The presence of NTPD1 and NT5E in the cell membranes of smooth muscle cells suggests important functional roles related to muscle contraction and relaxation during the voiding cycle.
Extracellular ET-1, produced in endothelial cells and glia cells, can adjust cerebrovascular tone via interactions with specific ET-A and -B receptors on the membranes of smooth muscle and endothelial cells [ 7, 31].
K+ channels contribute importantly to the resting membrane potential of smooth muscle and thus regulate the intracellular calcium level.
The increased intraluminal pressure results in the activation of non-selective cation channels in the plasma membrane of the smooth muscle cells, which causes membrane depolarization, Ca2+ influx through voltage-gated L-type Ca2+ channels and smooth muscle contraction (Davis and Hill, 1999).
These mutations cause an abnormal accumulation of Notch3 in the cytoplasmic membrane of vascular smooth muscle cells both in cerebral and extracerebral vessels, which appear as granular osmiophilic deposits on electron microscopy [4].
The major vascular action of CGRP action (conserved throughout the mammal species, including man) is the vasodilatation of large and small size arteries via direct activation of the calcitonin receptor-like receptor (CLR) associated to the receptor activity-modifying protein-1 (RAMP1) [4], which are primarily located on the plasma membrane of arterial smooth muscle cells.
However, ATP and ADP depolarize the membrane of the smooth muscular cell [ 43].
Cromakalim was reported to be an ATP-sensitive K+ channel opener [ 21], which may increase outflux of K+ and hyperpolarize the membrane of vascular smooth muscle cells and cause decrease of systolic pressure.
The depolarizing effect of hyperkalemia on the membrane of vascular smooth muscle cells counteracts and restricts the hyperpolarizing effect of EDHF, which was suggested to be responsible for the attenuated EDHF-mediated vasorelaxation under hyperkalemic cardioplegic exposure [ 17, 44].
Levosimendan has a vasodilatory effect via opening of ATP-sensitive potassium (KATP) channels in the plasma membrane of vascular smooth muscle cells, and also activates myocardial mitochondrial KATP (m-KATP) channels and exerts PreC effect against ischemia-reperfusion injury [ 13].
