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 pressu re that follows cessation of a 3-h intravenous infusion of vasopressin (20 ng.kg(-1).min(-1)) in hypertensive rats was investigated. Cessati on of the vasopressin infusion was associated with a large fall in pre ssure below preinfusion basal levels (30-50 mmHg) in both spontaneousl y 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 t he infusions of vasopressin in both SHR and DOCA-salt-hypertensive rat s but also in their appropriate normotensive controls. An equinatriure tic dose of furosemide failed to induce any change in pressure in SHR or normotensive controls. In contrast, furosemide decreased pressure i n the DOCA-salt-hypertensive group, although the decrease was not as l arge as with vasopressin. Replacement of the sodium losses that occurr ed during the vasopressin infusion failed to return pressure toward co ntrol levels in SHR but did increase pressure in the DOCA-salt-hyperte nsive group. The results indicate a major difference between the SHR a nd DOCA-salt-hypertensive models. In SHR, sodium losses do not contrib ute to the antihypertensive effect of vasopressin, but in contrast the se losses do contribute significantly to this antihypertensive effect in the DOCA-salt-hypertensive model.