Stretch-Induced Contraction and Ca2+ Mobilization in Vascular Smooth Muscle

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Abstract
The vascular system is receptive to both chemical and physical factors, and these factors elicit subsequent cellular responses such as contraction and relaxation. Quick stretch applied to cerebral and coronary arteries produces myogenic contraction by mobilization of at least two Ca2+ components, i.e., transmembrane influx and release from intracellular storage sites of Ca2+. The mechanical reception is more susceptible than pharmacological reception to chemical skinning, suggesting the importance of membrane lipids as a mechanosensor domain. Phospholipase C coupled to a cholera toxin- or pertussis toxin-insensitive GTP-binding protein, possibly a Gq class one, may play a role in the genesis of vascular contraction in response to stretch. Actuation of protein kinase C may affect more strongly the maintenance phase of stretch-induced contraction through the change in Ca2+ sensitivity of the contractile elements. The contractile reaction of vascular tissue to mechanical force such as stretch is a kind of physical response and thus requires cellular signal transduction, which may be mediated through a receptive site specific for a mechanical stimulus and the pathways of Ca2+ signaling that are common to pharmacological agonists.

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