Kurtz, Armin and Götz, Karl-Heinz and Hamann, Marlies and Wagner, Charlotte (1998) Stimulation of renin secretion by nitric oxide is mediated by phosphodiesterase 3. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 95 (8). pp. 4743-4747. ISSN 0027-8424
Full text not available from this repository.Abstract
This study aimed to characterize the cellular pathways along which nitric oxide (NO) stimulates renin secretion from the kidney. Using the isolated perfused rat kidney model we found that renin secretion stimulated 4- to 8-fold by low per fusion pressure (40 mmHg), by macula densa inhibition (100 mu mol/liter of bumetanide), and by adenylate cyclase activation (3 nmol/liter of isoproterenol) was markedly attenuated by the NO synthase inhibitor nitro-L-arginine methyl ester (L-Name) (1 mM) and that the inhibition by L-Name was compensated by the NO-donor sodium nitroprusside (SNP) (10 mu mol/liter). Similarly, inhibition of cAMP degradation by blockade of phosphodiesterase 1 (PDE-1) (20 mu mol/liter of 8-methoxymethyl-1-methyl-3-(3-methylpropyl)- xanthine) or of PDE-4 (20 mu mol/liter of rolipram) caused a 3- to 4-fold stimulation of renin secretion that was attenuated by L-Name and that was even overcompensated by sodium nitroprusside. Inhibition of PDE3 by 20 mu mol/liter of milrinone or by 200 nmol/liter of trequinsin caused a 5- to 6-fold stimulation of renin secretion that was slightly enhanced by NO synthase inhibition and moderately attenuated by NO donation. Because PDE3 is a cGMP-inhibited cAMP-PDE the role of endogenous cGMP for the effects of NO was examined by the use of the specific guanylate cyclase inhibitor 1-H-(1,2,4)oxodiazolo(4,3a)quinosalin-1-one (20 mu mol). In the presence of 1H-[1,2,4]oxodiazolo[4,3-a]quinoxalin-1-one the effect of NO on renin secretion was abolished, whereas PDE-3 inhibitors exerted their normal effects. These findings suggest that PDE3 plays a major role for the cAMP control of renin secretion. Our findings are compatible with the idea that the stimulatory effects of endogenous and exogenous NO on renin secretion are mediated by a cGMP-induced inhibition of cAMP degradation.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | JUXTAGLOMERULAR CELLS; GENE-EXPRESSION; RELAXING FACTOR; RELEASE; PRESSURE; INHIBITION; PHYSIOLOGY; SYNTHASE; BLOCKADE; CALCIUM |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Armin Kurtz |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 24 Feb 2023 11:04 |
| Last Modified: | 24 Feb 2023 11:04 |
| URI: | https://pred.uni-regensburg.de/id/eprint/49940 |
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