Experiments were performed in conscious rats to assess the contribution of V$\sb2$-vasopressinergic receptor activation to enhancement of baroreceptor reflex (BRR) sensitivity observed with vasopressin (AVP). All rats were chronically instrumented for measurement of cardiac output, arterial blood pressure and heart rate. Initial experiments were designed to determine if either blockade or activation of V$\sb2$-receptors alter BRR sensitivity. Administration of a specific V$\sb2$-receptor antagonist prior to AVP infusion diminished BRR sensitivity observed with AVP infusion. Administration of a specific V$\sb2$-receptor agonist enhanced BRR sensitivity compared to control. Further, treatment with either the V$\sb2$-antagonist or a specific V$\sb1$-antagonist prior to V$\sb2$-agonist infusion diminished the enhancement of BRR sensitivity observed with V$\sb2$-agonist administration. Finally, administration of either V$\sb2$- or V$\sb1$-antagonist prior to saline vehicle infusion did not diminish BRR sensitivity, indicating that basal levels of circulating vasopressin do not appear to affect BRR sensitivity. A second set of experiments was designed to asses the contribution of non-BRR mechanisms to the enhanced bradycardic response during V$\sb2$-agonist infusion. Although V$\sb2$-agonist infusion enhanced the bradycardic response to pressor doses of phenylephrine in intact rats, there was no effect in barodenervated rats. However, administration of pressor doses of AVP to barodenervated rats elicited a dose dependent bradycardia. A final set of experiments was designed to determine the physiological significance of vasopressinergic enhancement of BRR sensitivity. Vasopressinergic antagonists were administered during two situations of stimulated endogenous release of AVP: water deprivation and nonhypotensive hemorrhage. BRR sensitivity was not affected by water deprivation or by vasopressinergic antagonism prior to and following water deprivation. However, nonhypotensive hemorrhage enhanced BRR sensitivity, and either V$\sb2$- or V$\sb1$-antagonist administration attenuated the enhancement of BRR sensitivity. These data suggest that (1) either V$\sb2$-antagonist administration during AVP infusion or V$\sb2$-agonist administration alter BRR sensitivity, however, the specificity of the receptor activation is uncertain; (2) enhancement of bradycardic responses to pressor stimuli during V$\sb2$-agonist administration is indeed a baroreflex dependent phenomenon, although there may be a bradycardic response to AVP which is BRR-independent; and (3) BRR sensitivity may be enhanced in some situations of stimulated endogenous release of AVP, however, the specificity of the receptor activated is uncertain / acase@tulane.edu
| Identifer | oai:union.ndltd.org:TULANE/oai:http://digitallibrary.tulane.edu/:tulane_26613 |
| Date | January 1989 |
| Contributors | Brizzee, Barbara L (Author), Walker, Benjimen R (Thesis advisor) |
| Publisher | Tulane University |
| Source Sets | Tulane University |
| Language | English |
| Detected Language | English |
| Rights | Access requires a license to the Dissertations and Theses (ProQuest) database., Copyright is in accordance with U.S. Copyright law |
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