A narrow segment of the efferent arteriole controls efferent resistance in the hydronephrotic rat kidney

We microscopically examined the narrow segment of the efferent arteriole (NSEA) in the hydronephrotic kidney of rats in vivo. This segment is routinely found at the proximal efferent arteriole adjacent to the glomerulus and is characterized by a narrowing due to a cellular structure which bulges into the lumen. The existence of NSEA has been described in a previous study from our laboratory, but it was not examined in detail; its functional behavior in particular is still unknown. In the present study, we measured changes in luminal diameter of NSEA during reduction of renal perfusion pressure and in response to angiotensin II (Ang II), saralasin, and nitroprusside. The mean luminal diameter of NSEA at its narrowest point was 5.1 microns and its effective length was 8.4 microns. Reduction of renal perfusion pressure from 115 to 90, 70, and 40 mm Hg decreased NSEA diameter by 9, 15, and 23%, respectively. Topical application of saralasin (10(-5) M) or nitroprusside (10(-4) M) to the kidney dilated NSEA by 10 or 20%, respectively, and attenuated the pressure-dependent constriction of NSEA. Intravenous infusion of Ang II at rates of 50, 100, 200, and 400 ng/min/kg constricted NSEA lumen by 7, 15, 20, and 21%, respectively. The vascular bed of the hydronephrotic kidney was scanned morphologically, and a mathematical model was developed from these data. With this model, we could calculate the effect of segmental diameter changes on total renal resistance as well as flow and pressure at different vascular levels. NSEA contributed 4% to the total renal resistance and 20% to the efferent resistance under control conditions. Lowering of renal perfusion pressure increased the efferent arteriolar resistance up to 50% above the control value mainly as a result of constriction of NSEA. Our data indicate that efferent resistance increases at reduced renal perfusion pressure and leads to a stabilization of glomerular pressure. The rise of efferent resistance is mediated primarily by NSEA constriction, and the renin-angiotensin system is involved in this regulation.