Signal transduction in vascular smooth muscle.
BACKGROUND
Vascular smooth muscle participates in the normal control of vascular tone and in the pathological adaptation of arteries in hypertension and atherosclerosis. Growth factors and vasoconstrictors activate overlapping signalling pathways that include activation of phospholipase C isoforms, phospholipase D, protein kinase C, tyrosine kinases and mitogen-activated protein kinases.
Angiotensin II initiates a biphasic sequence of second messenger generation in vascular smooth muscle cells that appears to result from signalling that occurs in two distinct domains involving aggregated and sequestered receptors. It also activates membrane-associated reduced nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide phosphate oxidases that contribute to the control of the redox state of the cell.


CONCLUSIONS
Vasoactive agents generate a complex signalling pattern that controls both the normal and pathophysiological responses of vascular smooth muscle.
Alexander
R W
RW
Emory University School of Medicine, Division of Cardiology, Atlanta, Georgia 30322, USA.
Griendling
K K
KK
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D010084:Oxidation-Reduction; D010766:Phosphorylation; D011945:Receptors, Angiotensin / Q000378:metabolism; D015398:Signal Transduction; D014443:Tyrosine / Q000378:metabolism
D011945:Receptors, Angiotensin; D000804:Angiotensin II; D014443:Tyrosine