The major objective is to determine if endogenous vasopressin (reflexly stimulated secretion) contributes to the neural regulation of the circulation. The underlying hypothesis is that vasopressin at low concentrations may increase the gain of the arterial baroreflex to inhibit sympathetic nerve activity while at higher concentrations vasopressin may decrease the gain of the arterial baroreflex. At these higher concentrations of vasopressin, the reflex increase in sympathetic nerve activity to decreases in arterial pressure will be reduced. A second hypothesis is that the area postrema is necessary for the interaction of vasopressin with the arterial and cardiopulmonary baroreflexes. The third hypothesis is that circulating vasopressin may increase the arterial and cardiopulmonary inhibitions of vasopressin release thereby providing a mechanism whereby vasopressin might feedback to regulate its own release. Studies will be performed in conscious rabbits instrumented with arterial and venous catheters and electrodes on the renal, splanchnic and lumbar sympathetic nerves. By altering plasma vasopressin concentrations (osmotically or reflexly) we will be about to determine if endogenous vasopressin alters the arterial and cardiopulmonary baroreflex control of sympathetic nerve activity. The studies will be repeated in rabbits with lesion of the area postrema. We expect that in the lesioned rabbit the interactions of vasopressin with the arterial and cardiopulmonary baroreflex will be abolished. Additional studies are proposed to determine the arterial pressure, heart rate and sympathetic nerve responses to chemical and electrical stimulation of the area postrema.
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