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,
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