title: In vivo TRPC functions in the cardiopulmonary vasculature.
abstract: Cardiovascular diseases are the leading cause of death in the industrialized countries. The cardiovascular system includes the systemic blood circulation, the heart and the pulmonary circulation providing sufficient blood flow and oxygen to peripheral tissues and organs according to their metabolic demand. This review focuses on three major cell types of the cardiovascular system: myocytes of the heart as well as smooth muscle cells and endothelial cells from the systemic and pulmonary circulation. Ion channels initiate and regulate contraction in all three cell types, and the identification of their genes has significantly improved our knowledge of signal transduction pathways in these cells. Among the ion channels expressed in smooth muscle cells, cation channels of the TRPC family allow for the entry of Na(+) and Ca(2+). Physiological functions of TRPC1, TRPC3, TRPC4, TRPC5, TRPC6 and TRPC7 in the cardiovascular system, dissected by down-regulating channel activity in isolated tissues or by the analysis of gene-deficient mouse models, are reviewed. Possible functional roles and physiological regulation of TRPCs as homomeric or heteromeric channels in these cell types are discussed. Moreover, TRP channels may also be responsible for pathophysiological processes of the cardiovascular system like hypertension as well as cardiac hypertrophy and increased endothelial permeability.
authors: Institute for Pharmacology and Toxicology, School of Medicine, University of Marburg, 35043 Marburg, Germany. dietrica@staff.uni-marburg.de
authors: Alexander
authors: A
authors: Dietrich
authors: Hermann
authors: H
authors: Kalwa
authors: Beate
authors: B
authors: Fuchs
authors: Friedrich
authors: F
authors: Grimminger
authors: Norbert
authors: N
authors: Weissmann
authors: Thomas
authors: T
authors: Gudermann
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D006331:Heart Diseases / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000209:etiology; D051379:Mice; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000502:physiology*; D011652:Pulmonary Circulation; D051381:Rats; D050052:TRPC Cation Channels / Q000502:physiology*
chemical_list: D050052:TRPC Cation Channels