The central effects of a nitric oxide synthase inhibitor (N omega-nitro-L-arginine) on blood pressure and plasma renin.

An endothelium-derived relaxing factor has been identified as nitric oxide (NO). Peripheral and central administration of nitric oxide synthase inhibitors result in an increase in renal sympathetic nerve activity and an increase in blood pressure. The goal of our study was to determine if the increase in blood pressure following central NO synthase inhibition with N omega-nitro-L-arginine (L-NNA) is caused by the release of renin.

Time course of stimulation of renal renin messenger RNA by furosemide.

Renin secretion responds rapidly to a variety of stimuli; however, reported changes in renal renin messenger RNA (mRNA) levels in vivo have been observed only after prolonged stimulation. Studies were designed to test whether rapid changes in renin mRNA levels can be produced in vivo. In the first series, Sprague-Dawley rats received furosemide (10 mg/kg) intraperitoneally and a low sodium diet (0.

Analysis of active renin heterogeneity.

Active renin is a heterogeneous enzyme that can be separated into multiple forms with high-resolution isoelectric focusing. The isoelectric heterogeneity may result from differences in glycosylation between the different forms. In order to determine the relationship between active renin heterogeneity and differences in composition or attachment of oligosaccharides, two separate experiments were performed: (i) Tunicamycin, which interferes with normal glycosylation processing, increased the proportion of relatively basic renin forms secreted into the incubation media by rat renal cortical slices.