Differential modulation of the baroreceptor reflex by brain and plasma vasopressin.

Abstract

Plasma vasopressin sensitizes the baroreceptor reflex, whereas vasopressin given into the cerebral ventricle overrides the baroreceptor reflex by means of sympathetic stimulation. To test the hypothesis that arginine vasopressin stimulates two different receptor subtypes (V, and V 2 ) in the central nervous system, we measured the baroreceptor reflex (change in pulse interval vs change in blood pressure) after administering methoxamine (10-300 fj-glkg i.v.) in conscious rats. Animals were pretreated either with a V, vasopressin receptor antagonist administered intravenously or intracerebroventricularly, or with a V 2 receptor antagonist administered intravenously. The central V, antagonist caused sensitization of the baroreceptor reflex, whereas the intravenous V 2 antagonist attenuated it. The intravenous V! vasopressin antagonist had no effect on baroreceptor reflex sensitivity. When the experiments were repeated in rats with hereditary diabetes insipidus, neither antagonist influenced the baroreceptor reflex. Volume expansion lowered circulating vasopressin levels and also attenuated the baroreceptor reflex -effects similar to those observed with the intravenous V 2 antagonist. We conclude that vasopressin sensitizes the baroreceptor reflex through V 2 receptors accessible from the blood and inhibits the reflex through V, receptors in the brain that cannot be reached from the blood. These observations suggest a direct interaction between hormonal and neuronal vasopressin in cardiovascular control. (Hypertension 8 [Suppl II]: 11-157-11-162, 1986) KEY WORDS V| receptors vasopressin V 2 receptors baroreceptor reflex • central cardiovascular controlA RGININE vasopressin (AVP) is one of the most / \ potent circulating vasoconstrictor agents A. jk. known. 1 Plasma AVP induces vasoconstriction through specific receptors of the V, (vascular) subtype. However, unlike other circulating pressor hormones, such as angiotensin II, AVP increases blood pressure only at plasma concentrations well above those sufficient to produce an antidiuretic action through receptors of the V 2 (renal) subtype. 1 -2 This unique feature of AVP is due to the fact that circulating AVP sensitizes the baroreceptor reflex (BRR) and thereby counteracts its own vasoconstrictor action. 1

Effects of Arginine Vasopressin on Blood Pressure and Renal Prostaglandin E2 in Rabbits.

“…When changes in heart rate were analyzed in relation to blood pressure changes, the reduction in the heart rate relative to the increase in systolic blood pressure was not significantly attenuated in the group given AVP infusion, implying that the baroreflex was not depressed by continuous AVP infusion in the present study. This is consistent with the results of a previous study demonstrating that the baroreflex was sensitized through V2 receptors accessible from the blood [19]. Taken together, circulating AVP within a physiological range may regulate blood pressure mainly through vascular V1 receptors, possibly through down-regulation of V1 receptors.…”

Endogenous vasopressin and the central control of heart rate during dynamic exercise

“…Administration of a suppressor dose of vasopressin restricted to the NTS (mimicking stimulation of the long-descending vasopressinergic projections to this area) did not change the sensitivity of the baroreceptor reflex control of heart rate, but displaced the set point of the reflex toward higher heart rate values (37). This response contrasts with both the potentiation of the bradycardic response after intravenous vasopressin (38,39) and the blunting of reflex bradycardia following injection of vasopressin into the cerebrospinal fluid of conscious rats (26,39, see also Table 1). The peripheral hormone vasopressin sensitizes the baroreceptor reflex through V 2 receptors accessible from the blood, while neuronal V 1 receptors show highly specific responses such as inhibition of the reflex bradycardia by the neurohormone released into the cerebrospinal fluid, but displacement of the operating point of the reflex by the neurotransmitter vasopressin released directly in the NTS upon stimulation of projections originating in the PVN.…”

Selective elimination of hypothalamic neurons by grafted hypertension- inducing neural tissue

“…The high blood pressure in intact SHR may result from imbalance between the neuronal (parvocellular) and hormonal (magnocellular) components of the VP system (Unger et al, 1986) or, quite likely, may be due to a disequilibrium between the VP and other systems (Palkovits and Zaborszky, 1977;Olpe and Baltzer, 198 1;Unger et al, 1984) including OT. This situation differs from that in the normotensive Brattleboro rat developed by Valtin (1967) in which neither type of cell produces VP.…”