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Themed Issue Papers |
1 Graduate School of Engineering Science2 School of Health and Sport Sciences, Osaka University, Toyonaka, Japan 3 Institute of Health Science, Kyushu University, Kasuga, Japan
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(Received 27 July 2005;
accepted after revision 4 October 2005; first published online 6 October 2005)
Corresponding author N. Hayashi: Institute of Health Science, Kyushu University, 6-1 Kasuga-Kouen, Kasuga, Fukuoka, 816-8580, Japan. Email: naohayashi{at}ihs.kyushu-u.ac.jp
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Introduction |
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Recent studies have demonstrated that the function of the EPR is altered in heart failure, contributing to the abnormal cardiovascular response to exercise in rats (Li et al. 2004; Smith et al. 2003, 2005), dogs (Hammond et al. 2000) and humans (Middlekauff et al. 2004; Momen et al. 2004). The advantages of using rats are: (1) that the mechanically and metabolically sensitive components of the EPR can be isolated; (2) that the EPR can be stimulated in the absence of input from central command; (3) that cellular and molecular techniques not available in larger animals and humans are readily available; and (4) that models of human disease are readily available. However, this species had been little used in studies of the EPR till recently. This is because of the previous conflicting data in anaesthetized rats, in which activation of the EPR has been shown to elicit both a pressor (Ishide et al. 2002) and depressor response (Smith et al. 2001; Hayashi, 2003; Plowey & Waldrop, 2004) or no response at all (Vissing et al. 1991). These discrepancies could be due to an unknown effect of anaesthesia in this species (Smith et al. 2001; Hayashi, 2003). Smith et al. (2001) and Hayashi (2003) established a non-anaesthetized and decerebrated rat model and reported that the activation of the EPR by static muscle contraction increased blood pressure in this model (Smith et al. 2001; Hayashi, 2003), which is consistent with the data obtained in other species (Coote et al. 1971; McCloskey & Mitchell, 1972; Victor et al. 1988; Matsukawa et al. 1992; Wilson et al. 1994; Potts & Mitchell, 1998; Kramer & Waldrop, 2001). However, to date there have been no studies determining the sympathetic response to activation of the EPR in this model. Moreover, the role played by the sympathetic nervous system in regulation of the peripheral circulation has not been clarified. Thus, determination of the sympathetic and circulatory responses to activation of the EPR in the decerebrate rat model should provide information that can be used to improve our understanding of circulatory control during exercise in both health and disease.
In the present study, the decerebrate rat model was used to investigate renal sympathetic and circulatory responses mediated by the EPR. We focused on the kidneys because these organs receive about 20% of the cardiac output in resting humans (Rowell, 1986). In anaesthetized cats, it was reported that EPR increases renal sympathetic nerve activity (RSNA) and induces renal vasoconstriction (Victor et al. 1988; Matsukawa et al. 1992). We examined renal sympathetic and circulatory responses to static contraction of the triceps surae muscles in the decerebrate rat model described by Hayashi (2003). We also examined these responses to passive stretch of the muscles. Static contraction activates the EPR (both the muscle metabo- and mechanoreflexes), whereas passive stretch activates only mechanically sensitive muscle components of the EPR (Kaufman et al. 1983; Stebbins et al. 1988; Victor et al. 1988; Kaufman & Forster, 1996). In addition, renal circulatory responses were compared before and after renal denervation to assess the role of renal innervation.
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Methods |
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All experimental procedures were approved by the Research Ethic Committee of School of Health and Sport Sciences, Osaka University, and were conducted in accordance with the Guiding Principles in the Care and Use of Animals in the Fields of Physiological Sciences published by the Physiological Society of Japan. Male Sprague–Dawley rats (7–9 weeks old, weighing 250–350 g) were anaesthetized by inhalation of a mixture of halothane (< 4%) and oxygen. The trachea was cannulated, and the lungs were artificially ventilated with a ventilator (SN-480-7, Shinano, Tokyo, Japan). The left jugular vein and common carotid artery were cannulated for administration of drugs and recording of arterial blood pressure (AP), respectively. The carotid catheter was attached to a pressure transducer (P23XL-1, Ohmeda, Madison, WI, USA). Arterial pH was measured at 30 min intervals with a pH meter (B-212, Horiba, Kyoto, Japan), and was maintained within normal limits by infusing sodium bicarbonate solution (1M) intravenously or by changing the artificial ventilation minute volume. Needle electrodes were positioned on the back to record electrocardiogram (ECG). The ECG signal was amplified with a differential amplifier (AB-621G, Nihon Kohden, Tokyo, Japan). Heart rate (HR) was calculated beat to beat by detecting the time between successive R waves in the ECG. Body temperature was maintained adequately with a heating lamp. The rat was placed in a stereotaxic apparatus (ST-7, Narishige, Tokyo, Japan).
To record RSNA, the left kidney was exposed retroperitoneally through a left flank incision. The bundle of the renal nerve fibres was carefully dissected from other connective tissues. A piece of laboratory film was placed under the isolated bundle, and two tips of a bipolar electrode were placed between the nerve bundle and the film. The nerve bundle and the electrode tips were embedded in silicon gel. Once the gel had hardened, the silicon rubber was fixed to the surrounding tissue with a glue containing 
-cyanoacrylate. The third tip of the electrode, which served as an earth electrode, was attached to the adipose tissue near the nerve. A pool was formed around the nerve with laboratory film and filled with mineral oil. RSNA was confirmed by observing the decrease and increase in response to intravenous injection of phenylephrine (5 µg) and nitroprusside (5 µg), respectively. The RSNA signal was amplified with a differential amplifier (MEG2100, Nihon Kohden) with a band-pass filter of 150 Hz in low-cut frequency and of 1 kHz in high-cut frequency, and made audible. The left renal cortical blood flow (RCBF) was recorded with a laser-Doppler flowmetry with a needle-type probe (ALF21, Advance, Tokyo, Japan), which measures blood flow within a radius of 1 mm from the tip of the probe. The probe was placed and stabilized vertically on the dorsal surface of the kidney.
The left triceps surae muscles were isolated, and the left Achilles tendon was isolated by cutting the calcaneus bone. The left peroneal nerve was cut from the sciatic nerve. The common tibial nerve was carefully dissected and then placed on a shielded bipolar electrode connected to a stimulator (SEN-7203, Nihon Kohden) with an isolator (SS-202 J, Nihon Kohden). The electrode was stabilized with silicon gel, and the surgical opening was filled with warm mineral oil. The tension generated by the triceps surae muscles was recorded with a force transducer (TB-611T, Nihon Kohden) connected to the Achilles tendon. The hindlimb was fixed in space with a patellar precision clamp to prevent limb movement.
Decerebration at the mid-collicular level was performed according to the method described by Hayashi (2003). Dexamethasone (0.2 mg) was administered intravenously to minimize oedema. Immediately before decerebration, the right carotid artery was occluded permanently to reduce bleeding in the brain. The upper skull and dura matter were removed, and then cerebral tissue was removed by aspiration. The brain was then sectioned vertically with a blade at the mid-collicular level. All neural tissues rostral to the section as well as the cerebral tissues covering the cerebellum were aspirated. Small pieces of cotton gauze were set in the cranial vault to control bleeding, after which the halothane anaesthesia was withdrawn. The cranial vault was filled with agar. To replace the blood lost during decerebration (approximately < 1 ml), saline was given intravenously in an amount sufficient to maintain basal AP. Before the experiments, a recovery period of 90 min was allowed to eliminate the effects of anaesthesia and to stabilize the preparation.
Experimental protocols
The rat was stabilized in sternal recumbency. Before experimental protocols, the motor threshold (MT), which is the minimum current intensity necessary to evoke twitching of the triceps surae muscles, was determined by electrical stimulation of the tibial nerve with a pulse duration of 30 µs. The muscles were stretched to create a baseline tension of 30–50 g. After collecting 30 s of baseline data, static contraction of the triceps surae muscles for 30 s was evoked by electrical stimulation of the tibial nerve (30 Hz, 30 µs pulse duration, 2 x MT) in the spontaneously breathing decerebrate rat. This stimulation intensity did not activate the tibial afferents directly, since no response occurred during stimulation in the paralysed (vecuronium bromide, 0.03 mg kg–1) and artificially ventilated rat (Hayashi, 2003). Passive stretch of triceps surae muscles for 30 s was also evoked by mechanically stretching the left Achilles tendon at the same tension as the static contraction. In cases in which contraction or stretch made the rat move reflexively, the data were discarded.
To separate neural and non-neural components of the RCBF response to static contraction or passive stretch, the protocols were also performed in renal denervated (RD) rats. Left renal denervation was performed by cutting all nerves that could be visualized. In cases in which rats used in the control (CON) trial were also used in the RD trial, the animals were re-anaesthetized with a mixture of halothane (1%) and oxygen. After renal denervation, a recovery period of 90 min was allowed.
At the end of data collection, the left tibial nerve was cut distal to the electrode and electrically stimulated to ensure that the observed responses to static contraction were not due to direct stimulation of muscle afferents. In cases in which this stimulation increased AP, the data were discarded.
After all protocols, the rat was killed with an intravenous anaesthetic overdose (pentobarbitone sodium, 100 mg kg–1), and the background noise of RSNA and artifacts of RCBF were recorded.
Data acquisition and statistical analyses
AP, ECG, HR, RSNA, RCBF and tension generated by the triceps surae muscles were displayed continuously on a computer monitor and stored on hard disk by analog-to-digital conversion (Powerlab/8s, AD Instruments, Sydney Australia) at a sampling rate of 1 kHz. AP and HR were recorded in all rats (n = 33). The reflex responses to static contraction before renal denervation were investigated in 17 CON rats. RCBF was recorded in six rats, RSNA in six rats, and both RCBF and RSNA were recorded in five of these rats. The reflex circulatory responses to static contraction after renal denervation were investigated in 12 RD rats. Three of these rats were used for the RD protocol after the CON trial. The reflex responses to passive stretch before renal denervation were investigated in 20 CON rats. RCBF was recorded in five rats, RSNA in nine, and both RCBF and RSNA were recorded in six of these rats. The reflex circulatory responses to passive stretch after renal denervation were investigated in 13 RD rats. Four of these rats were used for the RD protocol after the CON trial. The reason why there is a discrepancy in the numbers of rats used is because some of the data were discarded if: (1) there was a vital change in the rat during the measurements; (2) muscle stimulation evoked spontaneous motor activity; or (3) electrical stimulation of the tibial nerve increased AP after cutting the nerve distal to the electrode.
Electrical artifacts of RCBF, which were less than 5% of the recorded RCBF at baseline, were subtracted from the recorded RCBF. Mean AP (MAP), HR and RCBF were calculated beat by beat and then averaged over every 1 s. The returned absolute value of the recorded RSNA was integrated by 1 s and subtracted by the 1 s integrated background noise. In RSNA and RCBF, the recorded absolute valude at steady state varied among rats. To quantify the RSNA and RCBF responses to contraction or stretch, relative changes from baseline were determined by taking the means of the values during the prestimulation period for 30 s. These values were considered to be 100% of baseline. Renal cortical vascular conductance (RCVC) was obtained by dividing RCBF by MAP, and the relative changes from baseline were quantified in the same way as for RSNA and RCBF.
The data are expressed as means ± S.E.M. Basal MAP and HR were determined by analysing 30 s of data immediately before the onset of the muscle stimulation. The baseline data between trials were compared by Student's unpaired t test. The reflex responses to static contraction or passive stretch were analysed statistically by two-way analysis of variance (ANOVA), to evaluate the effects of the muscle stimulation on the differences between the responses and baseline, and to evaluate the effects of renal denervation on the responses during contraction or stretch. Where significant F ratios were found by the ANOVA, post hoc analysis was performed with Tukey's procedure. The level of statistical significance was set at P < 0.05.
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Figure 1 shows examples of developed tension in triceps surae muscles, AP, HR, RCBF, RCVC, RSNA and 1 s integrated RSNA before and during left tibial nerve stimulation (2 x MT) in a CON rat (Fig. 1A) and a RD rat (Fig. 1C). The detailed data of RSNA before and during the stimulation are shown in Fig. 1B). In both rats, the stimulation generated muscle tension and increased AP and HR. In the CON rat, the stimulation did not induce marked changes in RCBF, but increased RSNA and decreased RCVC. In contrast, the stimulation increased RCBF and did not change RCVC in the RD rat. Figure 2 shows examples of developed tension in triceps surae muscles, AP, HR, RCBF, RCVC, RSNA and 1 s integrated RSNA before and during passive stretch of the Achilles tendon in a CON rat (Fig. 2A) and a RD rat (Fig. 2C). The developed tension was set at a similar level as that during static contraction. The detailed data of RSNA before and during the stretch are shown in Fig. 2B). The stretch increased AP and HR in both rats. In the CON rat, the stretch did not change RCBF, but increased RSNA and decreased RCVC. In contrast, the stretch increased RCBF and did not change RCVC in the RD rat.
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Discussion |
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Recent studies have investigated the effects of congestive heart failure (CHF) or disuse atrophy on the pressor response to activation of the EPR by using the decerebrate rat model. CHF increases the pressor response to activation of the EPR (Smith et al. 2003), and the exaggerated response is based on an enhanced muscle mechanoreflex (Smith et al. 2003; Li et al. 2004) and an attenuated muscle metaboreflex (Li et al. 2004; Smith et al. 2005). Disuse atrophy enhances the muscle mechanoreflex (Hayashi et al. 2005). These findings suggest that the diseases plastically change the nature of the neural arc of the EPR and then alter cardiovascular regulation during exercise through the arc. There have been no previous studies in which the sympathetic response to activation of the EPR in the decerebrate rat model has been investigated. The present study, in which we recorded sympathetic nerve activity in decerebrate rats, should provide an appropriate and useful model for investigating issues regarding the role played by the EPR in cardiovascular regulation during exercise in both health and disease. Furthermore, cellular and molecular tools not available in larger animals and humans may be used in this rat model.
The present observations of sympathetically mediated renal cortical vasoconstriction during the EPR or the muscle mechanoreflex support the results of previous studies in cats and humans. In anaesthetized cats, activation of the EPR both by static contraction or the muscle mechanoreflex by passive stretch of the triceps surae muscles increased RSNA and induced renal vasoconstriction (Matsukawa et al. 1992). In humans, renal vasoconstriction occurred during static handgrip exercise as well as during postexercise ischaemia (activation of the muscle metaboreflex; Middlekauff et al. 1997; Momen et al. 2003). In addition, involuntary biceps muscle contraction evoked by percutaneous electrical stimulation induced renal vasoconstriction within a few seconds from the onset of contraction, suggesting that the muscle mechanoreflex also induces renal vasoconstriction (Momen et al. 2003).
Although the present findings were consistent with those of a previous study in anaesthetized cats (Matsukawa et al. 1992), there is a conflict in that static muscle contraction significantly decreased renal blood flow (velocity) in anaesthetized cats (Matsukawa et al. 1992), whereas the muscle stimulation did not affect RCBF in the decerebrate rats. This may be due to species differences and/or the presence of anaesthesia. Moreover, the magnitude of activation of the EPR may also be different between the two studies. The developed tension in triceps surae muscles was relatively greater per animal weight in the previous study (Matsukawa et al. 1992) compared with the present study. Thus, the activation of the EPR in the present study may be less than in the previous study and may not be great enough to reduce RCBF.
The developed tension in static muscle contraction was small compared to another study using decerebrate rats (Smith et al. 2001). We can point out several differences in the procedures to evoke muscle contraction between the two studies: electrically stimulated nerves (ventral root and tibial nerves), stimulus parameter used to evoke contraction, the age and size of the animals, the position of the animals during muscle contraction and/or the preload tension prior to contraction.
By the use renal denervation, the decreases in RCVC during contraction or stretch were abolished, whereas the pressor response was not changed. In RD rats, vessels in organs other than the kidney might have been constricted more powerfully than in CON rats, compensating the pressor response to contraction or stretch. However, it is unclear whether this hypothetical mechanism exists.
The significant increases in HR response to activation of the EPR or the muscle mechanoreflex were abolished by renal denervation. The reason for the abolishment of the increase in HR is unclear. A possibility is that the denervation might also have abolished the nerve activity to the adrenal medulla. Muscular activity increases the secretion of adrenaline from the adrenal medulla, possibly due to adrenal sympathetic activation (Nishiyasu et al. 1998; Vissing et al. 1991), which is known to increase heart rate (Motomura et al. 1990).
The method used for decerebration in the present model left appropriate brainstem medullary sites intact necessary to mediate reflex responses to muscle contraction (Hayashi, 2003). Neuroanatomical and electrophysiological studies suggested that intact sites, such as nucleus tractus solitarii, rostral ventrolateral medulla (RVLM) and lateral tegmental field, receive input from afferents responsive to muscle contraction (Bauer et al. 1990; Iwamoto & Waldrop, 1996; Li et al. 1998; Toney & Mifflin, 2000). Neurones in the RVLM innervate preganglionic sympathetic nerves in the spinal cord monosynaptically and are responsible for basal sympathetic discharge (Sved et al. 2001). The activation of the RVLM during contraction and stretch would have contributed to increases in RSNA and renal sympathetic vasoconstriction in the present study.
In summary, to investigate the role played by the EPR in sympathetic regulation of the renal circulation in rats, we examined renal sympathetic and circulatory responses to static contraction of the triceps surae muscles in the decerebrate rat model. Static contraction increased AP, HR and RSNA and decreased RCVC. Likewise, passive stretch of the muscles induced similar responses. Renal denervation abolished the decreases in RCVC during contraction and stretch. We conclude that both the exercise pressor reflex and its mechanically sensitive component, the muscle mechanoreflex, induce renal cortical vasoconstriction through sympathetic activation in rats. The present experimental set-up, in which we recorded sympathetic nerve activity in decerebrate rats, should provide an effective approach for answering important issues regarding the function of the EPR in both health and disease.
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Acknowledgements |
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Author's present address
T. Yoshida: Graduate School of Medicine, Osaka University, Japan. S. Koba: Pennsylvania State University College of Medicine, USA.
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