Castrop, Hayo and Schweda, Frank and Mizel, Diane and Huang, Yuning and Briggs, Josie and Kurtz, Armin and Schnermann, Jurgen (2004) Permissive role of nitric oxide in macula densa control of renin secretion. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 286 (5). F848-F857. ISSN 1931-857X, 1522-1466
Full text not available from this repository. (Request a copy)Abstract
Experiments were performed in neuronal (nNOS)- and endothelial nitric oxide synthase ( eNOS)- deficient mice to study the role of nitric oxide ( NO) in macula densa control of renin secretion in vivo and in the isolated, perfused mouse kidney. Acute and chronic administration of loop diuretics was used as a method to stimulate macula densa-mediated renin secretion. Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg . kg(-1) . day(-1)) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOS-/- mice. Responses to furosemide were also maintained in eNOS-/- mice, but the administration of N-omega-nitro-L-arginine methyl ester (L-NAME) markedly attenuated the PRC response to furosemide in these mice. In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice. Bumetanide only marginally increased renin secretion in L-NAME-treated kidneys, but the bumetanide effect was normalized by S-nitroso-N-acetyl-penicillamine. Basal PRC was significantly reduced in male nNOS -/- mice compared with nNOS +/+ (189 +/- 28 vs. 355 +/- 57 ng ANG I . ml(-1) . h(-1); P = 0.017). There was no significant difference in PRC between eNOS -/-, and eNOS -/- mice. Basal renin secretion rates in perfused kidneys isolated from nNOS -/- or eNOS -/- mice were markedly reduced compared with wild-type controls. Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion. However, NO independent of its exact source permits the macula densa pathway of renin secretion to function normally.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | SYNTHASE KNOCKOUT MICE; JUXTAGLOMERULAR CELLS; GENE-EXPRESSION; RELAXING FACTOR; ANGIOTENSIN-II; BLOOD-PRESSURE; RELEASE; FUROSEMIDE; INHIBITION; KIDNEY; plasma renin; isolated; perfused kidney; neuronal nitric oxide synthase knockout; endothelial nitric oxide synthase knockout; furosemide; bumetanide |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Armin Kurtz |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 20 Jul 2021 08:39 |
| Last Modified: | 20 Jul 2021 08:39 |
| URI: | https://pred.uni-regensburg.de/id/eprint/37654 |
Actions (login required)
 |
View Item |
