Increased TRPP2 expression in vascular smooth muscle cells from high-salt intake hypertensive rats: The crucial role in vascular dysfunction.

Abstract

High-salt intake is a major risk factor in the development of hypertension. The underlying mechanism of high sodium on the cardiovascular system has received extensive attention. TRPP2 (Polycystin-2) is a Ca(2+) permeable nonselective cation channel that mediates Ca(2+) mobilization to control vascular smooth muscle cells (VSMCs) contraction. Here, we investigated TRPP2 expression change in VSMCs from high-salt intake hypertensive rats and role of TRPP2 in the development of high-salt diet-induced hypertension. After 4 ws of dietary treatment, systolic blood pressure was significantly elevated in high-salt intake rats (132 ± 3 mmHg) compared with regular diet control rats (104 ± 2 mmHg). Results from vessel tension and diameter measurements show that high-salt intake potentiated phenylephrine-induced contraction in denuded mesenteric artery and thoracic aorta. Immunoblot and immunofluorescence data indicate that TRPP2 expression in VSMCs from mesenteric artery and thoracic aorta was significantly increased in high-salt intake-induced hypertensive rats. However, agonist-induced contractions in denuded mesenteric artery and thoracic aorta were markedly decreased if TRPP2 was knocked down by specific shRNA. Our data demonstrate that high-salt intake increased TRPP2 expression in VSMCs, which in turn potentiated blood vessel response to contractors; this may participate in the development of hypertension.