This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kaley, G. Search for Related Content PubMed PubMed Citation Articles by Kaley, G. Related Collections Cerebrovascular disease/stroke Cell signalling/signal transduction Brain Circulation and Metabolism Cerebral Aneurysm, AVM, & Subarachnoid hemorrhage Lipid and lipoprotein metabolism

(Circulation Research. 2000;87:4.)
© 2000 American Heart Association, Inc.

Editorials

Regulation of Vascular Tone

Role of 20-HETE in the Modulation of Myogenic Reactivity

Gabor Kaley

From the Department of Physiology, New York Medical College, Valhalla, NY.

Correspondence to Gabor Kaley, PhD, Department of Physiology, New York Medical College, Valhalla, NY 10595.

Key Words: microcirculation • myogenic tone • 20-HETE • vascular smooth muscle • potassium channel

	Introduction

 
Bayliss¹ first suggested that distention (stretch) of the vascular wall, elicited by increases in intravascular pressure, acts as a facilitating stimulus on the vascular smooth muscle (VSM) to intensify its activity, eliciting constriction of blood vessels. Since this original hypothesis was offered, it has been recognized that this pressure-sensitive response, a constriction to elevation and a dilation to reduction of transmural pressure, originates from the smooth muscle layer of blood vessels and is independent of neural, hormonal, and metabolic influences.² Although it is most pronounced in arterioles, it can also be demonstrated frequently in all types of blood vessels and lymphatics. The myogenic response contributes to autoregulation of blood flow and is believed to be one of the primary mechanisms responsible for the basal tone of small blood vessels. Consequently, it also influences capillary hydrostatic pressure.

Although there is no general agreement as to the nature of the transduction mechanisms mediating the myogenic response, there is a consensus that stretch of the VSM membrane results in membrane depolarization, leading to augmented Ca²⁺ influx through increased voltage-gated Ca²⁺ channel activity and contraction of VSM via Ca²⁺-calmodulin–induced myosin light chain kinase phosphorylation. Among the mediators that have been proposed to be involved in the mechanotransduction of the stretch signal are activation of phospholipase C and A₂, the adenylate cyclase/cAMP/protein kinase A signaling pathway, protein kinase C– and tyrosine kinase–mediated mechanisms, and a variety of ion channels, as well as integrins and elements of the cytoskeleton of VSM.^{3 4}

In this issue . . . [Full Text of this Article]

This article has been cited by other articles:

				E. W. Inscho Mysteries of Renal Autoregulation Hypertension, February 1, 2009; 53(2): 299 - 306. [Full Text] [PDF]

				X. H. Collins, S. D. Harmon, T. L. Kaduce, K. B. Berst, X. Fang, S. A. Moore, T. V. Raju, J. R. Falck, N. L. Weintraub, G. Duester, et al. {omega}-Oxidation of 20-Hydroxyeicosatetraenoic Acid (20-HETE) in Cerebral Microvascular Smooth Muscle and Endothelium by Alcohol Dehydrogenase 4 J. Biol. Chem., September 30, 2005; 280(39): 33157 - 33164. [Abstract] [Full Text] [PDF]

				D. D. O'Leary, J. K. Shoemaker, M. R. Edwards, and R. L. Hughson Spontaneous beat-by-beat fluctuations of total peripheral and cerebrovascular resistance in response to tilt Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2004; 287(3): R670 - R679. [Abstract] [Full Text] [PDF]

				L. Storme, T. A. Parker, J. P. Kinsella, R. L. Rairigh, and S. H. Abman Chronic hypertension impairs flow-induced vasodilation and augments the myogenic response in fetal lung Am J Physiol Lung Cell Mol Physiol, January 1, 2002; 282(1): L56 - L66. [Abstract] [Full Text] [PDF]