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1 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
2 Institut fuer Physiologie, Universitaet Regensburg, Regensburg, Germany
* To whom correspondence should be addressed. E-mail: jurgens{at}intra.niddk.nih.gov.
were performed in nNOS and eNOS deficient mice to study the role of nitric oxide 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 of PRC in response to a 3 day infusion of bumetanide (50 mg kg-1d-1) or an acute i.p. injection of furosemide (50 mg/kg) were not markedly altered in nNOS-/- mice. Responses to furosemide were also maintained in eNOS-/- mice, but the administration of 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-/-. Bumetanide only marginally increased renin secretion in LNAME treated kidneys, but the bumetanide effect was normalized by SNAP. Basal plasma renin concentration (PRC) was significantly reduced in male nNOS-/- mice compared to nNOS+/+ (189±28 ng Ang I ml-1h-1 vs. 355±57 ng Ang I ml-1h-1; p=.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 to 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.
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