Referenced in: none

Automatically associated channels: Kir2.3

Title: Calcium activation of vascular smooth muscle. State of the art lecture.

Authors: C Van Breemen, P Leijten, H Yamamoto, P Aaronson, C Cauvin

Journal, date & volume: Hypertension, 1986 Jun , 8, II89-95

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/2424835

Abstract
Tension development in arterial smooth muscle is regulated by variations of calcium concentration in the submicromolar range. The receptor for Ca2+ is calmodulin, which through stimulation of myosin light chain kinase can activate sequentially two apparently different contractile states. A third possible contractile state may be related to C-kinase activation. These contractile states are thought to have different Ca2+ sensitivities. Ca2+ is supplied from two major sources: the sarcoplasmic reticulum and the extracellular space. The release of sarcoplasmic reticulum Ca2+ is mediated by the intracellular messenger inositol-1,4,5-trisphosphate (IP3) and perhaps by Ca2+ itself. These two messengers have the potential for amplification; for example, IP3 may release some Ca2+ that may subsequently cause Ca2+-induced Ca2+ release. The entry of Ca2+ from the extracellular space into the cytoplasm is mediated by a Ca2+ leak and by excitable Ca2+ channels and is modulated by a Ca2+ buffer barrier consisting of the superficial sarcoplasmic reticulum. Two types of adenosine 5'-triphosphate-driven Ca2+ pumps in the sarcoplasmic reticulum and plasmalemma are responsible for returning the cytoplasmic Ca2+ concentration to resting level after contraction and for maintaining Ca2+ homeostasis during the life of the cells.