Role of atrial natriuretic peptide in mediating the blood pressure-independent natriuresis elicited by systemic inhibition of nitric oxide.

Publisher: Springer Country of Publication: Germany NLM ID: 0154720 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1432-2013 (Electronic) Linking ISSN: 00316768 NLM ISO Abbreviation: Pflugers Arch Subsets: MEDLINE

Original Publication: Berlin, New York, Springer.

Blood Pressure* ; Natriuresis*; Atrial Natriuretic Factor/*blood ; Nitric Oxide/*metabolism; Animals ; Hemodynamics ; Kidney/drug effects ; Kidney/metabolism ; Kidney/physiology ; Male ; Nitric Oxide Synthase/antagonists & inhibitors ; Peptides, Cyclic/pharmacology ; Rats ; Rats, Sprague-Dawley ; Sodium/metabolism

While it is clearly recognized that increased intrarenal nitric oxide (NO) levels elicit natriuresis, confounding data showing that systemic nitric oxide synthase inhibition (NOSi) also increases sodium excretion (UNaV) poses a conundrum. This response has been attributed to the associated increases in arterial pressure (AP); however, the increases in AP and in UNaV are temporally dissociated. The changes in regional renal haemodynamics induced by NOSi could also contribute to the alterations of UNaV. To evaluate the roles of AP and non-AP mechanisms mediating the natriuresis, N ω-nitro-L-arginine methyl ester hydrochloride (L-NAME) was infused i.v. at doses ranging from 5 to 50 μg/kg/min in anaesthetized rats. UNaV, perfusion of the cortex (cortical blood flow, CBF) and medulla (medullary blood flow, MBF) with laser-Doppler flowmetry and glomerular filtration rate (GFR) were measured. UNaV increased from 0.6 ± 0.2 to 1.6 ± 0.1 μmol/kg/min (P < 0.05) with the lower nonpressor doses. With the higher doses, AP increased from 116 ± 4 to 122 ± 4 mmHg and UNaV increased from 1.1 ± 0.3 to 3.3 ± 0.7 μmol/min/g (P < 0.002). UNaV increased similarly in a group where renal AP was maintained at baseline levels. The associated reductions in CBF (17 ± 5 and 38 ± 5 %) and MBF (27 ± 6 and 52 ± 6 %) would be expected to attenuate rather than contribute to the natriuresis. Plasma atrial natriuretic peptide (ANP) concentrations increased significantly following NOSi. Anantin, a natriuretic peptide receptor-A blocker, prevented or reversed the L-NAME-induced natriuresis without altering the L-NAME-induced changes in AP or CBF. The results indicate that increased ANP and related natriuretic peptides mediate the AP-independent natriuresis, at least partly, elicited by systemic L-NAME infusion and help resolve the conundrum of natriuresis during systemic NOSi.

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P20 RR017659 United States RR NCRR NIH HHS; R01 HL018426 United States HL NHLBI NIH HHS; HL-18426 United States HL NHLBI NIH HHS; P30 GM103337 United States GM NIGMS NIH HHS; P20 RR-017659 United States RR NCRR NIH HHS

0 (Peptides, Cyclic)
133658-45-4 (anantin)
31C4KY9ESH (Nitric Oxide)
85637-73-6 (Atrial Natriuretic Factor)
9NEZ333N27 (Sodium)
EC 1.14.13.39 (Nitric Oxide Synthase)

Date Created: 20140624 Date Completed: 20151217 Latest Revision: 20211021

20221213

PMC4276550

10.1007/s00424-014-1557-4

24953240