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

Abstract

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.

Effects of enalapril and sodium depletion on the renin-angiotensin system in hydronephrotic mice

“…The results of this study confirmed that the kidney becomes hydronephrotic and loses its tubular structure when the left ureter is tied completely, so that it primarily consists of an arteriole system and glomeruli (Bührle et al 1986;Fretschner et al 1990). In the present study, there was clear biological and morphological evidence of continuing renin synthesis in the hydronephrotic kidney after ureteral ligation.…”

Contribution of endothelin receptors in renal microvessels in acute cyclosporine-mediated vasoconstriction in rats

“…Circumstantial evidence for CsA-induced constriction of large preglomerular vessels can also be derived from the findings that in this and previous studies on the hydronephrotic kidney [17,34] CsA reduced GBF by about 80%, whereas in normal kidneys the reduction in renal blood flow due to a comparable dose was half as much [16, 19 -23]. This difference may be related to the finding that the large preglomerular vessels contribute twice as much to the total renal resistance in the hydronephrotic kidney than in the normal kidney [35]. Preglomerular vasoconstriction due to CsA has been shown by Kon et al [16], who measured a reduction in glomerular capillary pressure due to increased preglomerular vascular resistance.…”

Evidence‐based treatment of hypertension in patients with diabetes mellitus

“…The glomerular microcirculation is unique in its construction because it is in series between two resistance vessels, the afferent and efferent arterioles. Although both afferent and efferent arterioles vasoconstrict to AII, there is experimental evidence to suggest that AII produces a greater efferent arteriolar vasoconstriction compared with the afferent arteriole [29–32]. The kidney is able to autoregulate intraglomerular pressures such that over a wide range of systolic blood pressures, the GFR remains remarkably constant.…”