HEMODYNAMIC-RESPONSE TO VASOPRESSIN DURING V-1-RECEPTOR ANTAGONISM INBAROREFLEX-DEFICIENT SUBJECTS

Six quadriplegic subjects and 6 control subjects received high-dose ar ginine vasopressin (AVP) infusions at rates of 500, 1,000, 2,000, and 4,000 mu U.kg(-1).min(-1) in consecutive 10-min intervals. Six additio nal quadriplegic subjects received low-dose AVP infusions at rates of 50, 100, 200, 400, and 800 mu U.kg(-1).min(-1). All subjects were stud ied once with and once without administration of a selective V-1-recep tor antagonist. During high-dose AVP infusions without V-1-receptor bl ockade, mean arterial pressure (MAP) increased from 80 +/- 4 to 87 +/- 5 mmHg (P < 0.05) in quadriplegic subjects but was unchanged in contr ol subjects. In the presence of V-1-receptor blockade, MAP decreased f rom 75 +/- 4 to 58 +/- 4 mmHg(P < 0.001), and heart rate (HR) increase d from 61 +/- 5 to 80 +/- 5 beats/min (P < 0.001) in quadriplegic subj ects. In the studies on control subjects, MAP decreased only from 75 /- 3 to 72 +/- 5 mmHg (P < 0.05), whereas HR increased from 64 +/- 4 t o 87 +/- 4 beats/min (P < 0.001). Plasma renin activity (PRA) increase d in both quadriplegic and control subjects. The effects of low-dose A VP infusions on MAP, HR, and PRA in quadriplegic subjects were similar to those observed during high-dose infusions. Thus, in the absence of baroreceptor-mediated sympathetic nervous system responses, a vasodil atory effect of AVP that is capable of producing marked reductions in MAP can be demonstrated in the presence of V-1-receptor blockade.