Salt-Dependent Inhibition of Epithelial Na+ Channel–Mediated Sodium Reabsorption in the Aldosterone-Sensitive Distal Nephron by Bradykinin

We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na channel (ENaC) via the bradykinin B2 receptor (B2R)-Gq/11-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physi...

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Veröffentlicht in:	Hypertension (Dallas, Tex. 1979) Tex. 1979), 2012-11, Vol.60 (5), p.1234-1241
Hauptverfasser:	Mamenko, Mykola, Zaika, Oleg, Doris, Peter A, Pochynyuk, Oleh
Format:	Artikel
Sprache:	eng
Schlagworte:	Aldosterone - metabolism Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Bradykinin - pharmacology Calcium - metabolism Captopril - pharmacology Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Epithelial Sodium Channels - metabolism In Vitro Techniques Male Medical sciences Membrane Potentials - drug effects Mice Mice, Inbred C57BL Mice, Knockout Nephrons - cytology Nephrons - drug effects Nephrons - metabolism Patch-Clamp Techniques Peptidyl-Dipeptidase A - metabolism Receptor, Bradykinin B1 - deficiency Receptor, Bradykinin B1 - genetics Receptor, Bradykinin B2 - deficiency Receptor, Bradykinin B2 - genetics Sodium - administration & dosage Sodium - metabolism Sodium Chloride - metabolism Time Factors
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Zusammenfassung:	We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na channel (ENaC) via the bradykinin B2 receptor (B2R)-Gq/11-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physiological role of BK cascade in regulation of ENaC in native tissue, aldosterone-sensitive distal nephron. Under normal sodium intake (0.32% Na), ENaC open probability (Po) was modestly elevated in B1R, B2R mice compared with wild-type mice. This difference is augmented during elevated Na intake (2.00% Na) and negated during Na restriction (
ISSN:	0194-911X 1524-4563
DOI:	10.1161/HYPERTENSIONAHA.112.200469