To determine the effects on pre- and post-glomerular vascular resistance of adrenocorticotrophin (ACTH)-induced hypertension in rats, before and after blockade of nitric oxide formation.
Four groups of Sprague–Dawley rats were studied. Measurements were made in ACTH- (Synacthen Depot, 0.25 mg/kg twice daily for 8 days) and sham-treated anaesthetized rats, before and after either N ω-nitro-l-arginine (l-NNA, 6 mg/kg) or vehicle.
Whole-kidney and single-nephron haemodynamics and function were measured. Glomerular capillary pressure was estimated from tubular stop-flow pressure measurements.
Blood pressure (P< 0.001), renal blood flow (RBF, P< 0.05) and glomerular filtration rate (P< 0.01) were increased following ACTH treatment compared with sham. There were no differences in either total renal, or pre- or post-glomerular vascular resistances, but stop-flow-estimated glomerular capillary pressure was elevated (P< 0.001) as was single-nephron glomerular filtration rate (SNGFR) (P< 0.001) and single-nephron blood flow (P< 0.01) in the ACTH- compared to the sham-treated rats. l-NNA treatment increased blood pressure by a similar extent in both ACTH- and sham-treated rats, but reduced RBF (P< 0.05) and glomerular filtration rate (GFR) (P< 0.05) more in the ACTH group; similar changes were seen in single-nephron values. l-NNA increased pre- and post-glomerular resistances to a greater extent in the ACTH group.
ACTH-induced hypertension produced glomerular hypertension and hyperfiltration, which may be due to nitric oxide-related vasodilatation of the renal vasculature.