Inhibition of aortic chemoreceptor discharge by pressor response to muscular contraction

1987 ◽  
Vol 62 (6) ◽  
pp. 2258-2263
Author(s):  
K. W. McCoy ◽  
D. M. Rotto ◽  
M. P. Kaufman
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Pressure Response ◽  
Hindlimb Muscles ◽  
Pressor Responses ◽  
Adrenergic Antagonist ◽  
Static Contraction

We have examined the effect of static contraction of the hindlimb muscles on the discharge of aortic chemoreceptors in chloralose-anesthetized cats. The responses of the chemoreceptors to contraction were dependent on the arterial pressure response to this maneuver. When contraction reflexly evoked a pressor response of at least 20 mmHg, the discharge of 26 chemoreceptors was reduced from control levels by 53% (P less than 0.01). The contraction-induced inhibition of chemoreceptor discharge was prevented by phentolamine, an alpha-adrenergic antagonist that also attenuated the contraction-induced pressor response. In addition, the inhibition evoked by contraction was simulated by injection of phenylephrine and inflation of an aortic balloon, both of which evoked pressor responses. However, when contraction failed to significantly change arterial pressure, the discharge of 20 aortic chemoreceptors was not significantly changed from control levels. We conclude that the reflex pressor response to static contraction inhibits the discharge of aortic chemoreceptors. This inhibition of discharge needs to be considered when interpreting the effects of aortic barodenervation on the cardiovascular responses to exercise.

Effects of barodenervation on cardiovascular responses to static muscular contraction

1985 ◽  
Vol 249 (4) ◽  
pp. H710-H714 ◽  
Author(s):  
T. G. Waldrop ◽  
J. H. Mitchell
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Skeletal Muscles ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Baroreceptor Reflex ◽  
Hindlimb Muscles ◽  
The Central Nervous System ◽  
Root Stimulation

The purpose of this study was to measure blood flow to various tissues during static muscular contraction in anesthetized cats and to evaluate if the baroreflex modulates the cardiovascular responses to muscular contraction. Contraction of the hindlimb muscles induced by ventral root stimulation caused increases in arterial pressure (delta 37.8 +/- 5.5 mmHg) and heart rate (delta 13.9 +/- 3.1 beats/min). Increases in blood flow to the heart, working skeletal muscles, and selected areas of the central nervous system occurred during muscular contraction. Blood flow to visceral organs did not change during muscular contraction. Baroreceptor-denervated cats showed a greater rise in arterial pressure (delta 55.5 +/- 5.5 mmHg) during muscular contraction than did the baroreceptor-intact cats. However, blood flow responses were similar in both groups. Thus the baroreceptor reflex modulates the pressor response without changing the alteration in blood flow during induced muscular contraction in anesthetized cats.

Arterial pressure responses to increasing interstitial potassium in hindlimb muscle of dogs

1984 ◽  
Vol 247 (4) ◽  
pp. R717-R721 ◽  
Author(s):  
K. J. Rybicki ◽  
M. P. Kaufman ◽  
J. L. Kenyon ◽  
J. H. Mitchell
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Potassium Concentration ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Gracilis Muscle ◽  
Hindlimb Muscle ◽  
Static Contraction ◽  
Anesthetized Dogs ◽  
Blood Pressure Responses

Static contraction of hindlimb skeletal muscle is known to increase reflexly arterial pressure and heart rate. Potassium is known to be released by the working muscle and is thought to activate the afferents responsible for the reflex cardiovascular responses to muscular contraction. However, it is not known whether potassium, at interstitial concentrations within the range observed during static contraction, is capable of stimulating these afferents. Thus we injected potassium into the gracilis artery of chloralose-anesthetized dogs while we measured interstitial potassium concentrations in the gracilis muscle with potassium-selective electrodes. In 16 dogs, we found that potassium injections, which increased interstitial potassium concentrations by 4.7 +/- 0.3 mM, increased mean arterial pressure by 18 +/- 3 mmHg and heart rate by 12 +/- 8 beats/min; cutting the obturator nerve abolished these increases. These heart rate and blood pressure responses were of short duration (20 +/- 7 s), even though interstitial potassium remained elevated for a period of several minutes. In 5 of the 16 dogs, static contraction of the gracilis muscle for 60 s increased interstitial potassium concentration by 4.3 +/- 0.3 mM. Our data are consistent with the hypothesis that potassium plays a role in causing the reflex cardiovascular responses to static muscular contraction.

Increasing gracilis muscle interstitial potassium concentrations stimulate group III and IV afferents

1985 ◽  
Vol 58 (3) ◽  
pp. 936-941 ◽  
Author(s):  
K. J. Rybicki ◽  
T. G. Waldrop ◽  
M. P. Kaufman
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Group Iv ◽  
Gracilis Muscle ◽  
Group Iii ◽  
Arterial Blood ◽  
Static Contraction ◽  
Anesthetized Dogs

Static muscular contraction reflexly increases arterial blood pressure and heart rate. One possible mechanism evoking this reflex is that potassium accumulates in the interstitial space of a working muscle to stimulate group III and IV afferents whose activation in turn evokes a pressor response. The responses of group III and IV muscle afferents to increases in interstitial potassium concentrations within the range evoked by static contraction are unknown. Thus we injected potassium chloride into the gracilis artery of anesthetized dogs while we measured both gracilis muscle interstitial potassium concentrations with potassium-selective electrodes and the impulse activity of afferents in the gracilis nerve. We found that increasing interstitial potassium concentrations to levels similar to those seen during static contraction stimulated 14 of 16 group III and 29 of 31 group IV afferents. The responses of the afferents to potassium were concentration dependent. The typical response to potassium consisted of a burst of impulses, an effect that returned to control firing rates within 26 s, even though interstitial potassium concentrations remained elevated for several minutes. Although our results suggest that potassium may play a role in initiating the reflex cardiovascular responses to static muscular contraction, the accumulation of this ion does not appear to be solely responsible for maintaining the pressor response for the duration of the contraction.

VR-1 receptor blockade attenuates the pressor response to capsaicin but has no effect on the pressor response to contraction in cats

2005 ◽  
Vol 288 (4) ◽  
pp. H1867-H1873 ◽  
Author(s):  
Angela E. Kindig ◽  
Todd B. Heller ◽  
Marc P. Kaufman
Keyword(s):  
Popliteal Artery ◽  
Pressor Response ◽  
Muscular Contraction ◽  
Triceps Surae ◽  
Exercise Pressor Reflex ◽  
Pressor Responses ◽  
Static Contraction ◽  
Pressor Reflex ◽  
The Right

Vanilloid type 1 (VR-1) receptors are stimulated by capsaicin and hydrogen ions, the latter being a by-product of muscular contraction. We tested the hypothesis that activation of VR-1 receptors during static contraction contributes to the exercise pressor reflex. We established a dose of iodoresinaferatoxin (IRTX), a VR-1 receptor antagonist, that blocked the pressor response to capsaicin injected into the arterial supply of muscle. Specifically, in eight decerebrated cats, we compared pressor responses to capsaicin (10 μg) injected into the right popliteal artery, which was subsequently injected with IRTX (100 μg), with those to capsaicin injected into the left popliteal artery, which was not injected with IRTX. The pressor response to capsaicin injected into the right popliteal artery averaged 49 ± 9 mmHg before IRTX and 9 ± 2 mmHg after IRTX ( P < 0.05). In contrast, the pressor response to capsaicin injected into the left popliteal artery averaged 46 ± 10 mmHg “before” and 43 ± 6 mmHg “after” ( P > 0.05). We next determined whether VR-1 receptors mediated the pressor response to contraction of the triceps surae. During contraction without circulatory occlusion, the pressor response before IRTX (100 μg) averaged 26 ± 3 mmHg, whereas it averaged 22 ± 3 mmHg ( P > 0.05) after IRTX ( n = 8). In addition, during contraction with occlusion, the pressor responses averaged 35 ± 3 mmHg before IRTX injection and 49 ± 7 mmHg after IRTX injection ( n = 7). We conclude that VR-1 receptors play little role in evoking the exercise pressor reflex.

Role for the median preoptic nucleus in centrally evoked pressor responses

1987 ◽  
Vol 252 (6) ◽  
pp. R1165-R1172 ◽  
Author(s):  
T. P. O'Neill ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
Receptor Site ◽  
Cardiovascular Responses ◽  
Pressor Effect ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
Median Preoptic Nucleus ◽  
Pressor Responses ◽  
Angiotension Ii

Recent evidence suggests an important role for the median preoptic nucleus (MnPO) in cardiovascular responses evoked by angiotension II (ANG II). We therefore planned to determine whether selective inactivation of this nucleus would produce deficits in pressor responsiveness to centrally administered ANG II and carbachol. Chronic disruption of MnPO by electrolytic lesion produced pressor deficits to centrally administered ANG II and carbachol but did not change resting arterial pressure. In addition, blockade of neuronal activity in MnPO produced by the microinjection of the local anesthetic lidocaine reversibly attenuated pressor responses to these agents without producing any change in resting arterial pressure. The microinjection of ANG II itself into sites in which lidocaine blocked ANG II pressor responses had no effect on arterial pressure but did produce drinking. These data suggest that the MnPO, although not acting as a receptor site for the pressor effect of ANG II, plays an important role in mediating the pressor response evoked by centrally administered ANG II and carbachol.

Sympathoadrenal mechanisms in cardiovascular responses to naloxone after hemorrhage

1987 ◽  
Vol 252 (1) ◽  
pp. H40-H46 ◽  
Author(s):  
P. C. Rutter ◽  
S. J. Potocnik ◽  
J. Ludbrook
Keyword(s):  
Arterial Pressure ◽  
Adrenal Medulla ◽  
Adrenal Glands ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Plasma Epinephrine ◽  
Pressor Responses ◽  
Noradrenergic Nerves ◽  
Total Adrenalectomy

Five rabbits were allotted to each of six treatments on a matched-individual basis. Treatments were none, sham, total adrenalectomy with adrenocorticoid replacement, intravenous guanethidine (15 mg X kg-1 X day-1), adrenalectomy + guanethidine, and adrenal medullectomy. The conscious rabbits were bled 20 ml/kg over 5 min. Naloxone (6 mg/kg) was injected intravenously. The responses of arterial pressure and of plasma epinephrine (E) and norepinephrine (NE) concentrations were measured. Factorial analysis was used to calculate the effects of sympathetic noradrenergic nerves (SYM) and the adrenal medulla (ADR) on the responses. In combination, SYM + ADR fully accounted for the pressor response observed in normal and sham-treated rabbits. SYM and ADR each made independent and approximately equal contributions to the response, but the SYM X ADR interaction was strongly antagonistic. The responses of plasma E and NE were fully accounted for by the adrenal glands and sympathetic nerves, respectively. The pressor responses after total adrenalectomy and adrenal medullectomy were similar. Thus hemorrhage-stimulated adrenal corticosteroid release was not essential to naloxone's action, and adrenal enkephalins were not responsible for naloxone's action on sympathetic pathways.

Effect of ischemia on responses of group III and IV afferents to contraction

1984 ◽  
Vol 57 (3) ◽  
pp. 644-650 ◽  
Author(s):  
M. P. Kaufman ◽  
K. J. Rybicki ◽  
T. G. Waldrop ◽  
G. A. Ordway
Keyword(s):  
Impulse Activity ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Group Iv ◽  
Triceps Surae ◽  
Arterial Supply ◽  
Group Iii ◽  
Hindlimb Muscles ◽  
Static Contraction ◽  
Static Contractions

Static contraction of the hindlimb muscles of cats reflexly increases cardiovascular function, an effect that is potentiated by occlusion of the arterial supply to the working muscles. Although group III and IV afferents are known to be stimulated by and to cause the reflex cardiovascular responses to static muscular contraction, little is known about the responses of these afferents to static contraction when the arterial supply to a working muscle is occluded. We therefore recorded the impulse activity of 24 group III afferents and 30 group IV afferents with endings in the triceps surae while we statically contracted this muscle group, both when the abdominal aorta was occluded and when it was patent. A chi 2 analysis revealed that ischemia increased the responses to static contractions of a significantly higher percentage of group IV afferents than group III afferents (46.7% vs. 12.5%, respectively; P less than 0.02). In addition, two patterns of responses to ischemic contraction were observed. The first pattern was displayed by afferents (n = 10) that were stimulated by nonischemic contraction but were stimulated more by ischemic contraction. The second pattern was displayed by afferents (n = 7) that were not stimulated by nonischemic contraction but were stimulated by ischemic contraction. We conclude that afferents displaying both patterns are likely to contribute to the reflex cardiovascular responses to ischemic contraction.

mu-Opioid receptors in NTS elicit pressor responses via sympathetic pathways

1987 ◽  
Vol 252 (1) ◽  
pp. H156-H162 ◽  
Author(s):  
A. H. Hassen ◽  
G. Feuerstein
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Baroreflex Function ◽  
Sprague Dawley Rats ◽  
Pressor Responses ◽  
Adrenergic Antagonist ◽  
Atropine Methyl Nitrate ◽  
Mu Receptors

We have evaluated the relative contributions of the sympathetic and parasympathetic nervous systems to the increased mean arterial pressure (MAP) and heart rate (HR) elicited by the selective mu-agonist D-Ala2, MePhe4, Gly-ol5 enkephalin (DAGO) following microinjection (100 nl) into the nucleus of tractus solitarius (NTS) of anesthetized, artificially ventilated Sprague-Dawley rats. The effects of anesthesia and central opioid-receptor activation on baroreflex function were also examined. All cardiovascular responses elicited by DAGO were eliminated by complete C1 spinal transection. Pretreatment with the alpha-adrenergic antagonist phentolamine attenuated the increase in MAP, but not the tachycardia; the beta-blocker propranolol abolished the tachycardia but not the pressor response to DAGO. Adrenalectomy, vagotomy, or pretreatment with atropine methyl nitrate were all without effect. Baroreflexes were attenuated in animals anesthetized with pentobarbital sodium, but were present in urethan-anesthetized rats. DAGO attenuated the increases in MAP and HR elicited following carotid occlusion, but not the bradycardia elicited by a phenylephrine-induced pressor response. These data indicate that mu-receptors in the NTS elicit cardiovascular responses that are mediated by increased sympathetic nerve activity, and accompanied by selective attenuation of baroreflex function.

Mechanisms of centrally administered ET-1-induced increases in systemic arterial pressure and AVP secretion

1997 ◽  
Vol 272 (1) ◽  
pp. E126-E132 ◽  
Author(s):  
N. F. Rossi ◽  
D. S. O'Leary ◽  
H. Chen
Keyword(s):  
Arterial Pressure ◽  
Peak Plasma ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Fold Increase ◽  
Systemic Arterial Pressure ◽  
Sympathetic Outflow ◽  
Central Administration ◽  
Eta Receptor ◽  
The Central Nervous System

Endothelins (ET) within the central nervous system (CNS) alter systemic cardiovascular responses and arginine vasopressin (AVP) secretion. These experiments were designed to ascertain whether the rise in systemic arterial pressure after central administration of ET-1 is mediated by enhancing sympathetic outflow and/or circulating AVP. In Long-Evans (LE/LE) rats, intracerebroventricular injection of 1-10 pmol ET-1 dose dependently increased mean arterial pressure (MAP). Peak response occurred 7-12 min after ET-1 and was inhibited by ETA receptor antagonism. Systemic vasopressin (V1) receptor blockade did not inhibit the pressor response, and rats with central diabetes insipidus (DI/DI) displayed an identical rise in MAP. Ganglionic blockade prevented ET-1-induced hemodynamic effects. Peak plasma AVP levels occurred 60 min after ET-1, as the pressor response began to wane. In sinoaortic-denervated LE/LE rats, ET-1 elicited a 10-fold increase in AVP secretion that coincided with the hemodynamic changes and was blocked by BQ-123. Thus ET-1 via ETA receptors within the CNS induced a concentration-dependent increase in systemic arterial pressure mediated by enhanced sympathetic outflow but not by circulating AVP. Reflex baroreceptor activation attenuated AVP release.

Regional hemodynamic and baroreflex effects of endothelin in rats

1989 ◽  
Vol 257 (3) ◽  
pp. H918-H926 ◽  
Author(s):  
M. M. Knuepfer ◽  
S. P. Han ◽  
A. J. Trapani ◽  
K. F. Fok ◽  
T. C. Westfall
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Nerve Activity ◽  
Anesthetized Rats ◽  
Pressor Responses ◽  
Regional Hemodynamics ◽  
Potent Vasoconstrictor ◽  
Baroreceptor Reflex Control

Endothelin is a peptide with potent, long-lasting pressor effects characterized by increases in mesenteric and hindquarters vascular resistance and bradycardia following an initial, transient depressor response. This study examined the mechanisms of action of endothelin on regional hemodynamics in conscious, freely moving rats and on baroreflex sensitivity both in conscious and chloralose-anesthetized rats. The pressor response to endothelin (0.67 nmol/kg) was attenuated by nifedipine (25 micrograms/kg) and augmented by chloralose anesthesia. The bradycardia was attenuated by pentolinium (10 mg/kg), atropine methyl sulfate (0.5 mg/kg), or chloralose anesthesia. Hindquarter vaso-constriction was attenuated by nifedipine, pentolinium, and atropine, whereas mesenteric vasoconstriction was less sensitive to blockade. The vasopressin V1 antagonist, [d(CH2)5Tyr(Me)]-AVP (20 micrograms/kg), indomethacin (5 mg/kg), or verapamil (150 micrograms/kg) did not affect any of these cardiovascular responses. Renal sympathetic nerve activity was reduced similarly in chloralose-anesthetized rats to pressor responses elicited by either phenylephrine or endothelin, and the slope of the baro-reflex function curve after endothelin was similar to that of phenylephrine. These results suggest that endothelin is a potent vasoconstrictor in which its action on visceral and skeletal muscle vasculature is mediated by somewhat different mechanisms. Endothelin does not alter baroreceptor reflex control of sympathetic nerve activity or heart rate.

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