Potential effect of resistin on the ET-1-increased reactions of blood pressure in rats and Ca2+ signaling in vascular smooth muscle cells

• Published in: Journal of cellular physiology 2012-04, Vol.227 (4), p.1610-1618
• Main Authors: Chuang, Tung-Yueh, Au, Lo-Chun, Wang, Li-Chun, Ho, Low-Tone, Yang, De-Ming, Juan, Chi-Chang
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Blood Pressure - drug effects; Blood Pressure - physiology; Calcium Channels - genetics; Calcium Channels - physiology; Calcium Signaling - drug effects; Calcium Signaling - physiology; Cell Line; Endothelin-1 - pharmacology; Endothelin-1 - physiology; Gene Expression; Male; MAP Kinase Signaling System; Membrane Glycoproteins - antagonists & inhibitors; Membrane Glycoproteins - genetics; Membrane Glycoproteins - physiology; Myocytes, Smooth Muscle - drug effects; Myocytes, Smooth Muscle - physiology; Rats; Rats, Sprague-Dawley; Resistin - pharmacology; Resistin - physiology; RNA, Small Interfering - genetics; Stromal Interaction Molecule 1
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.22878

Resistin and endothelin‐1 (ET‐1) are upregulated in people with type II diabetes mellitus, central obesity, and hypertension. ET‐1 signaling is involved in Ca2+‐contraction coupling and related to blood pressure regulation. The aim of this study is to investigate the role of resistin on ET‐1‐increased blood pressure and Ca2+ signaling. The blood pressure and cytosolic Ca2+ of vascular smooth muscle cells (VSMCs) of Sprague–Dawley rats were detected. The data demonstrated that resistin accelerated and prolonged ET‐1‐induced increases in blood pressure and had significant effects on ET‐1‐increased Ca2+ reactions. Resistin‐enhanced ET‐1‐increased Ca2+ reactions were reversed by blockers of store‐operated Ca2+ entry (SOCE) and extracellular‐signal‐regulated kinase (ERK). The endogenous expression of Orai and stromal interaction molecular (STIM) were characterized in the VSMCs. Furthermore, resistin‐enhanced ET‐1 Ca2+ reactions and the resistin‐dependent activation of SOCE were abolished under STIM1‐siRNA treatment, indicating that STIM1 plays an important role in resistin‐enhanced ET‐1 Ca2+ reactions in VSMCs. Resistin appears to exert effects on ET‐1‐induced Ca2+ increases by enhancing the activity of ERK‐dependent SOCE (STIM1‐partcipated), and may accelerate and prolong ET‐1‐increased blood pressure via the same pathway. J. Cell. Physiol. 227: 1610–1618, 2012. © 2011 Wiley Periodicals, Inc.