| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Department of 1 Anesthesiology and Physiology, Medical College of Wisconsin2 Veterans Affairs Medical Center, Milwaukee, WI 53295, USA
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
1-antagonist prazosin (1.59 µM). Tension was decreased by the addition of the P2 antagonist PPADs (P < 0.05). Prazosin abolished tension at all constant frequencies (P < 0.05). P2 and 1-antagonism decreased tension with 8 and 30 Hz burst pattern field stimulation. However, the magnitude of decrease in tension with prazosin was less with burst patterns compared to the same average constant frequencies (P < 0.05). It appears that P2X receptors and 1-receptors in the femoral artery are sensitive to frequency and patterns of electrical stimulation.
(Received 12 June 2006;
accepted after revision 7 September 2006; first published online 14 September 2006)
Corresponding author P. S. Clifford: Anesthesia Research 151, Veterans Affairs Medical Center, Milwaukee, WI 53295, USA. Email: pcliff{at}mcw.edu
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Our understanding of how the complex patterns of natural neural activity code for different neurotransmitters is incomplete. Previous research suggests that sympathetic neurones fire in series of bursts with periods of interburst quiescence (Habler et al. 1993; Macefield & Wallin, 1999). These periods of quiescence do not appear to result in a loss of vasoconstriction (Nilsson et al. 1985; Hardebo, 1992); therefore, they may be a valuable part of the coding for different neurotransmitters. We created a series of stimulation patterns to test the relative importance of firing patterns on neurotransmitter-mediated vasoconstriction in the femoral artery. Burst patterns were designed to mimic common sympathetic neurone firing patterns (Macefield et al. 1999; Macefield & Wallin, 1999; Elam et al. 2003) during periods of increased sympathetic activity. As a comparison, vessels were also exposed to constant frequency stimulation, in which there is a consistent interval between each electrical impulse. The purpose of this study was: (1) to compare adrenergic- or non-adrenergic-mediated vasoconstriction with repeating burst patterns versus constant frequency stimulation at the same average frequency; and (2) to compare the effect of the number of impulses within a burst and instantaneous frequency on adrenergic- or non-adrenergic-mediated vasoconstriction. We hypothesized that vasoconstrictor responses at lower frequencies and impulse numbers would be predominantly P2X receptor-mediated, whereas vasoconstriction in response to higher frequencies and impulse numbers would be 1-receptor-mediated in rat femoral artery rings.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Experimental procedures described below were approved by the Institutional Animal Care and Use Committees of the Medical College of Wisconsin and Veterans Affairs Medical Center. The femoral arteries were taken from male Sprague–Dawley rats (body weight, 339.6 ± 10.5 g) after induction of general anaesthesia with pentobarbitone (40 mg kg–1 I.P., killed via pneumothorax). The vessels were placed in a Krebs–Henseleit buffer solution (Sigma, St Louis, MO, USA) with Hepes (10 mM; Sigma), sodium bicarbonate (25 mM; ICN, Aurora, OH, USA), and calcium chloride (0.95 mM; ICN) added. They were dissected free of connective tissue and cut into ring segments (2 mm in length). Three to four vessel segments per rat were mounted on tungsten triangular holders, connected to force transducers and positioned in 15 ml tissue baths containing modified Krebs–Henseleit buffer solution. Baths were continuously bubbled with a mixture of 5% CO2–95% O2. The tension of the vessel segments was set to 0.5 g and allowed to stabilize for 30 min at pH 7.4 and 37°C (Zhou et al. 1993).
Field stimulation was delivered via two parallel platinum electrodes placed on either side of the vessel. The electrical current was supplied using a custom-made constant voltage stimulator set to deliver 15 V using a 2 ms pulse width. The data were collected using a Powerlab 16/30 with Chart software (version 5.2; ADI Instruments, Colorado Springs, CO, USA). The frequency and pattern of stimulation were controlled through the stimulator function in Chart.
A length–tension curve was contructed to determine the optimal baseline tension using 60 Hz field stimulation for a total time of 10 s. Baseline tension was increased by 0.5 g until the developed tension failed to increase by 10% in response to stimulation (Spier et al. 1999). Viability of the smooth muscle was assessed by contraction in response to phenylephrine (10–5 M; Baxter Healthcare Corp., Irvine, CA, USA), and the viability of the endothelium was assessed by at least 20% relaxation in response to acetylcholine (10–5 M, Sigma; Schneider et al. 1994).
Protocols
Series 1.
Vessels from six rats were stimulated with two burst pattern protocols consisting of pairs, triplets, quadruplets and sextuplets for 144 impulses per pattern with 5 min rest between each pattern (see Fig. 1). The burst patterns were performed using 8 and 30 Hz as the instantaneous frequency. The order of the stimulation sets was randomized and the vessels repeatedly rinsed for 15 min in between sets. The specific 1-antagonist prazosin (1.59 µM) was added 5 min before field stimulation to one organ bath, and the purinergic-2 (P2) antagonist pyridoxal-phosphate-6-azophenyl-2'4'-disulphonic acid (0.42 M; PPADs; Sigma) was added to one tissue bath per rat. This concentration of PPADs abolishes the response to the agonist ,ß-methylene ATP (Kluess et al. 2005). During four of the 8 Hz pattern experiments, both prazosin and PPADs were added to one tissue bath.
|
Five minutes before beginning the stimulation protocols, prazosin (1.59 µM) was added to one tissue bath per rat and PPADs (0.42 M) was added to one tissue bath per rat. The remaining untreated vessel segments were used as controls.
On a separate day, femoral rings from four rats were stimulated at constant frequencies of 2, 3, 4 and 6 Hz. This protocol was repeated after adding both prazosin and PPADs to the bath. Double blocking was performed on a separate day because in our experience, femoral artery rings begin to lose tension when they are subjected to more than two sets of stimulation.
Series 3.
We have previously established that the femoral artery of the rat contains P2X and 1-adrenergic receptors in sufficient quantities to allow a dose–response curve to be contructed (Kluess et al. 2005). However, it is less clear whether there are neuropeptide Y1 and 2-adrenergic receptors on the femoral artery. The neuropeptide Y1 specific agonist [Leu31,Pro34]neuropeptide Y (10–4
M) was added to the organ baths. This dose of [Leu31,Pro34]neuropeptide Y was chosen because it was higher than the highest dose used in several studies looking at neuropeptide Y1-mediated vasoconstriction (Pernow et al. 1987; Cressier et al. 1995; Gradin et al. 2003). Since the role of neuropeptide Y1 postjunctional receptors may include potentiation of 1-mediated vasoconstriction (Grassi et al. 1996; Pernow et al. 1986), [Leu31,Pro34]neuropeptide Y (10–4
M) was added 1 min before the addition of noradrenaline (10–6
M). The experiments were performed consecutively in the same vessel segments.
We also wished to establish whether 2-adrenergic receptors are present on the femoral artery of the rat. The 2-receptor specific agonist 5-bromo-N-(2-imidazolin-2-yl)-6-quinoxalinamine (UK-14,304; 10–5
M) was added to the organ baths. This dose of UK-14 304 was higher than that used in studies by Flavahan & Vanhoutte (1986b) and Chotani et al. (2000).
Data analysis
Results are expressed as means ± S.E.M. unless stated otherwise. Data are presented as developed tension (peak tension minus baseline tension) and as a percentage change from control [(developed tension with antagonist minus developed tension control)/developed tension control) x 100].
Differences between control and antagonist in series 1 and 2 were assessed using two-way-repeated measures ANOVA followed by Tukey's post hoc test when appropriate. Differences between series 1 and series 2 were assessed using a two-way ANOVA followed by Tukey's post hoc test when appropriate. Differences were considered significant when P < 0.05.
To determine whether different stimulation patterns or receptor blockade resulted in a change in the time to half-maximal tension (t
) or the slope, tension data from 6 Hz constant stimulation, 30 Hz sextuplets and 8 Hz sextuplets were fitted with non-linear regression analysis. A curve fit was considered adequate if the correlation coefficient (r) was greater than 0.90. The t and the slope of the curve were calculated. Data for t or slope were compared using a one-way ANOVA followed by Tukey's post hoc test when appropriate.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Raw data traces from individual femoral artery rings during 8 Hz sextuplet and 30 Hz sextuplet burst pattern stimulation and during 6 Hz constant frequency stimulation are shown in Fig. 2. At the onset of all patterns of field stimulation, there was a brief delay and then tension in the rings increased exponentially.
|
1-antagonist, resulted in a –68 ± 12% change from control values (P < 0.05; n
= 6). When PPADs and prazosin were added together, tension was abolished (P < 0.05 versus control values; n
= 4).
|
Series 2
During 2–6 Hz constant frequency stimulation (Fig. 3C), PPADs (n = 5) attenuated tension on average by –67 ± 7% (P < 0.05 from control values). Prazosin (n = 5) abolished tension at all constant frequencies (on average, –100 ± 4%; P < 0.05 from control and PPADs values). Double blocking with both prazosin and PPADs (n = 4) also abolished tension (P < 0.05 from control and PPADs values).
Comparison of constant with burst pattern protocols
In order to compare changes in tension as a result of receptor antagonism more easily, data were expressed as a percentage change from control values. A summary of the percentage change with PPADs for 8 Hz burst pattern, 30 Hz burst pattern and constant frequency is presented in Fig. 4A and for prazosin in Fig. 4B. The percentage change in tension with PPADs was not significantly different between the burst pattern and constant frequency stimulation, indicating that the effect of PPADs was similar for the two stimulation protocols. However, the percentage decrease in tension with prazosin was significantly greater for constant frequency stimulation compared with the burst patterns (P < 0.05).
|
or the slope among 8 Hz sextuplets (n
= 4), 30 Hz sextuplets (n
= 6) and 6 Hz constant frequency (n
= 5) field stimulation patterns. There was also no difference in the t or slope with PPADs.
|
Tension was not increased above baseline values with the addition of [Leu31,Pro34]neuropeptide Y (from 0.50 ± 0.01 to 0.54 ± 0.17 g; n
= 5). The -adrenergic agonist noradrenaline caused a significant increase in tension (-adrenergic agonist, 1.47 ± 0.13 g), but prior addition of [Leu31,Pro34]neuropeptide Y did not potentiate this response (1.53 ± 0.03 g; n
= 5). The addition of UK-14,304, a specific 2-agonist, did not cause an increase in tension above baseline (from 0.36 ± 0.02 to 0.38 ± 0.03 g; n
= 4).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1-adrenergic receptors contribute to vasoconstriction during field stimulation with all frequencies and patterns. With constant frequency stimulation, P2X receptors did not produce vasoconstriction themselves, but potentiated 1-mediated vasoconstriction. In contrast, with burst patterns, P2X receptors caused vasoconstriction and potentiated 1-mediated vasoconstriction. Therefore, it appears that P2X and 1-adrenergic receptor-mediated vasoconstriction are sensitive to different electrical stimulation frequencies and patterns. Burst pattern stimulation
Based on previous research and sympathetic neurone recordings, the burst patterns used in this study were repeating pairs, triplets, quadruplets or sextuplets with a quiescent period between bursts (Hardebo, 1992; Macefield et al. 1999; Macefield & Wallin, 1999). The length of time in quiescence depended on the instantaneous frequency (frequency within a burst) and the number of impulses in a burst (duration of each epoch was 1000 ms). A low (8 Hz) and a high instantaneous frequency (30 Hz) were used with the expectation that a higher instantaneous frequency would cause greater tension. With the 8 Hz burst patterns, there were no differences in tension development among the patterns of pairs, triplets, quadruplets and sextuplets. However, with the 30 Hz burst pattern, developed tension with the sextuplets pattern was significantly greater than that with the pairs, triplets or quadruplets pattern. Overall, there was no difference in the developed tension with 8 Hz patterns compared with 30 Hz patterns.
P2X antagonism resulted in a decrease in tension with 8 and 30 Hz burst patterns. There was no significant difference in P2X antagonism with the pairs, triplets, quadruplets or sextuplets patterns. It is particularly difficult to compare our results to those of others, since most researchers have used a single burst, rather than a repeating pattern. However, Johnson et al. (2001) saw a non-significant increase in vascular resistance with couplets, but the increase in vascular resistance with a train of 20 impulses was attenuated by purinergic blockade. In contrast, Hardebo (1992) used the protocol most similar to our 30 Hz sextuplets pattern and did not see an effect of P2X antagonism in the rabbit ear artery. Differences between species and vessels used may explain the differences in results.
Antagonism of 1 receptors resulted on average in a 68 and 77% decrease from control values with 8 and 30 Hz burst pattern stimulation, respectively. The residual tension was abolished with the addition of PPADs. This suggests that the residual tension is the proportion of tension mediated by the P2X receptors (on average 32% for 8 Hz burst pattern and 23% for 30 Hz burst pattern). In agreement with this finding, previous studies have shown that as much as half of the tension developed by natural nerve patterns is resistant to 1-antagonism (Sjoblom-Widfeldt & Nilsson, 1990; Johnson et al. 2001).
Furthermore, we tested for the presence of 2-receptors and neuropeptide Y1 receptors on the femoral artery. In agreement with others, we found that the femoral artery did not contain 2-receptors and neuropeptide Y1 receptors in sufficient quantities to result in vasoconstriction in response to receptor-specific agonists (Thom et al. 1985; Flavahan et al. 1987; Guimaraes & Moura, 2001). Addition of a neuropeptide Y1 agonist did not cause potentiation of 1-mediated vasoconstriction. These data highlight the fact that 2-receptors and neuropeptide Y1 receptors contribute little to vasoconstriction in the femoral artery and explain the focus of the present study on 1-receptors and P2X receptors.
Constant frequency stimulation
As expected (Nilsson et al. 1985; Flavahan & Vanhoutte, 1986b; Sjoblom-Widfeldt & Nilsson, 1990; Hardebo, 1992; Haniuda et al. 1997; Ren & Burnstock, 1997; Morris, 1999; Zhang & Ren, 2001), tension produced by field stimulation was greater at 6 Hz compared with lower frequencies. P2X antagonism attenuated developed tension at all frequencies, a finding that is consistent with previous investigations employing constant frequency stimulation (Evans & Cunnane, 1992; Haniuda et al. 1997; Ren & Burnstock, 1997).
Antagonism of 1-adrenergic receptors abolished tension with constant frequency stimulation. This finding is in agreement with others and suggests that P2X receptors produce little to no vasoconstriction themselves during constant frequency stimulation (Flavahan & Vanhoutte, 1986b; Johnson et al. 2001; Tanaka et al. 2003; Tarasova et al. 2003). However, this finding is in contrast to the results of Evans & Cunnane (1992), Haniuda et al. (1997) and Ren & Burnstock (1997), who saw no effect of -adrenergic blockade at frequencies below 5 Hz. It is difficult to resolve the differences among these studies considering differences in vessels, species and stimulation protocols, but a predominance of the papers that support our findings are studies in the rat, while the dissenters are mostly studies in the rabbit.
Comparison of burst and constant frequency stimulation
It is clear from the data above that constant frequency field stimulation favours 1-mediated vasoconstriction, while both 1-receptors and P2X receptors contribute to vasoconstriction with burst pattern stimulation. However, the increased contribution to vasoconstriction from the P2X receptor with burst patterns does not result in an additive increase in tension development. There are two possible explanations for this finding, including neurotransmitter release and postjunctional receptor interactions. Although we did not measure noradrenaline or ATP release from the nerve end terminals, our findings are consistent with the idea that more ATP and less noradrenaline is released with burst patterns. However, Hardebo (1992) has previously shown that more noradrenaline is released with burst pattern compared with constant stimulation. Release of ATP was not measured in that study.
An alternative explanation was presented by Bao & Stjarne (1993), who found evidence to suggest that P2X receptors may inhibit 1-receptors, perhaps through an intracellular mechanism. Further support for this idea comes from Johnson et al. (2001), who also found evidence that ATP has a dual role of potentiating and inhibiting the effect of noradrenaline. It is hypothesized that the potentiating role is mediated by prejunctional P2X receptors (Boehm, 1999; Papp et al. 2004), but the inhibiting role is mediated by postjunctional P2X receptors (Bao & Stjarne, 1993). This issue could be resolved by simultaneous measurement of ATP and noradrenaline at the synapse.
Significance
The femoral artery, although a conduit vessel, is unique in that sympathetic vasoconstriction is mediated only by P2X receptors and 1-receptors, which makes it an excellent model for investigating the interactions between 1-receptors and P2X receptors. One of the potential limitations of this study is the use of field stimulation rather than naturally occurring sympathetic nerve activity to induce endogenous release of neurotransmitters. It is unknown whether endogenous release of sympathetic neurotransmitters is similar with field stimulation and natural nerve activity, although Johnson et al. (2001) found that the vascular response of the tail artery to field stimulation and natural nerve activity were comparable.
Sympathetic nerve activity increases during application of stressors such as heat, exercise, cardiovascular disease and ageing. The pattern of firing from a single sympathetic neurone changes by increasing the number of impulses within a burst and the number of bursts within a period of time. This has been demonstrated in people with chronic heart failure, but we know little about specific pattern changes with thermal stress, exercise and ageing. Our data add to the literature by showing that repeated patterns of bursts have an influence on the relative contributions of different neurotransmitters on vascular tone. The higher average frequency of our burst patterns suggests that P2X receptors can play an important role in producing vasoconstriction even with high levels of sympathetic activity. However, these data also suggest that as the pattern of sympathetic activity tends towards shorter quiescent periods (constant frequency), the ability of P2X receptors to directly mediate vascular tone declines. The overall impact of a loss of P2X-mediated vasoconstriction in skeletal muscle is unknown, but Thompson & Kenney (2004) have shown that a loss of non-adrenergic-mediated vasoconstriction in the skin impairs the ability to respond to thermal stress.
In conclusion, using a stimulation pattern modelled after that found in vivo, vasoconstriction in the femoral artery is mediated by 1-receptors and P2X receptors. We found that P2X receptors are active at all stimulation frequencies and play a dual role of vasoconstriction and potentiation of 1-receptor-mediated vasoconstriction. This study underscores the importance of the pattern of stimulation in better understanding the interaction among adrenergic and purinergic receptors.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
,ß-methylene ATP and suramin in rat tail artery. Br J Pharmacol 110, 1421–1428.[Medline]Boehm S (1999). ATP stimulates sympathetic transmitter release via presynaptic P2X purinoceptors. J Neurosci 19, 737–746.
Bradley E, Law A, Bell D & Johnson CD (2003). Effects of varying impulse number on cotransmitter contributions to sympathetic vasoconstriction in rat tail artery. Am J Physiol Heart Circ Physiol 284, H2007–H2014.
Chotani MA, Flavahan S, Mitra S, Daunt D & Flavahan NA (2000). Silent 2C-adrenergic receptors enable cold-induced vasoconstriction in cutaneous arteries. Am J Physiol Heart Circ Physiol 278, H1075–H1083.
Cressier F, Criscione L & Hofbauer KG (1995). Mechanism of interaction between neuropeptide Y and angiotensin II in the rabbit femoral artery. Eur J Pharmacol 272, 57–65.[CrossRef][Medline]
Elam M, Sverrisdottir YB, Rundqvist B, Mckenzie D & Wallin BG (2003). Pathological sympathoexitation: how is it achieved? Acta Physiol Scand 177, 405–411.[CrossRef][Medline]
Evans RJ & Cunnane TC (1992). Relative contributions of ATP and norepinephrine to the nerve evoked contraction of the rabbit jejunal artery. Dependence on stimulation parameters. Naunyn-Schmiedebergs Arch Pharmacol 345, 424–430.[Medline]
Flavahan NA, Cooke JP, Shepherd JT & Vanhoutte PM (1987). Human postjunctional alpha-1 and alpha-2 adrenoceptors diffrential distribution in arteries of the limbs. J Pharmacol Exp Ther 241, 361–365.
Flavahan NA & Vanhoutte PM (1986a). Effect of cooling on alpha-1 and alpha-2 adrenergic responses in canine saphenous and femoral veins. J Pharmacol Exp Ther 238, 139–147.
Flavahan NA & Vanhoutte PM (1986b). Sympathetic purinergic vasoconstriction and thermosensitivity in a canine cutaneous vein. J Pharmacol Exp Ther 239, 784–789.
Franco-Cereceda A & Liska J (1998). Neuropeptide Y Y1 receptors in vascular pharmacology. Eur J Pharmacol 349, 1–14.[CrossRef][Medline]
Gradin KA, Li JY, Andersson O & Simonsen U (2003). Enhanced neuropeptide Y immunoreactivity and vasoconstriction in mesenteric small arteries from spontaneously hypertensive rats. J Vasc Res 40, 252–265.[CrossRef][Medline]
Grassi C, Deriu F, Roatta S, Santarelli R, Azzena GB & Passatore M (1996). Sympathetic control of skeletal muscle function: possible co-operation between noradrenaline and neuropeptide Y in rabbit jaw muscles. Neurosci Lett 212, 204–208.[CrossRef][Medline]
Guimaraes S & Moura D (2001). Vascular adrenoceptors: an update. Pharmacol Rev 53, 319–356.
Habler HJ, Janig W, Krummel M & Peters OA (1993). Respiratory modulation of the activity in postganglionic neurons supplying skeletal muscle and skin of the rat hindlimb. J Neurophysiol 70, 920–930.
Haniuda K, Nakane T & Chiba S (1997). Different contributions of ATP and norepinephrine to neurotransmission in the isolated canine intermediate auricular artery. Eur J Pharmacol 333, 163–168.[CrossRef][Medline]
Hardebo JE (1992). Influence of impulse pattern on noradrenaline release from sympathetic nerves in cerebral and some peripheral vessels. Acta Physiol Scand 144, 333–339.[Medline]
Johnson CD, Coney AM & Marshall JM (2001). Roles of norepinephrine and ATP in sympathetically evoked vasoconstriction in rat tail and hindlimb in vivo. Am J Physiol Heart Circ Physiol 281, H2432–H2440.
Kennedy C, Saville VL & Burnstock G (1986). The contributions of noradrenaline and ATP to the responses of the rabbit central ear artery to sympathetic nerve stimulation depend on the parameters of stimulation. Eur J Pharmacol 122, 291–300.[CrossRef][Medline]
Kluess HA, Buckwalter JB, Hamann JJ & Clifford PS (2005). Acidosis attenuates P2X purinergic vasoconstriction in skeletal muscle arteries. Am J Physiol Heart Circ Physiol 288, H129–H132.
Macefield VG, Rundqvist B, Sverrisdottir YB, Wallin BG & Elam M (1999). Firing properties of single muscle vasoconstrictor neurons in the sympathoexitation associated with congestive heart failure. Circulation 100, 1708–1713.
Macefield VG & Wallin BG (1999). Firing properties of single vasoconstrictor neurones in human subjects with high levels of muscle sympathetic activity. J Physiol 516, 293–301.
Morris JL (1999). Cotransmission from sympathetic vasoconstrictor neurons to small cutaneous arteries in vivo. Am J Physiol Heart Circ Physiol 277, H58–H64.
Nilsson H, Ljung B, Sjoblom N & Wallin BG (1985). The influence of the sympathetic impulse pattern on contractile responses of rat mesenteric arteries and veins. Acta Physiol Scand 123, 303–309.[Medline]
Papp L, Balazsa T, Kofalvi A, Erdelyi F, Szabo G, Vizi S & Sperlagh B (2004). P2X receptor activation elicits transporter-mediated noradrenaline release from rat hippocampal slices. J Pharmacol Exp Ther 310, 973–980.
Pernow J, Ohlen A, Hokfelt T, Nilsson O & Lundberg JM (1987). Neuropeptide Y: presence in perivascular nonadrenergic neurons and vasoconstrictor effects on skeletal muscle blood vessels in experimental animals and man. Regul Pept 19, 313–324.[CrossRef][Medline]
Pernow J, Saria A & Lundberg JM (1986). Mechanisms underlying pre- and postjunctional effects of neuropeptide Y in sympathetic vascular control. Acta Physiol Scand 126, 239–249.[Medline]
Ren LM & Burnstock G (1997). Prominent sympathetic purinergic vasoconstriction in the rabbit splenic artery: potentiation by 2,2'-pyridylisatogen tosylate. Br J Pharmacol 120, 530–536.[CrossRef][Medline]
Schneider F, Bucher B, Schott C, Andre A, Julou-Schaeffer G & Stoclet JC (1994). Effect of bacterial liposaccaride on function of rat small femoral arteries. Am J Physiol Heart Circ Physiol 266, H191–H198.
Sjoblom-Widfeldt N & Nilsson H (1990). Sympathetic transmission in small mesenteric arteries: influence of impulse pattern. Acta Physiol Scand 138, 523–528.[Medline]
Spier SA, Laughlin MH & Delp MD (1999). Effects of acute and chronic exercise on vasoconstrictor responsiveness of rat abdominal aorta. J Appl Physiol 87, 1752–1757.
Tanaka K, Yang XP & Chiba S (2003). Purinergic and adrenergic cotransmission in canine isolated and perfused gastroepiploic arteries. Clin Exp Pharmacol Physiol 30, 678–683.[CrossRef][Medline]
Tarasova O, Sjoblom-Widfelt N & Nilsson H (2003). Transmitter characteristics of cutaneous, renal and skeletal muscle arteries in the rat. Acta Physiol Scand 177, 157–166.[CrossRef][Medline]
Thom S, Calvete J, Hayes R, Martin G & Sever P (1985). Human vascular smooth muscle responses mediated by 2 mechanisms in vivo and in vitro. Clin Sci 68, 147s–150s.[Medline]
Thompson CS & Kenney WL (2004). Altered neurotransmitter control of reflex vasoconstriction in aged human skin. J Physiol 558, 697–704.
Zhang W & Ren LM (2001). Sympathetic cotransmission in rabbit saphenous artery in vitro: effect of electric stimulation and potentiation by ,ß-methylene ATP. Acta Pharmacol Sin 22, 907–912.[Medline]
Zhou Z, Price JM, Sutton ET & Baker CH (1993). Effect of muscle length on the in vitro comparison of femoral arteries before and after endotoxin shock. Am J Physiol Heart Circ Physiol 265, H1160–H1166.
|
Acknowledgements |
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
