Renal function contributes to antihypertensive effect of vasopressin in DOCA-salt but not spontaneous hypertension.

The contribution of sodium losses to the dramatic fall in blood pressure that follows cessation of a 3-h intravenous infusion of vasopressin (20 ng.kg-1.min-1) in hypertensive rats was investigated. Cessation of the vasopressin infusion was associated with a large fall in pressure below preinfusion basal levels (30-50 mmHg) in both spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt-hypertensive rats. In contrast, pressure returned to control levels in normotensive rats. Sodium excretion rates increased markedly during the infusions of vasopressin in both SHR and DOCA-salt-hypertensive rats but also in their appropriate normotensive controls. An equinatriuretic dose of furosemide failed to induce any change in pressure in SHR or normotensive controls. In contrast, furosemide decreased pressure in the DOCA-salt-hypertensive group, although the decrease was not as large as with vasopressin. Replacement of the sodium losses that occurred during the vasopressin infusion failed to return pressure toward control levels in SHR but did increase pressure in the DOCA-salt-hypertensive group. The results indicate a major difference between the SHR and DOCA-salt-hypertensive models. In SHR, sodium losses do not contribute to the antihypertensive effect of vasopressin, but in contrast these losses do contribute significantly to this antihypertensive effect in the DOCA-salt-hypertensive model.