TRP Channels in the Cardiopulmonary Vasculature

Chapter
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 704)

Abstract

Transient receptor potential (TRP) channels are expressed in almost every human tissue, including the heart and the vasculature. They play unique roles not only in physiological functions but, if over-expressed, also in pathophysiological disease states. Cardiovascular diseases are the leading cause of death in the industrialized countries. Therefore, TRP channels are attractive drug targets for more effective pharmacological treatments of these diseases. This review focuses on three major cell types of the cardiovascular system: cardiomyocytes as well as smooth muscle cells and endothelial cells from the systemic and pulmonary circulation. TRP channels initiate multiple signals in all three cell types (e.g. contraction, migration) and are involved in gene transcription leading to cell proliferation or cell death. Identification of their genes has significantly improved our knowledge of multiple signal transduction pathways in these cells. Some TRP channels are important cellular sensors and are mostly permeable to Ca2+, while most other TRP channels are receptor activated and allow for the entry of Na+, Ca2+ and Mg2+. Physiological functions of TRPA, TRPC, TRPM, TRPP and TRPV channels in the cardiovascular system, dissected by down-regulating channel activity in isolated tissues or by the analysis of gene-deficient mouse models, are reviewed. The involvement of TRPs as homomeric or heteromeric channels in pathophysiological processes in the cardiovascular system like heart failure, cardiac hypertrophy, hypertension as well as edema formation by increased endothelial permeability will be discussed.

Keywords

Smooth Muscle Cell Cardiac Hypertrophy Transient Receptor Potential Autosomal Dominant Polycystic Kidney Disease Transient Receptor Potential Channel 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media B.V. 2011

Authors and Affiliations

  1. 1.Walther-Straub-Institute for Pharmacology and Toxicology, School of Medicine,Ludwig-Maximilians-University MünchenMunichGermany
  2. 2.Walther-Straub-Institute for Pharmacology and Toxicology, School of Medicine,Ludwig-Maximilians-University MünchenMunichGermany

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