Abstract
Intrinsic arterial myogenic function comprises the degree of constriction (myogenic tone), the arterial constriction to an increase in intraluminal pressure and vice versa (myogenic response), and forced dilation at high intraluminal pressure. Although the development of myogenic tone at 40-60 mmHg involves the influx of calcium (Ca2+) through voltage- dependent Ca2+ channels and an elevation in arterial intracellular Ca2+ (Ca2+ i), myogenic responses between 60-140 mmHg involves predominantly Rho kinase (ROK)-mediated changes in Ca2+ sensitivity. In the cerebral circulation an impaired myogenic response results in impaired cerebral autoregulation and susceptibility hypertension-induced cerebral haemorrhage. An impaired cerebral artery myogenic response, due to blunted ROK mediated changes in Ca2+ sensitivity, may be a consequence of defective mechanotransduction of the intraluminal pressure stimulus; this may be a result of abnormalities in the extracellular matrix. In the coronary circulation distinctions between the mechanisms involved in the development of myogenic tone and the myogenic response have not been clearly defined. However, coronary artery myogenic tone is dependent on both Ca2+ entry through voltage –dependent Ca2+ channels and protein kinase C (PKC) activity. Impaired coronary myogenic tone has been observed in animal models of disease but the implications of these findings are currently uncertain.
Keywords: Autoregulation, cerebral haemorrhage, cerebral arteries, coronary arteries, in vitro studies, myogenic response, SHRSP.
Current Vascular Pharmacology
Title:Myogenic Properties of Brain and Cardiac Vessels and their Relation to Disease
Volume: 12 Issue: 6
Author(s): Ashley S. Izzard and Anthony M. Heagerty
Affiliation:
Keywords: Autoregulation, cerebral haemorrhage, cerebral arteries, coronary arteries, in vitro studies, myogenic response, SHRSP.
Abstract: Intrinsic arterial myogenic function comprises the degree of constriction (myogenic tone), the arterial constriction to an increase in intraluminal pressure and vice versa (myogenic response), and forced dilation at high intraluminal pressure. Although the development of myogenic tone at 40-60 mmHg involves the influx of calcium (Ca2+) through voltage- dependent Ca2+ channels and an elevation in arterial intracellular Ca2+ (Ca2+ i), myogenic responses between 60-140 mmHg involves predominantly Rho kinase (ROK)-mediated changes in Ca2+ sensitivity. In the cerebral circulation an impaired myogenic response results in impaired cerebral autoregulation and susceptibility hypertension-induced cerebral haemorrhage. An impaired cerebral artery myogenic response, due to blunted ROK mediated changes in Ca2+ sensitivity, may be a consequence of defective mechanotransduction of the intraluminal pressure stimulus; this may be a result of abnormalities in the extracellular matrix. In the coronary circulation distinctions between the mechanisms involved in the development of myogenic tone and the myogenic response have not been clearly defined. However, coronary artery myogenic tone is dependent on both Ca2+ entry through voltage –dependent Ca2+ channels and protein kinase C (PKC) activity. Impaired coronary myogenic tone has been observed in animal models of disease but the implications of these findings are currently uncertain.
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Cite this article as:
Izzard S. Ashley and Heagerty M. Anthony, Myogenic Properties of Brain and Cardiac Vessels and their Relation to Disease, Current Vascular Pharmacology 2014; 12 (6) . https://dx.doi.org/10.2174/15701611113116660150
DOI https://dx.doi.org/10.2174/15701611113116660150 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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