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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Nitric oxide participates in calcium-mediated regulation of renin release
1Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, MI 48202-2689.
Abstract:
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(-4) mol/L NG-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 < .05). When calcium was eliminated from the incubation medium, basal renin release doubled (to 133.1 +/- 15.2 [ng Ang I/h]/mg per 30 minutes incubation, P < .001). Without calcium, inhibiting nitric oxide synthesis had no further effect on renin release (126.8 +/- 17.7 [ng Ang I/h]/mg per 30 minutes incubation). High-calcium medium (7.8 mmol/L) reduced basal renin release by half (30.8 +/- 4.8 [ng Ang I/h]/mg per 30 minutes incubation, P < .001), but inhibiting nitric oxide synthesis in high-calcium medium stimulated renin release by 50% (46.9 +/- 6.2 [ng Ang I/h]/mg per 30 minutes incubation, P < .005). Addition of the calmodulin inhibitor W-7 completely reversed the inhibition of renin by high-calcium medium.(ABSTRACT TRUNCATED AT 250 WORDS)
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