Nitric Oxide Participates in Calcium-Mediated Regulation of Renin Release

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 1994-01, Vol.23 (1 Suppl I), p.I-40-I-44
• Main Author: Beierwaltes, William H
• Format: Article
• Language: English
• Subjects: Angiotensin II - pharmacology; Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Calcium - pharmacology; Calmodulin - antagonists & inhibitors; Egtazic Acid - pharmacology; Endocrine kidney. Renin-angiotensin-aldosterone system; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Isoproterenol - pharmacology; Kidney Cortex - drug effects; Kidney Cortex - enzymology; Kinetics; Male; Nitric Oxide - antagonists & inhibitors; Nitric Oxide - metabolism; omega-N-Methylarginine; Rats; Rats, Sprague-Dawley; Renin - metabolism; Sulfonamides - pharmacology; Vertebrates: endocrinology
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.hyp.23.1_suppl.i40

The regulation of renin release is unusual in that intracellular calcium reportedly acts as an inhibitory second messenger. Increased calcium not only inhibits renin release but is a cofactor in nitric oxide synthesis. Also, nitric oxide can inhibit renin release. This study was done in vitro using rat renal cortical slices to determine whether calcium-mediated renin inhibition could be in part due to the concurrent production of nitric oxide. Renin concentration in the incubation medium was determined by radioimmunoassay for angiotensin I (Ang I) generation (in nanograms Ang I per hour per milligram per 30 minutes of incubation). In all studies, n=6 to 17. In normal-calcium incubation medium (2.6 mmol/L), 10 mol/L N-monomethyl L-arginine, which blocks nitric oxide synthesis, caused an 18% increase in basal renin release (78.6±8.9 versus 66.7±5.8 [ng Ang I/h]/mg per 30 minutes incubation, P