Effects of activation of vasopressin-V-1-receptors on regional kidney blood flow and glomerular arteriole diameters

Objectives We tested whether vasoconstriction of juxtamedullary glomerular arterioles contributes to vasopressin V-1-receptor-mediated reductions in m edullary perfusion (MBF). Design and methods The left kidney of pentobarbitone anaesthetized rabbits was denervated, a perivascular flow probe placed around the renal artery an d laser-Doppler flow probes positioned in the inner medulla end on the cort ical surface. Rabbits then received a 30 min intravenous infusion of [Phe(2 ), IIe(3),Orn(8)] vasopressin (V-1-AG; 30 ng/kg per min; n = 7) or its vehi cle (n = 7). Kidneys were perfusion fixed at the final recorded mean arteri al pressure (MAP) and filled with methacrylate casting material. Diameters of afferent and efferent arterioles were determined by scanning electron mi croscopy. Results V1-AG increased MAP (19 +/- 3%) and reduced MBF (30 +/- 8%) but not cortical perfusion or total renal blood flow. Vehicle-treatment did not si gnificantly affect these variables. After vehicle- and V-1-AG-treatment, ju xtamedullary afferent arteriole luminal diameter averaged 15.35 +/- 1.31 an d 15.88 +/- 1.86 mum, respectively (P = 0.92), while juxtamedullary efferen t arteriole luminal diameter averaged 17.75 +/- 1.86 and 18.36 +/- 2.24 mum , respectively (P = 0.93), Conclusions VI-AG reduced MBF but did not significantly affect juxtamedulla ry arteriolar diameter. Our results therefore do not support a role for jux tamedullary arterioles in producing V-1-receptor-mediated reductions in MBF , suggesting that downstream vascular elements (e,g, outer medullary descen ding vasa recta) might be involved.