Premium
Pendrin gene ablation enhances vascular contractility
Author(s) -
Sutliff Roy L.,
Walp Erik R.,
Bonsall Robert,
Ramosevac Semra,
Eaton Douglas C.,
Kim Young Hee,
Pham Truyen D.,
Wall Susan M.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.774.15
Subject(s) - pendrin , contractility , endocrinology , medicine , phenylephrine , chemistry , blood pressure , gene , transporter , biochemistry
Pendrin, encoded by Slc26a4, is expressed in the apical regions of a subset of renal intercalated cells, where it mediates Cl − absorption and HCO 3 − secretion through apical Cl − /HCO 3 − exchange. Pendrin null mice have reduced blood pressure and a blunted hypertensive response to aldosterone. The purpose of this study was to determine if pendrin is expressed in blood vessels and to determine if the lower blood pressure observed in pendrin null mice occurs from changes in vascular contractility. Mice were pair‐fed a balanced, NaCl‐replete diet for 7 days. Aortas were removed from wild‐type and pendrin null mice, denuded and isometrically mounted. Aortic contraction was studied using potassium chloride (KCl; 0‐80 mM) and phenylephrine (PE; 0.1 nM‐10 ìM). The sensitivity to the contractile agents was unaffected by pendrin gene ablation. However, the maximum contractile responses to KCl (14.6 ± 1.2 and 9.8 ± 1.2; N=5‐6) and PE (18.5 ± 1.3 and 12.6 ± 1.6; N=5‐6) were significantly greater in aortas from pendrin knockout mice when normalized to cross sectional area. However, in aorta Slc26a4 mRNA was detected at very low levels. Thus, pendrin gene ablation enhances vascular contractility, through an indirect effect of pendrin in the vasculature. The increased vascular contractility observed in these mutant mice is likely a compensatory response to the reduced blood pressure, rather than a cause of the blood pressure change.