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Review Article |
1 Baker Heart Research Institute, Melbourne, Victoria, Australia
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Abstract |
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(Received 20 December 2006;
accepted after revision 14 February 2007; first published online 15 February 2007)
Corresponding author D. N. Mayorov: Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia. Email: dmitry.mayorov{at}baker.edu.au
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Introduction |
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TopAbstractIntroductionReferences |
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Given that a wide variety of AT1 receptor signalling pathways exists in neurones (Richards et al. 1999; Sumners et al. 2002), the precise molecular mechanisms that underlie central cardiovascular actions of Ang II during emotional stress remain to be determined. Growing evidence, however, indicates that reactive oxygen species (ROS), and in particular superoxide (·O2–) and hydrogen peroxide, are important intracellular messengers of many of the actions of Ang II (Griendling & Ushio-Fukai, 2000; Zimmerman et al. 2002). This review summarizes current knowledge of central redox-sensitive mechanisms underlying the pressor effect of emotional stress. Additionally, it presents initial evidence that ·O2– may be less important in the activation of central pressor pathways that mediate autonomic cardiovascular arousal associated with appetitive events, such as food anticipation and feeding.
The role of ·O2– in the excitatory actions of exogenous brain Ang II
It is well established that ROS are important intracellular messengers of many physiological and pathological effects of circulating Ang II (Griendling & Ushio-Fukai, 2000). Growing evidence also indicates that ROS are critically involved in the excitatory actions of brain Ang II. Firstly, Ang II increased ·O2– production and neuronal firing rate in neuronal cell cultures (Zimmerman et al. 2002; Sun et al. 2005) and in the hypothalamus and brainstem of rats (Erdos et al. 2006). These effects were prevented by losartan, indicating a role for AT1 receptors in activating redox-sensitive pathways in neurones (Zimmerman et al. 2002; Sun et al. 2005). Secondly, the adenoviral vector-mediated overexpression of ·O2– dismutase (SOD) abolished the pressor effects of I.C.V. Ang II in mice (Zimmerman et al. 2002). Thirdly, I.C.V. administration of SOD mimetics attenuated sympathoexcitatory responses to central Ang II in rabbits with chronic heart failure (CHF) and in rats (Gao et al. 2004; Lu et al. 2004; Campese et al. 2005). Finally, tempol markedly attenuated the Ang II-induced increase in neuronal firing rate in primary cultures from the hypothalamus and brainstem (Sun et al. 2005).
We have recently conducted a series of experiments to examine the role of ·O2– in the actions of exogenous Ang II in the rostral ventrolateral medulla (RVLM) of conscious rabbits. This brain region forms a final common pathway for sympathoactivation (Dampney, 1994) and, as such, is critical for the regulation of the cardiovascular stress response (Pezzone et al. 1993; Jansen et al. 1995; Mayorov & Head, 2002). Additionally, the RVLM is a major site of the sympathoexcitatory action of Ang II in various species (Sasaki & Dampney, 1990; Averill et al. 1994; Fontes et al. 1997). Microinjection of a SOD mimetic, tempol, markedly attenuated the pressor response to Ang II in the RVLM (Fig. 1), without altering resting cardiovascular parameters (Mayorov et al. 2004). Conversely, local microinjection of 3-carbamoyl proxyl (3-CP), which is structurally close to tempol but has a much lower ·O2– scavenging capacity (Krishna et al. 1992), did not alter the response to Ang II. However, a ·O2– scavenger, tiron, which is not chemically related to tempol, but has a similar ·O2– scavenging activity (Mok et al. 1998), mirrored the effect of tempol on the pressor response to Ang II (Fig. 1). These data suggest that the ·O2– scavenging capacity of tempol and tiron is critical for the expression of their inhibitory effects. Likewise, microinjection of tempol into the RVLM markedly attenuated the pressor effect of local injection of Ang II, while 3-CP was much less efficient in blocking this effect in rats (Chan et al. 2005).
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The role of ·O2– in the central regulation of cardiovascular stress response
Given that brain Ang II has recently emerged as an important stress hormone (Yang et al. 1996; Saavedra et al. 2004), and that the activation of AT1 receptors in the hypothalamus and RVLM is required for full expression of the cardiovascular response to emotional stress (Kubo et al. 2001; Mayorov & Head, 2003), it is plausible that local ROS may underlie, at least in part, the excitatory actions of Ang II during stress. To test this hypothesis, we have recently conducted a series of experiments using bilateral microinjections of ·O2– scavengers directly into the RVLM of conscious rabbits and a model of mild emotional stress in animals, air-jet stress (Mayorov et al. 2004). These studies have shown that administration of tempol or tiron into the RVLM, but not into nearby medullary regions, markedly attenuated the pressor, tachycardic and renal sympathoexcitatory responses to air-jet stress (Fig. 2). This decrease could not be attributed to changes in basal parameters because resting BP, HR or renal sympathetic nerve activity (RSNA) remained unaltered. Local microinjection of 3-CP did not change the stress response, further indicating that the observed effects of tempol and tiron are likely to relate to the ·O2– scavenging capacity of these agents.
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In regard to stress response, similar intrinsic links between Ang II and ·O2– may also exist in other brain regions controlling autonomic and neuroendocrine outputs to the periphery. Among these regions, the dorsomedial hypothalamus (DMH) appears to be of primary importance in the regulation of the fight-or-flight response (Stotz-Potter et al. 1996; Lowry et al. 2003; McDougall et al. 2004; De Matteo et al. 2006a). Recent evidence also suggests that, within the DMH, AT1 receptors play an essential role in modulating the cardiovascular and behavioural components of this response. Firstly, microinjection of a selective AT1 antagonist, candesartan, into this region attenuated the pressor and tachycardic effects of air-jet stress in rabbits in a dose-dependent manner (De Matteo et al. 2006a). Secondly, AT1 receptor blockade in the DMH distinctly reduced the anxiety-like and cardiovascular components of sodium lactate-induced panic-like responses in ‘panic-prone’ rats (Shekhar et al. 2006). In the same hypothalamic region, administration of tempol or tiron markedly decreased the cardiovascular effects of air-jet stress (De Matteo et al. 2006b), indicating that local ·O2– is critically implicated in the regulation of the fight-or-flight response. It should be noted, however, that although these observations indicate that the AT1 receptor and ·O2– are involved in the regulation of stress response in the DMH, conclusive evidence that both substances activate the same signalling pathway is yet to be provided.
Does ·O2– modulate cardiovascular reactivity via a non-specific inactivation of nitric oxide?
It is well known that ·O2– can avidly react with and inactivate nitric oxide (NO) in vascular tissues, leading to functional NO deficiency, widespread accumulation of protein nitration products and cardiovascular abnormalities. It is possible that a similar interaction might also occur at the CNS level, and the observed effects of ·O2– scavengers in the RVLM on the stress response (Mayorov et al. 2004) might in fact be mediated by a NO deficit. Indeed, several observations suggest that NO exerts a predominantly excitatory action in the RVLM of conscious rabbits. Firstly, administration of NO donors into the RVLM increased BP in a dose-dependent manner (Mayorov, 2005). Secondly, microinjection of NO itself into the RVLM evoked a distinct, dose-dependent increase in BP (Mayorov, 2005). Finally, administration of a NO synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), but not its inactive enantiomer D-NAME, attenuated the RSNA baroreflex gain (i.e. the sympathoexcitatory response to a given decrease in BP), indicating an excitatory role of endogenous NO in modulating this reflex (Mayorov, 2005). These results are in line with several previous findings that NO donors, unless given in high doses, evoke neuronal excitation in the RVLM (Hirooka et al. 1996; Martins-Pinge et al. 1997; Morimoto et al. 2000; Chan et al. 2001).
The NO inactivation by ·O2– per se may thus explain the attenuation of the stress response. However, the interaction of ·O2– with NO in the RVLM appears not to be essential for expression of its facilitatory effect on the cardiovascular response to emotional stress. Firstly, local administration of L-NAME, at doses that inhibited baroreflex transmission, did not affect the pressor response to local injection of Ang II (Fig. 1) or to air-jet stress (Mayorov et al. 2004; Mayorov, 2005). Secondly, co-microinjection of L-NAME and tempol into the RVLM elicited the same attenuation of the pressor response to stress as did tempol alone. The lack of the effect of NOS inhibition on the pressor response to stress cannot be attributed to insufficient exposure to stress or to an inadequate dose of L-NAME used. Indeed, co-microinjection of L-NAME and tempol into this region abolished an attenuation in the stress-induced tachycardia observed after local injection of tempol alone (Mayorov et al. 2004). Remarkably, in the same experimental model, AT1 receptor blockade in the RVLM decreased the pressor, but not tachycardic response to air-jet stress (Mayorov & Head, 2003). These findings suggest that the HR component of stress response may be regulated in the RVLM by a NO-sensitive mechanism that is independent of local AT1 receptors and ·O2–. However, there is little evidence that NO is essential for the manifestation of the acute cardiovascular response to emotional stress in the RVLM of rabbits.
The enzymatic sources of the stress-induced ·O2– production in the brain
Exact subcellular mechanisms by which ROS can modulate neuronal activity in the brain are currently an area of intensive investigation. The major enzymatic sources of ·O2– generation in the brain include NADPH oxidase, xanthine oxidase, mitochondrial respiration and uncoupled NOS (Pou et al. 1992; Atlante et al. 2001; Wang et al. 2004; Gao et al. 2005). Accumulating evidence indicates that NADPH oxidase is a key source of the Ang II-stimulated ·O2– production in the brain, similar to its role in the Ang II-induced ·O2– generation in vascular tissues (Griendling et al. 2000b). Firstly, administration of NADPH inhibitors, diphenyleneiodonium chloride (DPI) and apocynin, into the RVLM or brain ventricles attenuated the pressor response to Ang II in rats (Chan et al. 2005; Erdos et al. 2006). Secondly, microinjection of DPI or antisense oligonucleotides to p22phox or p47phox subunit of NADPH oxidase into the RVLM partly prevented the Ang II-induced increase in local ·O2– production (Chan et al. 2005). Thirdly, extracellular application of a selective NADPH oxidase inhibitor, gp91ds-tat, decreased by half the Ang II-induced increase in neuronal firing in primary cultures from the hypothalamus and brainstem (Sun et al. 2005). Finally, adenoviral-mediated expression of a dominant-negative isoform of Rac1, a critical component for NADPH oxidase activation and ·O2– production, inhibited the Ang II-induced influx of extracellular Ca2+ in neurones (Zimmerman et al. 2005).
It is plausible that NADPH oxidase also produces ·O2– in response to endogenously released Ang II or other stress mediators because bilateral microinjection of apocynin into the RVLM markedly attenuated the pressor and tachycardic response to air-jet stress, without altering resting haemodynamic parameters in rabbits (Fig. 3). Apart from acute settings, NADPH oxidase may be important in the AT1 receptor-dependent regulation of ·O2– levels in chronic conditions, such as hypertension or CHF. For instance, it has been shown that elevated ·O2– levels in the RVLM of rabbits with CHF are accompanied by increases in mRNA and protein expression of AT1 receptor and p40phox, p47phox, and gp91phox subunits of NADPH oxidase (Gao et al. 2004). The contribution of other subcellular sources of ·O2– generation in the RVLM in response to acute and chronic stress is yet to be determined. Little effect of microinjection of L-NAME into the RVLM on the pressor response to air-jet stress (Mayorov et al. 2004) suggests, however, that one putative source of ·O2–, uncoupled NOS, is unlikely to be critical in ·O2– production in this region during acute stress.
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It is well established that ROS can influence multiple intracellular signalling events by activating receptor and non-receptor tyrosine kinases, inhibiting protein tyrosine phosphatases, and regulating redox-sensitive transcription factors and intracellular Ca2+ homeostasis (Gelband et al. 1997; Griendling et al. 2000a). In particular, it has been shown that ROS mediate Ang II stimulation of important intracellular signals, such as mitogen-activated protein kinases (MAPKs), including p38 MAPK and p42/44 MAPK. In particular, it has been shown that microinjection of Ang II into the RVLM resulted in AT1 receptor-dependent phosphorylation (activation) of p38 MAPK and p42/44 MAPK via a redox-sensitive, NADPH oxidase-dependent mechanism (Chan et al. 2005). Conversely, inhibition of MAPKs abolished the stimulatory effect of Ang II on noradrenaline reuptake in neuronal cultures from the hypothalamus and brainstem (Yang & Raizada, 1998), and markedly attenuated the pressor effect of Ang II in the RVLM of rats (Seyedabadi et al. 2001; Chan et al. 2005). It is noteworthy that in the study by Seyedabadi et al. (2001), the pressor response to glutamate remained unaltered, indicating that the effects of MAPK inhibition could not be attributed to non-specific changes in neuronal excitability in the RVLM.
The role of MAPKs, in presympathetic brain areas, in the regulation of cardiovascular stress responses is yet to be determined. However, it has been reported that repeated restraint stress activated p42/44 MAPK in the rostral ventromedial medulla, an essential part of the descending pain modulation system in rats (Imbe et al. 2004). Moreover, accumulating evidence indicates that various psycho- and physicoemotional stressors, including social threat, novel cage, air-jet and tail-shock stress, produce robust activation of p38 MAPK and/or p42/44 MAPK in the hippocampus, cortex and cerebellum of mice, rats and rabbits (Zhen et al. 2001; Yang et al. 2004; Murphy et al. 2005; Pardon et al. 2005). These findings suggest that MAPK activation may represent an early neural event in the initiation of behavioural, neuroendocrine and autonomic stress responses. However, the functional importance of MAPKs in the regulation of stress responses remains elusive, as does the role of central Ang II and ·O2– in the stress-induced MAPK activation.
The role of brain ·O2– in cardiovascular arousal associated with positive affect
Apart from aversive emotional events, appetitive stimuli are capable of inducing a prompt, sympathetically mediated rise in BP and HR in animal models (Del Bo et al. 1985; Braesicke et al. 2005). Similarly, activated positive emotions are associated with increased BP and HR in humans (Pressman & Cohen, 2005). Anticipation and eating palatable food is one of the most well-studied models of appetitive or positively motivated behaviour in animals (Randall et al. 1985; Reynolds & Berridge, 2002; Valdes et al. 2005). In particular, it is well established that food presentation and feeding are normally accompanied in animals by distinct increases in BP, HR and sympathetic activity (Del Bo et al. 1985; Matsukawa & Ninomiya, 1985; Diamond & LeBlanc, 1987; Valdes et al. 2005). This feeding-associated arousal is initiated by activation of descending inputs from higher CNS centres rather than viscero-sympathetic reflexes resulting from food intake (Matsukawa & Ninomiya, 1985; Diamond & LeBlanc, 1987; Matsukawa & Ninomiya, 1987). One of these descending inputs is likely to originate from the DMH, which forms a critical part of CNS circuits controlling food intake and energy balance (Bellinger & Bernardis, 2002). This possibility is supported by our recent findings that chemical stimulation of the DMH with a glutamate analogue, kainic acid, evoked hypertension, tachycardia and a vigorous drive to eat in rabbits (De Matteo et al. 2006a). Conversely, pharmacological blockade of glutamate receptors in the DMH with kynurenic acid attenuated cardiovascular responses to feeding, without altering eating behaviour (interest in food). Thus, apart from its role in the cardiovascular defence response, the DMH is likely to be important in mediating autonomic arousal associated with appetitive stimuli.
Unexpectedly, we found that the pressor and tachycardic response to feeding was not altered by AT1 receptor blockade in the DMH of rabbits (De Matteo et al. 2006a). Likewise, microinjection of the ·O2– scavengers tempol and tiron into the DMH did not attenuate the cardiovascular response to feeding (Mayorov et al. 2005), which was in contrast to their inhibitory effects on the stress response (De Matteo et al. 2006b). Thus, neither Ang II nor ·O2– in the DMH appears to be essential for cardiovascular arousal associated with appetitive feeding behaviour. Given that feeding behaviour is a key determinant of circadian rhythms of BP, HR and locomotor activity in the rabbit (Van den Buuse & Malpas, 1997), it is possible that redox regulation of AT1 receptor signalling also plays little role in cardiovascular arousal associated with circadian rhythms of wakefulness and physical activity. Taken together, the above data suggest that the redox-sensitive component of AT1 receptor signalling may be intrinsically linked to the activation of central pathways regulating the fight-or-flight response, but not to pressor responses to non-aversive arousing stimuli. However, further studies are clearly necessary to validate this possibility.
Summary
Evidence suggests that brain ·O2– is required for full expression of the acute cardiovascular response to psychoemotional stress. Within the DMH and RVLM, the AT1 receptor–·O2– signalling cascades are primarily associated with pressor pathways that regulate the sympathetic cardiovascular component of the fight-or-flight response. By contrast, ·O2– may be less important in the activation of central pressor pathways that mediate autonomic cardiovascular arousal associated with appetitive events, such as food anticipation and feeding. These findings may be of clinical significance because they suggest that targeted inhibition of the AT1 receptor–·O2– signalling pathway, in the brain, may selectively reduce cardiovascular reactivity to negative emotional stressors, and thus decrease the risk of hypertension and heart disease.
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References |
|---|
|
TopAbstractIntroductionReferences |
|---|
Atlante A, Calissano P, Bobba A, Giannattasio S, Marra E & Passarella S (2001). Glutamate neurotoxicity, oxidative stress and mitochondria. FEBS Lett 497, 1–5.[CrossRef][Medline]
Averill DB, Tsuchihashi T, Khosla MC & Ferrario CM (1994). Losartan, nonpeptide angiotensin II-type 1 (AT1) receptor antagonist, attenuates pressor and sympathoexcitatory responses evoked by angiotensin II and L-glutamate in rostral ventrolateral medulla. Brain Res 665, 245–252.[CrossRef][Medline]
Baltatu O, Campos LA & Bader M (2004). Genetic targeting of the brain renin-angiotensin system in transgenic rats: impact on stress-induced renin release. Acta Physiol Scand 181, 579–584.[CrossRef][Medline]
Bellinger LL & Bernardis LL (2002). The dorsomedial hypothalamic nucleus and its role in ingestive behavior and body weight regulation: lessons learned from lesioning studies. Physiol Behav 76, 431–442.[CrossRef][Medline]
Braesicke K, Parkinson JA, Reekie Y, Man MS, Hopewell L, Pears A, Crofts H, Schnell CR & Roberts AC (2005). Autonomic arousal in an appetitive context in primates: a behavioural and neural analysis. Eur J Neurosci 21, 1733–1740.[Medline]
Campese VM, Shaohua Y & Huiquin Z (2005). Oxidative stress mediates angiotensin II-dependent stimulation of sympathetic nerve activity. Hypertension 46, 533–539.
Carrasco GA & Van de Kar LD (2003). Neuroendocrine pharmacology of stress. Eur J Pharmacol 463, 235–272.[CrossRef][Medline]
Chan SH, Hsu KS, Huang CC, Wang LL, Ou CC & Chan JY (2005). NADPH oxidase-derived superoxide anion mediates angiotensin II-induced pressor effect via activation of p38 mitogen-activated protein kinase in the rostral ventrolateral medulla. Circ Res 97, 772–780.
Chan SHH, Wang LL, Wang SH & Chan JYH (2001). Differential cardiovascular responses to blockade of nNOS or iNOS in rostral ventrolateral medulla of the rat. Br J Pharmacol 133, 606–614.[CrossRef][Medline]
Cierco M & Israel A (1994). Role of angiotensin AT1 receptor in the cardiovascular response to footshock. Eur J Pharmacol 251, 103–106.[CrossRef][Medline]
Dampney RAL (1994). Functional organization of central pathways regulating the cardiovascular system. Physiol Rev 74, 323–364.
Del Bo A, Le Doux JE & Reis DJ (1985). Sympathetic nervous system and control of blood pressure during natural behaviour. J Hypertens 3 (Suppl. 3), S105–S106.
De Matteo R, Head GA & Mayorov DN (2006a). Angiotensin II in dorsomedial hypothalamus modulates cardiovascular arousal caused by stress but not feeding in rabbits. Am J Physiol Regul Integr Comp Physiol 290, R257–R264.
De Matteo R, Head GA & Mayorov DN (2006b). Tempol in the dorsomedial hypothalamus attenuates the hypertensive response to stress in rabbits. Am J Hypertens 19, 396–402.[CrossRef][Medline]
Diamond P & LeBlanc J (1987). Hormonal control of postprandial thermogenesis in dogs. Am J Physiol Endocrinol Metab 253, E521–E529.
Erdos B, Broxson CS, King MA, Scarpace PJ & Tumer N (2006). Acute pressor effect of central angiotensin II is mediated by NAD(P)H-oxidase-dependent production of superoxide in the hypothalamic cardiovascular regulatory nuclei. J Hypertens 24, 109–116.[Medline]
Esler M (1998). Stress, stressors and cardiovascular disease. In Repatriation Medical Authority Consensus Conference on Stress and Challenge – Health and Disease, ed. Morris P, Raphael B & Bordujenko A, pp. 198–206. Australian Government Repatriation Medical Authority Publications, Brisbane, Australia.
Esler MD, Thompson JM, Kaye DM, Turner AG, Jennings GL, Cox HS, Lambert GW & Seals DR (1995). Effects of aging on the responsiveness of the human cardiac sympathetic nerves to stressors. Circulation 91, 351–358.
Fontes MAP, Pinge MCM, Naves V, Campagnole-Santos MJ, Lopes OU, Khosla MC & Santos RAS (1997). Cardiovascular effects produced by microinjection of angiotensins and angiotensin antagonists into the ventrolateral medulla of freely moving rats. Brain Res 750, 305–310.[CrossRef][Medline]
Gao L, Wang W, Li YL, Schultz HD, Liu D, Cornish KG & Zucker IH (2004). Superoxide mediates sympathoexcitation in heart failure: roles of angiotensin II and NAD(P)H oxidase. Circ Res 95, 937–944.
Gao L, Wang W, Li YL, Schultz HD, Liu D, Cornish KG & Zucker IH (2005). Sympatho-excitation by central Ang II: The roles for AT1 receptor upregulation and NAD(P)H oxidase in the RVLM. Am J Physiol Heart Circ Physiol 288, H2271–H2279.
Gelband CH, Sumners C, Lu D & Raizada MK (1997). Angiotensin receptors and norepinephrine neuromodulation: implications of functional coupling. Regul Pept 72, 139–145.[CrossRef][Medline]
Goldstein DS (1995). Clinical assessment of sympathetic responses to stress. Ann N Y Acad Sci 771, 570–593.[Medline]
Griendling KK, Sorescu D, Lassègue B & Ushio-Fukai M (2000a). Modulation of protein kinase activity and gene expression by reactive oxygen species and their role in vascular physiology and pathophysiology. Arterioscler Thromb Vasc Biol 20, 2175–2183.
Griendling KK, Sorescu D & Ushio-Fukai M (2000b). NAD(P)H oxidase: role in cardiovascular biology and disease. Circ Res 86, 494–501.
Griendling KK & Ushio-Fukai M (2000). Reactive oxygen species as mediators of angiotensin II signaling. Regul Pept 91, 21–27.[CrossRef][Medline]
Hirasawa R, Hashimoto K & Ota Z (1990). Role of central angiotensinergic mechanism in shaking stress-induced ACTH and catecholamine secretion. Brain Res 533, 1–5.[CrossRef][Medline]
Hirooka Y, Polson JW & Dampney RA (1996). Pressor and sympathoexcitatory effects of nitric oxide in the rostral ventrolateral medulla. J Hypertens 14, 1317–1324.[CrossRef][Medline]
Huang BS & Leenen FH (1996). Brain ‘ouabain’ and angiotensin II in salt-sensitive hypertension in spontaneously hypertensive rats. Hypertension 28, 1005–1012.
Imbe H, Murakami S, Okamoto K, Iwai-Liao Y & Senba E (2004). The effects of acute and chronic restraint stress on activation of ERK in the rostral ventromedial medulla and locus coeruleus. Pain 112, 361–371.[CrossRef][Medline]
Jansen ASP, Nguyen XV, Karpitskiy V, Mettenleiter TC & Loewy AD (1995). Central command neurons of the sympathetic nervous system: basis of the fight-or-flight response. Science 270, 644–646.
Jezova D, Ochedalski T, Kiss A & Aguilera G (1998). Brain angiotensin II modulates sympathoadrenal and hypothalamic pituitary adrenocortical activation during stress. J Neuroendocrinol 10, 67–72.[CrossRef][Medline]
Kario K, McEwen BS & Pickering TG (2003). Disasters and the heart: a review of the effects of earthquake-induced stress on cardiovascular disease. Hypertens Res 26, 355–367.[CrossRef][Medline]
Kawazoe T, Kosaka H, Yoneyama H & Hata Y (2000). Acute production of vascular superoxide by angiotensin II but not by catecholamines. J Hypertens 18, 179–185.[CrossRef][Medline]
Krishna MC, Grahame DA, Samuni A, Mitchell JB & Russo A (1992). Oxoammonium cation intermediate in the nitroxide-catalyzed dismutation of superoxide. Proc Natl Acad Sci U S A 89, 5537–5541.
Kubo T, Numakura H, Endo S, Hagiwara Y & Fukumori R (2001). Angiotensin receptor blockade in the anterior hypothalamic area inhibits stress-induced pressor responses in rats. Brain Res Bull 56, 569–574.[CrossRef][Medline]
Lovallo WR & Gerin W (2003). Psychophysiological reactivity: mechanisms and pathways to cardiovascular disease. Psychosom Med 65, 36–45.
Lowry CA, Plant A, Shanks N, Ingram CD & Lightman SL (2003). Anatomical and functional evidence for a stress-responsive, monoamine-accumulating area in the dorsomedial hypothalamus of adult rat brain. Horm Behav 43, 254–262.[CrossRef][Medline]
Lu N, Helwig BG, Fels RJ, Parimi S & Kenney MJ (2004). Central Tempol alters basal sympathetic nerve discharge and attenuates sympathetic excitation to central ANG II. Am J Physiol Heart Circ Physiol 287, H2626–H2633.
McDougall SJ, Widdop RE & Lawrence AJ (2004). Medial prefrontal cortical integration of psychological stress in rats. Eur J Neurosci 20, 2430–2440.[CrossRef][Medline]
McDougall SJ, Widdop RE & Lawrence AJ (2005). Central autonomic integration of psychological stressors: focus on cardiovascular modulation. Auton Neurosci 123, 1–11.[CrossRef][Medline]
Martins-Pinge MC, Baraldi-Passy I & Lopes OU (1997). Excitatory effects of nitric oxide within the rostral ventrolateral medulla of freely moving rats. Hypertension 30, 704–707.
Matsukawa K & Ninomiya I (1985). Transient responses of heart rate, arterial pressure, and head movement at the beginning of eating in awake cats. Jpn J Physiol 35, 599–611.[Medline]
Matsukawa K & Ninomiya I (1987). Changes in renal sympathetic nerve activity, heart rate and arterial blood pressure associated with eating in cats. J Physiol 390, 229–242.
Mayorov DN (2005). Selective sensitization by nitric oxide of sympathetic baroreflex in rostral ventrolateral medulla of conscious rabbits. Hypertension 45, 901–906.
Mayorov DN & Head GA (2001). Influence of rostral ventrolateral medulla on renal sympathetic baroreflex in conscious rabbits. Am J Physiol Regul Integr Comp Physiol 280, R577–R587.
Mayorov DN & Head GA (2002). Ionotropic glutamate receptors in the rostral ventrolateral medulla mediate sympathetic responses to acute stress in conscious rabbits. Auton Neurosci 98, 20–23.[CrossRef][Medline]
Mayorov DN & Head GA (2003). AT1-receptors in the RVLM mediate pressor responses to emotional stress in rabbits. Hypertension 41, 1168–1173.
Mayorov DN, Head GA & De Matteo R (2004). Tempol attenuates excitatory actions of angiotensin II in the rostral ventrolateral medulla during emotional stress. Hypertension 44, 101–106.
Mayorov DN, Head GA & De Matteo R (2005). Brain angiotensin II and superoxide modulate the acute hypertensive response to emotional stress but not feeding. J Physiol 567.P, 20P.
Mok JS, Paisley K & Martin W (1998). Inhibition of nitrergic neurotransmission in the bovine retractor penis muscle by an oxidant stress: effects of superoxide dismutase mimetics. Br J Pharmacol 124, 111–118.[CrossRef][Medline]
Morimoto S, Sasaki S, Miki S, Kawa T, Nakamura K, Itoh H, Nakata T, Takeda K, Nakagawa M & Fushiki S (2000). Nitric oxide is an excitatory modulator in the rostral ventrolateral medulla in rats. Am J Hypertens 13, 1125–1134.[CrossRef][Medline]
Murphy ES, Harding JW, Muhunthan K, Holtfreter KL & Wright JW (2005). Role of mitogen-activated protein kinases during recovery from head-shake response habituation in rats. Brain Res 1050, 170–179.[CrossRef][Medline]
Pardon MC, Roberts RE, Marsden CA, Bianchi M, Latif ML, Duxon MS & Kendall DA (2005). Social threat and novel cage stress-induced sustained extracellular-regulated kinase1/2 (ERK1/2) phosphorylation but differential modulation of brain-derived neurotrophic factor (BDNF) expression in the hippocampus of NMRI mice. Neuroscience 132, 561–574.[CrossRef][Medline]
Pezzone MA, Lee WS, Hoffman GE, Pezzone KM & Rabin BS (1993). Activation of brainstem catecholaminergic neurons by conditioned and unconditioned aversive stimuli as revealed by c-Fos immunoreactivity. Brain Res 608, 310–318.[CrossRef][Medline]
Pou S, Pou WS, Bredt DS, Snyder SH & Rosen GM (1992). Generation of superoxide by purified brain nitric oxide synthase. J Biol Chem 267, 24173–24176.
Pressman SD & Cohen S (2005). Does positive affect influence health? Psychol Bull 131, 925–971.[CrossRef][Medline]
Rajagopalan S, Kurz S, Munzel T, Tarpey M, Freeman BA, Griendling KK & Harrison DG (1996). Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone. J Clin Invest 97, 1916–1923.[Medline]
Randall DC, Skinner TL & Billman GE (1985). A comparison of the autonomic nervous control of the heart during classical aversive vs appetitive conditioning in dog. J Auton Nerv Syst 13, 125–136.[CrossRef][Medline]
Reynolds SM & Berridge KC (2002). Positive and negative motivation in nucleus accumbens shell: bivalent rostrocaudal gradients for GABA-elicited eating, taste ‘liking’/‘disliking’ reactions, place preference/avoidance, and fear. J Neurosci 22, 7308–7320.
Richards EM, Raizada MK, Gelband CH & Sumners C (1999). Angiotensin II type 1 receptor-modulated signaling pathways in neurons. Mol Neurobiol 19, 25–41.[Medline]
Rozanski A, Blumenthal JA & Kaplan J (1999). Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 99, 2192–2217.
Saavedra JM, Ando H, Armando I, Baiardi G, Bregonzio C, Jezova M & Zhou J (2004). Brain angiotensin II, an important stress hormone: regulatory sites and therapeutic opportunities. Ann N Y Acad Sci 1018, 76–84.
Saiki Y, Watanabe T, Tan N, Matsuzaki M & Nakamura S (1997). Role of central ANG II receptors in stress-induced cardiovascular and hyperthermic responses in rats. Am J Physiol 272, R26–R33.[Medline]
Sasaki S & Dampney RAL (1990). Tonic cardiovascular effects of angiotensin II in the ventrolateral medulla. Hypertension 15, 274–283.
Seyedabadi M, Goodchild AK & Pilowsky PM (2001). Differential role of kinases in brain stem of hypertensive and normotensive rats. Hypertension 38, 1087–1092.
Shastri S, Gopalakrishnan V, Poduri R & Di Wang H (2002). Tempol selectively attenuates angiotensin II evoked vasoconstrictor responses in spontaneously hypertensive rats. J Hypertens 20, 1381–1391.[CrossRef][Medline]
Shekhar A, Johnson PL, Sajdyk TJ, Fitz SD, Keim SR, Kelley PE, Gehlert DR & DiMicco JA (2006). Angiotensin-II is a putative neurotransmitter in lactate-induced panic-like responses in rats with disruption of GABAergic inhibition in the dorsomedial hypothalamus. J Neurosci 26, 9205–9215.
Stotz-Potter EH, Willis LR & DiMicco JA (1996). Muscimol acts in dorsomedial but not paraventricular hypothalamic nucleus to suppress cardiovascular effects of stress. J Neurosci 16, 1173–1179.
Sumners C, Fleegal MA & Zhu MY (2002). Angiotensin At-1 receptor signalling pathways in neurons. Clin Exp Pharmacol Physiol 29, 483–490.[CrossRef][Medline]
Sun C, Sellers KW, Sumners C & Raizada MK (2005). NAD(P)H oxidase inhibition attenuates neuronal chronotropic actions of angiotensin II. Circ Res 96, 659–666.
Valdes JL, Farias P, Ocampo-Garces A, Cortes N, Seron-Ferre M & Torrealba F (2005). Arousal and differential Fos expression in histaminergic neurons of the ascending arousal system during a feeding-related motivated behaviour. Eur J Neurosci 21, 1931–1942.[CrossRef][Medline]
Van den Buuse M & Malpas SC (1997). 24-Hour recordings of blood pressure, heart rate and behavioural activity in rabbits by radiotelemetry: effects of feeding and hypertension. Physiol Behav 62, 83–89.[CrossRef][Medline]
Wang G, Anrather J, Huang J, Speth RC, Pickel VM & Iadecola C (2004). NADPH oxidase contributes to angiotensin II signaling in the nucleus tractus solitarius. J Neurosci 24, 5516–5524.
Watanabe T, Fujioka T, Hashimoto M & Nakamura S (1998). Stress and brain angiotensin II receptors. Crit Rev Neurobiol 12, 305–317.[Medline]
Yang CH, Huang CC & Hsu KS (2004). Behavioral stress modifies hippocampal synaptic plasticity through corticosterone-induced sustained extracellular signal-regulated kinase/mitogen-activated protein kinase activation. J Neurosci 24, 11029–11034.
Yang H & Raizada MK (1998). MAP kinase-independent signaling in angiotensin II regulation of neuromodulation in SHR neurons. Hypertension 32, 473–481.
Yang G, Wan Y & Zhu Y (1996). Angiotensin II – an important stress hormone. Biol Signals 5, 1–8.[Medline]
Zanzinger J & Czachurski J (2000). Chronic oxidative stress in the RVLM modulates sympathetic control of circulation in pigs. Pflugers Arch 439, 489–494.[CrossRef][Medline]
Zhen X, Du W, Romano AG, Friedman E & Harvey JA (2001). The p38 mitogen-activated protein kinase is involved in associative learning in rabbits. J Neurosci 21, 5513–5519.
Zimmerman MC, Lazartigues E, Lang JA, Sinnayah P, Ahmad IM, Spitz DR & Davisson RL (2002). Superoxide mediates the actions of angiotensin II in the central nervous system. Circ Res 91, 1038–1045.
Zimmerman MC, Sharma RV & Davisson RL (2005). Superoxide mediates angiotensin II-induced influx of extracellular calcium in neural cells. Hypertension 41, 1–7.[CrossRef]
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