Development of high sodium renal hypertension during chronic blockade of the vascular effects of vasopressin.

Studies in sodium-dependent models of hypertension have shown that arginine-vasopressin (AVP) plays an important role in the maintenance of blood pressure, predominantly through its vasoconstrictor action. In addition to AVP, the sympathetic nervous system (SNS) also acts to maintain blood pressure in high sodium one-kidney, figure-8 renal wrap hypertension. The purpose of this study was to determine if chronic blockade of vascular AVP (V1) receptors affected the induction of high sodium renal hypertension and the contribution of the SNS to the maintenance of blood pressure. Rats receiving chronic s.c. administration of a V1 antagonist, d(CH2)5Tyr(Me)AVP, or vehicle were subjected to renal wrapping or sham surgery, V1 receptor blockade was confirmed periodically by an 80 +/- 3% reduction of the pressor response to a bolus injection of 10 mU/kg of AVP. d(CH2)5Tyr(Me)AVP did not affect the development of hypertension or the associated changes in plasma sodium, potassium, osmolality and hematocrit. In renal-wrapped rats, ganglionic blockade caused a greater fall in blood pressure in animals treated with d(CH2)5Tyr(Me)AVP than in vehicle-treated animals. However, this apparent increase in SNS function was not responsible for the hypertension in d(CH2)5Tyr(Me)AVP-treated, renal-wrapped rats, inasmuch as ganglionic blockade lowered blood pressure a similar amount in normotensive d(CH2)5Tyr(Me)AVP-treated, sham-operated rats and blood pressure remained elevated after combined blockade of the SNS, AVP and the renin-angiotensin systems. These results indicated that chronic blockade of V1 receptors did not alter the induction of high sodium renal hypertension and the mechanism of the elevated blood pressure was not through an activation of the SNS or other neurohumoral mechanisms.