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In a rat model, V2 receptors do not have inherent or synergistic vasoactive action with V1 receptors, nor do they enhance reflex buffering of the pressor response to vasopressin.
To determine the contribution of V1 and V2 receptor activity on the enhancement of reflex buffering of the pressor response to arginine-vasopressin (AVP), mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of phenylephrine, AVP, or Phe2Orn8OT, a potent, selective V1-receptor agonist in the absence and presence of Val4DArg8VP, a potent, selective V2-receptor agonist. 2. There were no significant differences in MAP responses to the V1 agonist in the absence and presence of the V2 agonist in either conscious intact or autonomic-blocked rats. 3. Autonomic blockade with methscopolamine and hexamethonium increased the pressor sensitivity to phenylephrine threefold. In contrast, the pressor sensitivities to AVP and Phe2Orn8OT were increased 14-fold and 11-fold, respectively, by autonomic blockade. 4. V2-receptor activity does not have any inherent vasocative action or synergistic vasoactive action with V1-receptor activity. 5. V2 receptors do not play a role in enhancing reflex buffering of the pressor response to AVP; V1 receptors are suggested to play the role.
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Shimizu et al. (1991) studied this question.
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