PHOSPHOINOSITIDE-DERIVED 2ND MESSENGERS AND THE REGULATION OF CA2-MUSCLE( IN VASCULAR SMOOTH)

Vascular smooth muscle and the phosphoinositide signalling pathway: Va scular smooth muscle tone can be regulated by an array of agonists whi ch act via receptor-mediated transmembrane signalling pathways to modi fy the concentrations of key intracellular second messengers. Followin g agonist stimulation the phosphoinositide signalling pathway initiate s the contraction process in vascular smooth muscle, via the second me ssengers myo-inositol 1,4,5-trisphosphate and sn-1,2-diacylglycerol. D iversity of calcium-regulatory mechanisms: The vascular smooth muscle cell apparently sustains the contraction with a number of diverse mech anisms, which act to increase intracellular Ca2+ by regulating both Ca 2+ influx across the plasma membrane and Ca2+ release from intracellul ar calcium stores, or may act in the apparent absence of elevated cyto solic Ca2+ concentrations. Future research: The exact nature of these physiological interactions and their exact function are not yet fully understood. In particular, identification of the natural role of speci fic phospholipase C-delta, phospholipase C-gamma and protein kinase C isozymes and also the various ryanodine and myo-inositol 1,4,5-trispho sphate receptor subtypes present in vascular smooth muscle will prove critical to future understanding of the regulation of vascular smooth muscle tone in both the normal and the hypertensive phenotype.