Enhanced renal vasoconstrictor responsiveness to vasopressin after renal denervation

Previous studies from our laboratory and others demonstrated a relative insensitivity of the renal vasculature to the vasoconstrictor influences of arginine vasopressin (AVP). Experiments were therefore conducted to identify the possible roles of renal sympathetic withdrawal and V2-vasopressinergic receptor-mediated vasodilation in this response. Renal hemodynamic responses to AVP or saline vehicle were examined in the presence or absence of either selective V1-vasopressinergic-receptor blockade or nonselective vasopressinergic-receptor antagonism in conscious intact and renal-denervated rats. Our results indicate that renal denervation profoundly augmented AVP-induced renal vasoconstriction, whereas no differences were observed in the responses to V1-receptor blockade versus combined V1, V2-receptor antagonism. These findings are consistent with a role for renal sympathoinhibition in mediating the relative insensitivity of the renal bed to the vasoconstrictor effects of AVP in conscious rats but do not support a modulatory influence of V2-receptor activity in this response.