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.
Resta
T C
TC
Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque 87131-5218, USA.
Walker
B R
BR
D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000494:pharmacology / Q000502:physiology*; D003714:Denervation; D006439:Hemodynamics / Q000187:drug effects; D007668:Kidney / Q000098:blood supply* / Q000294:innervation; D008297:Male; D009392:Nephrectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000187:drug effects; D014661:Vasoconstriction
D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin