Exercise training normalizes renal blood flow responses to acute hypoxia in experimental heart failure: role of the α1-adrenergic receptor.

Autor:	Pügge C; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska., Mediratta J; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska., Marcus NJ; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska., Schultz HD; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska., Schiller AM; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska., Zucker IH; Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska izucker@unmc.edu.
Jazyk:	angličtina
Zdroj:	Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2016 Feb 01; Vol. 120 (3), pp. 334-43. Date of Electronic Publication: 2015 Nov 25.
DOI:	10.1152/japplphysiol.00320.2015
Abstrakt:	Recent data suggest that exercise training (ExT) is beneficial in chronic heart failure (CHF) because it improves autonomic and peripheral vascular function. In this study, we hypothesized that ExT in the CHF state ameliorates the renal vasoconstrictor responses to hypoxia and that this beneficial effect is mediated by changes in α1-adrenergic receptor activation. CHF was induced in rabbits. Renal blood flow (RBF) and renal vascular conductance (RVC) responses to 6 min of 5% isocapnic hypoxia were assessed in the conscious state in sedentary (SED) and ExT rabbits with CHF with and without α1-adrenergic blockade. α1-adrenergic receptor expression in the kidney cortex was also evaluated. A significant decline in baseline RBF and RVC and an exaggerated renal vasoconstriction during acute hypoxia occurred in CHF-SED rabbits compared with the prepaced state (P < 0.05). ExT diminished the decline in baseline RBF and RVC and restored changes during hypoxia to those of the prepaced state. α1-adrenergic blockade partially prevented the decline in RBF and RVC in CHF-SED rabbits and eliminated the differences in hypoxia responses between SED and ExT animals. Unilateral renal denervation (DnX) blocked the hypoxia-induced renal vasoconstriction in CHF-SED rabbits. α1-adrenergic protein in the renal cortex of animals with CHF was increased in SED animals and normalized after ExT. These data provide evidence that the acute decline in RBF during hypoxia is caused entirely by the renal nerves but is only partially mediated by α1-adrenergic receptors. Nonetheless, α1-adrenergic receptors play an important role in the beneficial effects of ExT in the kidney. (Copyright © 2016 the American Physiological Society.)
Databáze:	MEDLINE
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