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Smooth muscle cells rapidly redifferentiate in culture, entering a so-called proliferative or synthetic state characterized by reduced expression of contractile proteins, changes in cytoskeletal architecture, loss of dense bodies and disappearance of excitability mechanisms.
In most smooth muscles, PKC has contraction-promoting effects such as phosphorylation of Ca 2+ channels or other proteins that regulate cross-bridge cycling. Activator Ca 2+ binds to calmodulin, leading to activation of myosin light chain kinase (MLC kinase).
We describe here a number of pathways by which vascular smooth muscle contraction and stiffness are directly regulated and hence will affect blood pressure.
14 sie 2023 · Smooth muscle contraction depends on calcium influx. Calcium increases within the smooth muscle cell through two different processes. First, depolarization, hormones, or neurotransmitters cause calcium to enter the cell through L-type channels located in the caveolae of the membrane.
Smooth muscle contraction (left) requires five steps to perform: After the increase of intracellular Ca 2+ concentrations from either the extracellular fluid or the sarcoplasmic reticulum (1), these ions bind to a protein called calmodulin (2).
The mechanisms of smooth muscle contraction, beginning with increased cytoplasmic calcium levels. The steps of smooth muscle contraction are listed below (as shown in figure 10): Cytoplasmic levels of calcium (Ca 2+) increase in smooth muscle cells from both extracellular and intracellular sources.
1 cze 2011 · In the isolated smooth muscle cells, ATP could cause a lasting depolarization favoring muscle contraction, which could be reversed by subsequent application of PGE 2, with the activation of cAMP-dependent K + channels resulting in membrane hyperpolarization that would relax the muscle. This study has provided for the first time the details how ...
