Vasopressin V2-receptor-mediated hypotensive response in man
article
The V2-agonist desamino-8-D-arginine vasopressin (DDAVP), injected at 400 ng/kg in 10 min intravenously, lowered systolic blood pressure from 160 ± 9 to 142 ± 2 mmHg (mean ± s.e.m.), diastolic blood pressure from 104 ± 3 to 89 ± 5 mmHg and increased the heart rate from 68 ± 4 to 91 ± 6 beats/min. Plasma renin increased from 27 ± 5 to 73 ± 15 μ.U/ml and noradrenaline from 280 ± 35 to 576 ± 82 pg/ml. We have previously suggested that the hypotensive effect of DDAVP might be due to antagonism of the V1-mediated pressor effect of DDAVP. Experiments in vitro showed such antagonism only at very high concentrations of DDAVP (pA2 6-7). The plasma levels of DDAVP in the patients, approximately 10-9 mol/l, are probably too low to cause V1-antagonism. Patients with hereditary nephrogenic diabetes insipidus are resistant to the Vr mediated antidiuretic action of vasopress1n and DOAVP, and to the Vrmediated stimulatory effect on the release of clotting factor VIII:C and the tissue-type plasminogen activator (t-PA), suggesting a more general Vr receptor defect. These patients also showed no changes in blood pressure. heart rate. plasma renin and noradrenaline after DDAVP. Thus, vasodilation and baroreflex-induced increased sympathetic activi ty in response to DDAVP appears to depend on Vr receptor activation.
TNO Identifier
268237
Source
Journal of hypertension, 5(suppl 5), pp. S107-S109.
Pages
S107-S109
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