Effect of a converting-enzyme inhibitor on vasa recta blood flow in rat kidney

• Published in: The American journal of physiology Vol. 254; no. 4 Pt 2; pp. F492 - F499
• Main Authors: Hansell, P, Sjöquist, M, Ulfendahl, H R
• Format: Journal Article
• Language: English
• Published: United States 01-04-1988
• Subjects: Animals; Captopril - pharmacology; Erythrocytes - physiology; Female; Kidney Medulla - blood supply; Kinetics; Male; Rats; Rats, Inbred Strains; Regional Blood Flow - drug effects
• ISSN: 0002-9513
• DOI: 10.1152/ajprenal.1988.254.4.f492

In young anesthetized Munich-Wistar rats, red cell flux (Qrbc) was measured in the vasa recta of the exposed renal papilla by means of fluorescently labeled erythrocytes. To study the vasoreactivity of the juxtamedullary vasculature and its sensitivity to converting-enzyme inhibition, measurements of Qrbc were made before and after continuous intravenous infusion of the angiotensin I converting-enzyme inhibitor captopril (3 mg.h-1.kg body wt-1). A time control group that received vehicle alone was studied in parallel. Captopril acts as a vasodilator and reduces systemic arterial pressure. Captopril treatment increased Qrbc by 40 +/- 4% (n = 9, P less than 0.001) and decreased blood pressure by 9% (P less than 0.001). In the time control group no statistically significant change occurred in either Qrbc (+6 +/- 8%, n = 10) or blood pressure (-1%). Urine samples were taken from the papillary tip. In neither of the groups did the urine osmolality show a statistically significant change. In the time control group the values before and after intravenous infusion were 1,006 +/- 61 and 1,091 +/- 70 mosmol/kg H2O, respectively, and in the captopril-treated animals the corresponding values were 1,150 +/- 85 and 1,210 +/- 60 mosmol/kg H2O, respectively. These results confirm the suggestion that there is high vasoreactivity in the juxtamedullary vasculature and that this region is sensitive to inhibition of angiotensin I-converting enzyme, the latter sensitivity implying that angiotensin II plays a role in the regulation of juxtamedullary vascular resistance.