Mechanisms of smooth muscle contraction

Abstract

Work performed with differentiated contractile smooth muscle tissue over the last two decades has made clear that covalent modification of myosin by phosphorylation of the 20-kDa myosin light chains is a significant mode of regulation of contractile activity in smooth muscle, particularly in regard to the generation of phasic contractions and the initial development of tonic contractions. This regulatory mechanism appears to be of unique importance in smooth muscle compared with striated muscle. It is equally clear, however, that there is an important role for protein kinase C in the regulation of smooth muscle tone maintenance, particularly in vascular smooth muscle. Several possible signal transduction cascades involving protein kinase C are outlined. Increasing evidence suggests a link between protein kinase C and actin-based regulatory mechanisms. This review places emphasis on relating up-to-date biochemical facts to the physiological realities of the smooth muscle cell.

Agonistic AT1 Receptor Autoantibody Increases in Serum of Patients with Refractory Hypertension and Improves Ca2+ Mobilization in Cultured Rat Vascular Smooth Muscle Cells

“…The definitive role of AT 1 -AAs in the pathogenesis of primary hypertension is unclear, but Ang II is known to cause the contraction of VSMCs in blood vessels. And increased [Ca 2+ ]i is the signal activating the contractile apparatus of VSMCs to cause a contraction (13). We studied the AT 1 receptor agonistic response with the trace of intracellular free Ca 2+ of VSMCs when exposed to AT 1 -AAs.…”

“…Function of vascular smooth muscle cells (VSMCs) is important in the regulation of BP. Because intracellular Ca 2+ ([Ca 2+ ] i ) is a major determinant of VSMCs tone and function (13), we investigated and compared the ability of angiotensin II (Ang II) and AT 1 -AAs to stimulate the intracellular Ca 2+ mobilization and cellular proliferation of rat VSMCs.…”

Intravascular pressure-evoked changes in intracellular calcium [Ca2+]i and tone in rat mesenteric and rabbit cerebral arteries in vitro

“…It is possible that differences in activity of such a mechanism could account for our observations. Alterations in [Ca 2+ ] i sensitivity of contraction have been extensively studied in the context of receptor agonist-induced tone in isolated blood vessels 15,16 and a number of mechanisms including inhibition of myosin phosphatase or activation of protein kinase C and mitogen activated protein kinases have been implicated in these effects. Whether similar mechanisms are involved in the pressurerelated enhancement of [Ca 2+ ] i sensitivity is uncertain but a recent study has proposed protein kinase C as an important modulator of [Ca 2+ ] i sensitivity in pressurized rat cerebral arteries.…”

The Proteome of Mouse Cerebral Arteries

“…It is well established that intracellular-free calcium (iCa 2 þ ) binds with calmodulin, which then binds and activates the myosin light-chain kinase. 19 The activated kinase complex then phosphorylates myosin on the 20-kDa light chains, resulting in smooth muscle contraction. 19 Conversely, dephosphorylation of myosin light chains induces relaxation (Figure 4).…”