Objectives: We tested whether vasoconstriction of juxtamedullary glomerular arterioles contributes to vasopressin V1-receptor-mediated reductions in medullary perfusion (MBF).
Design and methods: The left kidney of pentobarbitone anaesthetized rabbits was denervated, a perivascular flow probe placed around the renal artery and laser-Doppler flow probes positioned in the inner medulla and on the cortical surface. Rabbits then received a 30 min intravenous infusion of [Phe2,Ile3,Orn8]vasopressin (V1-AG; 30 ng/kg per min;n = 7) or its vehicle (n = 7). Kidneys were perfusion fixed at the final recorded mean arterial pressure (MAP) and filled with methacrylate casting material. Diameters of afferent and efferent arterioles were determined by scanning electron microscopy.
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 significantly affect these variables. After vehicle- and V1-AG-treatment, juxtamedullary afferent arteriole luminal diameter averaged 15.35 ± 1.31 and 15.88 ± 1.86 μm, respectively (P = 0.92), while juxtamedullary efferent arteriole luminal
diameter averaged 17.75 ± 1.86 and 18.36 ± 2.24 μm, respectively (P = 0.93).
Conclusions: V1-AG reduced MBF but did not significantly affect juxtamedullary arteriolar diameter. Our results therefore do not support a role for juxtamedullary arterioles in producing V1-receptor-mediated reductions in MBF, suggesting that downstream vascular elements (e.g. outer medullary descending vasa recta) might be involved.
Department of Physiology, Monash University, Victoria, Australia.
Sponsorship: This work was supported by grants from the National Health and Medical Research Council of Australia (977713), the National Heart Foundation of Australia (G 98M 0125) and the Ramaciotti Foundations (A6370 & RA159/98).
Correspondence and requests for reprints to Dr Roger Evans, Department of Physiology, PO Box 13F, Monash University, Victoria, 3800, Australia. Tel: +61 3 9905 1466; fax: +61 3 9905 2566; e-mail: email@example.com
Received 28 August 2000 Revised 20 November 2000 Accepted 20 November 2000