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.