Experiments were performed on conscious, chronically instrumented rats to determine the role of arginine vasopressin (AVP) on the systemic and regional hemodynamic effects of 48-h water deprivation. Arterial and venous catheters as well as pulsed Doppler flow probes were implanted in rats to measure cardiac output (CO), mesenteric blood flow (MBF), renal blood flow (RBF), or hindquarter blood flow (HQBF). After adequate recovery from surgey, euhydrated animals were administered a specific V1-vasopressinergic antagonist [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg iv], a combined V1, V2-antagonist [d(CH2)5DTyr(Et)VAVP, 30 micrograms/kg iv], or saline vehicle (100 microliter/100 g). Neither antagonist was associated with any change in mean arterial blood pressure (MABP), heart rate (HR), systemic or regional flow or vascular resistance. All animals were subsequently water deprived for 48 h, at which time the experiments were repeated. Dehydration was associated with an increase in plasma AVP levels, hematocrit, and MABP but with a decrease in HR. Administration of either the combined V1, V2-antagonist or vehicle had no effect on any systemic or regional hemodynamic variables measured after 48-h dehydration. In contrast, although MABP, CO, MBF, and RBF were unaffected, V1-antagonism resulted in elevated HR, increased HQBF, and decreased hindquarter vascular resistance. In conclusion, AVP does not have a major effect on systemic hemodynamics in the dehydrated rat. However, certain beds may be affected by the relatively moderate levels of plasma AVP elicited during dehydration.
- Copyright © 1988 the American Physiological Society