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 (RA) and efferent arteriolar (RE) resistances increased, producing a fall in glomerular plasma flow (QA) and a rise in glomerular blood pressure (PGC). The glomerular capillary ultrafiltration coefficient (Kf) 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 RE; thus PGC was unaffected. Kf 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 RA rose; RE and PGC were unaffected, and Kf and SNGFR fell. These observations suggest that locally produced EDRF controls RA and Kf and that a rise in RE and PGC is only seen with systemic EDRF blockade when a large rise in BP occurs.