TY - JOUR
T1 - Vasopressin and angiotensin II in reflex regulation of heart rate
T2 - Effect of water deprivation
AU - Brooks, V. L.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1992
Y1 - 1992
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.
KW - V-vasopressin antagonist
KW - V/V-vasopressin antagonist
KW - baroreceptor reflex
KW - blood pressure
KW - conscious dogs
KW - nitroprusside
KW - renin-angiotensin system
KW - saralasin
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U2 - 10.1152/ajpregu.1992.263.4.r756
DO - 10.1152/ajpregu.1992.263.4.r756
M3 - Article
C2 - 1415785
AN - SCOPUS:0026806340
SN - 0002-9513
VL - 263
SP - R756-R761
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 4 32-4
ER -