Sensing pressure in the cardiovascular system: Gq-coupled mechanoreceptors and TRP channels.

Abstract

Despite the central physiological importance of cardiovascular mechanotransduction, the molecular identities of the sensors and the signaling pathways have long remained elusive. Indeed, how pressure is transduced into cellular excitation has only recently started to emerge. In both arterial and cardiac myocytes, the diacylglycerol-sensitive canonical transient receptor potential (TRPC) subunits are proposed to underlie the stretch-activated depolarizing cation channels. An indirect mechanism of activation through a ligand-independent conformational switch of Gq-coupled receptors by mechanical stress is invoked. Such a mechanism involving the angiotensin type 1 receptor and TRPC6 is proposed to trigger the arterial myogenic response to intraluminal pressure. TRPC6 is also involved in load-induced cardiac hypertrophy. In this review, we will focus on the molecular basis of pressure sensing in the cardiovascular system and associated disease states.

DOI: 10.1016/j.yjmcc.2009.03.020
0204060200920102011201220132014201520162017
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@article{SharifNaeini2010SensingPI, title={Sensing pressure in the cardiovascular system: Gq-coupled mechanoreceptors and TRP channels.}, author={Reza Sharif-Naeini and Joost H. A. Folgering and Delphine Bichet and Fabrice Duprat and Patrick Delmas and Amanda Jane Patel and Eric Honor{\'e}}, journal={Journal of molecular and cellular cardiology}, year={2010}, volume={48 1}, pages={83-9} }