LOCALLY PRODUCED EDRF CONTROLS PREGLOMERULAR RESISTANCE AND ULTRAFILTRATION COEFFICIENT

During systemic acute blockade of endogenous endothelial-derived relaxing factor (EDRF) with N-monomethyl-L-arginine (NMA), a significant rise in arterial blood pressure (BP) occurred in the anesthetized rat. Renal vasoconstriction was also seen, with complex changes in glomerular hemodynamics; both preglomerular (R(A)) and efferent arteriolar (R(E)) resistances increased, producing a fall in glomerular plasma flow (Q(A)) and a rise in glomerular blood pressure (P(GC)). The glomerular capillary ultrafiltration coefficient (K(f)) was reduced. The net effect was a small fall in single-nephron glomerular filtration rate (SNGFR). To determine the effects of local EDRF blockade, two additional groups were studied with intrarenal administration of NMA; in the first series, one-tenth of the systemic dose was given, which produced no change in BP, a small renal vasoconstriction with an increase in RA, but no change in R(E); thus P(GC) was unaffected. K(f) fell, and a small reduction in SNGFR was seen. With a larger intrarenal dose of NMA (one-fifth systemic) a moderate rise in BP occurred, but only R(A) rose; R(E) and P(GC) were unaffected, and K(f) and SNGFR fell. These observations suggest that locally produced EDRF controls R(A) and K(f) and that a rise in R(E) and P(GC) is only seen with systemic EDRF blockade when a large rise in BP occurs.