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Hypo‐Osmolality Pressor Stimulus is Linked to Transient Receptor Potential Vanilloid 4 (TRPV4) in the Portal Region
Author(s) -
Mai Tu,
McHugh Julia,
Diedrich Andre’,
Garland Emily M,
Robertson David
Publication year - 2013
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.27.1_supplement.884.7
Subject(s) - trpv4 , endocrinology , medicine , saline , transient receptor potential channel , ganglionectomy , receptor , pathology , alternative medicine
Patients with baroreflex impairment have a robust and sustained increase in blood pressure (BP) after water consumption. Using a sino‐aortic denervated mouse model (SAD), we identified hypo‐osmolality as the stimulus for this osmopressor response (OPR). However, the mechanism of the OPR is still unclear. We tested the hypothesis that decreased osmolality is sensed in the portal area after water consumption and that TRPV4 channels are essential for the response. We infused 0.45% or 0.9% saline directly into the portal vein of SAD wild type (WT) and TRPV4 −/− mice. An immediate pressor response occurred in WT mice after 0.45% saline but not after 0.9% saline infusion (0.45%: 16 ± 6 vs. 0.9%: − 6 ± 2 mmHg, p=0.03). On the other hand, infusion of 0.45% saline into TRPV4 −/− mice failed to stimulate a pressor response (−5 ±2 mmHg, p=0.03 for comparison with WT). We further explored the possible mechanism of OPR by using celiac ganglionectomized (CGX) and sham WT mice. Both CGX and sham mice had a robust increase in BP after water infusion into the duodenum (CGX: 10 ± 2 vs. SHAM: 12 ± 1 mmHg, p=0.5). However, the response was shortened by ganglionectomy. Ten minutes after water, BP had returned to normal in CGX, while it remaining elevated in sham mice (CGX: 0.3 ± 2 vs. 9 ± 1.7 mmHg, p=0.01). We conclude that TRPV4 channels in the portal region are essential for the OPR, and the celiac ganglia play an important role in maintaining BP elevation.