Pressor contributions from angiotensin and vasopressin after polyethylene glycol

Abstract

Isosmotic volume depletion was induced by subcutaneous injection of 5 ml of polyethylene glycol (PEG; 20 M; 30%) in Long-Evans rats and in rats deficient in hypothalamic vasopressin (Brattleboro rats). In the PEG-treated Long-Evans rats, captopril caused a hypotension that was greater than that seen in saline-injected controls. Pretreatment with the vasopressin (V1 receptor) antagonist d(CH2)5DAVP did not, itself, cause a fall in blood pressure, but it enhanced the hypotensive effect of captopril in the PEG-treated Long-Evans rats. The PEG-treated Brattleboro rats had similar resting blood pressures to the PEG-treated Long-Evans rats, but in the former group, captopril caused a more profound and progressive hypotension than was seen in any of the present experimental regimes used in the Long-Evans rats. This suggests that, during hypovolemia induced by PEG, Brattleboro rats were either more dependent on the renin-angiotensin system for the maintenance of arterial blood pressure than were Long-Evans rats treated acutely with a vasopressin (V1) receptor antagonist or less able to recruit sympathoadrenal mechanisms to compensate for the sudden loss of the renin-angiotensin system.