Km. Huch et al., HEMODYNAMIC-RESPONSE TO VASOPRESSIN DURING V-1-RECEPTOR ANTAGONISM INBAROREFLEX-DEFICIENT SUBJECTS, American journal of physiology. Regulatory, integrative and comparative physiology, 37(1), 1995, pp. 156-163
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.