Plasma vasopressin as influenced by acute and chronic blockade of the renin-angiotensin system.

The activation of the renin-angiotensin system that occurs during the development of congestive heart failure (CHF) may be accompanied by continued secretion of vasopressin (AVP) in response to non-osmotic stimuli. Increased supine plasma AVP levels (by radio-immunoassay) were found in 31 patients with moderate to severe CHF (11.49 +/- 1.00 pg/ml s.e.m.) 24 h after the last diuretic dose, which correlated with plasma renin activity (PRA) (r = 0.37, P less than 0.05). However, acute inhibition of converting enzyme with captopril did not decrease plasma AVP levels (14.9 +/- 3.9 versus 14.0 +/- 2.8 pg/ml, n = 8). Indeed, in six out of eight patients, plasma AVP actually increased following captopril - presumably secondary to haemodynamic changes. Readministration of captopril after 4 months of captopril treatment, 12 h after the last dose, again did not change AVP levels (9.58 +/- 1.2 versus 13.1 +/- 1.9 pg/ml), whereas changes in haemodynamics, PRA and angiotensin II were as expected and similar to the first test. These results suggest that the acute haemodynamic action of captopril in CHF is not mediated via suppression of vasopressin, although in some patients with non-osmotic vasopressin, excess activation of the renin-angiotensin-aldosterone system might constitute a factor.