Effect of Epithelial Sodium Channel Blockade on the Myogenic Response of Rat Juxtamedullary Afferent Arterioles

The mechanotransduction mechanism underlying the myogenic response is poorly understood, but evidence implicates participation of epithelial sodium channel (ENaC)-like proteins. Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfuse...

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Veröffentlicht in:	Hypertension (Dallas, Tex. 1979) Tex. 1979), 2009-11, Vol.54 (5), p.1062-1069
Hauptverfasser:	Guan, Zhengrong, Pollock, Jennifer S, Cook, Anthony K, Hobbs, Janet L, Inscho, Edward W
Format:	Artikel
Sprache:	eng
Schlagworte:	Amiloride - analogs & derivatives Amiloride - pharmacology Analysis of Variance Animals Arterial hypertension. Arterial hypotension Arterioles - drug effects Arterioles - physiology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Disease Models, Animal Experimental diseases Juxtaglomerular Apparatus - blood supply Juxtaglomerular Apparatus - drug effects Male Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Probability Random Allocation Rats Rats, Sprague-Dawley Reference Values Sodium Channel Blockers - pharmacology Vasoconstriction - drug effects Vasodilation - drug effects
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Zusammenfassung:	The mechanotransduction mechanism underlying the myogenic response is poorly understood, but evidence implicates participation of epithelial sodium channel (ENaC)-like proteins. Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfused juxtamedullary nephron technique. Papillectomy was used to isolate myogenic influences by eliminating tubuloglomerular feedback signals. Autoregulatory responses were assessed by manipulating perfusion pressure in 30-mm Hg steps. Under control conditions, arteriolar diameter increased by 15% from 13.0±1.3 to 14.7±1.2 μm (P
ISSN:	0194-911X 1524-4563
DOI:	10.1161/HYPERTENSIONAHA.109.137992