Vasopressin and angiotensin II in reflex regulation of heart rate

Effect of water deprivation

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15 Citations (Scopus)

Abstract

This study tested the hypothesis that endogenous angiotensin II (ANG II) and vasopressin enhance baroreflex-mediated increases in heart rate in water- replete dogs and in dogs water deprived to chronically elevate plasma ANG II and vasopressin concentrations. The baroreflex was assessed by examining the heart rate response to infusion of increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 μg · kg-1 · min-1). The effect on the baroreflex of pretreating the dogs with the competitive ANG II antagonist saralasin, a V1- vasopressin antagonist, or a combined V1/V2-vasopressin antagonist, alone or in combination, was determined. Nitroprusside infusion produced dose- dependent increases in heart rate, and the heart rate response was greater in water-deprived dogs in association with higher plasma levels of ANG II and vasopressin than in water-replete dogs. ANG II blockade alone depressed reflex increases in heart rate in water-deprived but not water-replete dogs. In both water-replete and water-deprived dogs, blockade of V1-vasopressin receptors reduced the heart rate response to hypotension, but this effect could be produced only when ANG II receptors were also blocked. In addition, administration of saralasin and the V1/V2-vasopressin antagonist led to a further reduction of the reflex tachycardia. These data suggest that endogenous vasopressin, acting at both V1- and V2-receptors, can amplify the increase in heart rate produced by hypotension. In addition, the results further support a physiological role for chronic elevations in endogenous ANG II in the maintenance of normal baroreflex function.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume263
Issue number4 32-4
StatePublished - 1992

Fingerprint

Water Deprivation
Vasopressins
Angiotensin II
Reflex
Heart Rate
Vasopressin Receptors
Dogs
Water
Baroreflex
Saralasin
Nitroprusside
Hypotension
Nijmegen Breakage Syndrome
Angiotensin Receptors
Tachycardia
Maintenance

Keywords

  • baroreceptor reflex
  • blood pressure
  • conscious dogs
  • nitroprusside
  • renin-angiotensin system
  • saralasin
  • V-vasopressin antagonist
  • V/V-vasopressin antagonist

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Vasopressin and angiotensin II in reflex regulation of heart rate: Effect of water deprivation",
abstract = "This study tested the hypothesis that endogenous angiotensin II (ANG II) and vasopressin enhance baroreflex-mediated increases in heart rate in water- replete dogs and in dogs water deprived to chronically elevate plasma ANG II and vasopressin concentrations. The baroreflex was assessed by examining the heart rate response to infusion of increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 μg · kg-1 · min-1). The effect on the baroreflex of pretreating the dogs with the competitive ANG II antagonist saralasin, a V1- vasopressin antagonist, or a combined V1/V2-vasopressin antagonist, alone or in combination, was determined. Nitroprusside infusion produced dose- dependent increases in heart rate, and the heart rate response was greater in water-deprived dogs in association with higher plasma levels of ANG II and vasopressin than in water-replete dogs. ANG II blockade alone depressed reflex increases in heart rate in water-deprived but not water-replete dogs. In both water-replete and water-deprived dogs, blockade of V1-vasopressin receptors reduced the heart rate response to hypotension, but this effect could be produced only when ANG II receptors were also blocked. In addition, administration of saralasin and the V1/V2-vasopressin antagonist led to a further reduction of the reflex tachycardia. These data suggest that endogenous vasopressin, acting at both V1- and V2-receptors, can amplify the increase in heart rate produced by hypotension. In addition, the results further support a physiological role for chronic elevations in endogenous ANG II in the maintenance of normal baroreflex function.",
keywords = "baroreceptor reflex, blood pressure, conscious dogs, nitroprusside, renin-angiotensin system, saralasin, V-vasopressin antagonist, V/V-vasopressin antagonist",
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T1 - Vasopressin and angiotensin II in reflex regulation of heart rate

T2 - Effect of water deprivation

AU - Brooks, Virginia

PY - 1992

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N2 - This study tested the hypothesis that endogenous angiotensin II (ANG II) and vasopressin enhance baroreflex-mediated increases in heart rate in water- replete dogs and in dogs water deprived to chronically elevate plasma ANG II and vasopressin concentrations. The baroreflex was assessed by examining the heart rate response to infusion of increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 μg · kg-1 · min-1). The effect on the baroreflex of pretreating the dogs with the competitive ANG II antagonist saralasin, a V1- vasopressin antagonist, or a combined V1/V2-vasopressin antagonist, alone or in combination, was determined. Nitroprusside infusion produced dose- dependent increases in heart rate, and the heart rate response was greater in water-deprived dogs in association with higher plasma levels of ANG II and vasopressin than in water-replete dogs. ANG II blockade alone depressed reflex increases in heart rate in water-deprived but not water-replete dogs. In both water-replete and water-deprived dogs, blockade of V1-vasopressin receptors reduced the heart rate response to hypotension, but this effect could be produced only when ANG II receptors were also blocked. In addition, administration of saralasin and the V1/V2-vasopressin antagonist led to a further reduction of the reflex tachycardia. These data suggest that endogenous vasopressin, acting at both V1- and V2-receptors, can amplify the increase in heart rate produced by hypotension. In addition, the results further support a physiological role for chronic elevations in endogenous ANG II in the maintenance of normal baroreflex function.

AB - This study tested the hypothesis that endogenous angiotensin II (ANG II) and vasopressin enhance baroreflex-mediated increases in heart rate in water- replete dogs and in dogs water deprived to chronically elevate plasma ANG II and vasopressin concentrations. The baroreflex was assessed by examining the heart rate response to infusion of increasing doses of nitroprusside (0.3, 0.6, 1.5, and 3.0 μg · kg-1 · min-1). The effect on the baroreflex of pretreating the dogs with the competitive ANG II antagonist saralasin, a V1- vasopressin antagonist, or a combined V1/V2-vasopressin antagonist, alone or in combination, was determined. Nitroprusside infusion produced dose- dependent increases in heart rate, and the heart rate response was greater in water-deprived dogs in association with higher plasma levels of ANG II and vasopressin than in water-replete dogs. ANG II blockade alone depressed reflex increases in heart rate in water-deprived but not water-replete dogs. In both water-replete and water-deprived dogs, blockade of V1-vasopressin receptors reduced the heart rate response to hypotension, but this effect could be produced only when ANG II receptors were also blocked. In addition, administration of saralasin and the V1/V2-vasopressin antagonist led to a further reduction of the reflex tachycardia. These data suggest that endogenous vasopressin, acting at both V1- and V2-receptors, can amplify the increase in heart rate produced by hypotension. In addition, the results further support a physiological role for chronic elevations in endogenous ANG II in the maintenance of normal baroreflex function.

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KW - V-vasopressin antagonist

KW - V/V-vasopressin antagonist

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M3 - Article

VL - 263

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 4 32-4

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