title: Angiotensin-(1-7) attenuates hyposmolarity-induced ANP secretion via the Na+-K+ pump.
abstract: The alteration in osmolarity challenges cell volume regulation, a vital element for cell survival. Hyposmolarity causes an increase in cell volume. Recently, it has been reported that the renin-angiotensin system (RAS) plays a role in cell volume regulation. We investigated the effect of angiotensin-(1-7) [Ang-(1-7)] on hyposmolarity-induced atrial natriuretic peptide (ANP) secretion in normal and diabetic (DM) rat atria and modulation of the effect of Ang-(1-7) by the Na(+)-K(+) pump. Using isolated control rat atria, we observed that perfusion of hyposmotic solution into the atria increased ANP secretion. When Ang-(1-7) [0.1 microM or 1 microM] was perfused in a hyposmolar solution, it decreased the hyposmolarity-induced ANP secretion in a dose-dependent manner. This effect of Ang-(1-7) could be mediated by the Na(+)-K(+) pump, since ouabain, an Na(+)-K(+) pump inhibitor, significantly decreased the effect of Ang-(1-7) on hyposmolarity-induced ANP secretion. In contrast, N(omega) Nitro-l-arginine methyl ester hydrochloride (l-NAME) did not modify the effect of Ang-(1-7) on the hyposmolarity-induced ANP secretion. Interestingly, the ANP secretion was increased robustly by the perfusion of the hyposmolar solution in the DM atria, as compared to the control atria. However, the inhibitory effect of Ang-(1-7) on the hyposmolarity-induced ANP secretion was not observed in the DM atria. In the DM atria, atrial contractility was significantly increased. Taken together, we concluded that Ang-(1-7) attenuated hyposmolarity-induced ANP secretion via the Na(+)-K(+) pump and a lack of Ang-(1-7) response in DM atria may partly relate to change in Na(+)-K(+) pump activity.
authors.affiliation: Department of Physiology, Diabetic Research Center, Chonbuk National University Medical School, Jeonju, South Korea.
authors.forename: Amin
authors.initials: A
authors.lastname: Shah
authors.forename: Young-Bin
authors.initials: YB
authors.lastname: Oh
authors.forename: Gao
authors.initials: G
authors.lastname: Shan
authors.forename: Chang Ho
authors.initials: CH
authors.lastname: Song
authors.forename: Byung-Hyun
authors.initials: BH
authors.lastname: Park
authors.forename: Suhn Hee
authors.initials: SH
authors.lastname: Kim
mesh_terms: D000803:Angiotensin I; D000804:Angiotensin II / Q000819:agonists / Q000037:antagonists & inhibitors / Q000494:pharmacology* / Q000502:physiology; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000503:physiopathology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D006325:Heart Atria / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D009994:Osmolar Concentration; D010446:Peptide Fragments / Q000819:agonists / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013312:Stress, Physiological / Q000187:drug effects; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D010446:Peptide Fragments; C472610:atrial natriuretic peptide, rat; D000804:Angiotensin II; D009569:Nitric Oxide; D009320:Atrial Natriuretic Factor; D000803:Angiotensin I; D000254:Sodium-Potassium-Exchanging ATPase; D006152:Cyclic GMP; C118790:angiotensin I (1-7)