Nanojunctions of the Sarcoplasmic Reticulum Deliver Site- and Function-Specific Calcium Signaling in Vascular Smooth Muscles

Author(s):  
A.M. Evans
1982 ◽  
Vol 243 (5) ◽  
pp. H641-H662 ◽  
Author(s):  
H. Kuriyama ◽  
Y. Ito ◽  
H. Suzuki ◽  
K. Kitamura ◽  
T. Itoh

Contraction-relaxation cycles in vascular smooth muscles are largely dependent on the regulation of free Ca2+ in the myoplasm, as is the case in skeletal and cardiac muscles. In this article we describe the varieties of contraction-relaxation cycles of vascular smooth muscles determined at cellular and subcellular levels. To discuss the excitation-contraction and pharmacomechanical coupling mechanisms in vascular tissues, passive and active membrane properties and ionic movements measured by various procedures are briefly introduced. In vascular smooth muscles the sources of Ca2+ contributing to the activation of contractile proteins are extra- and intracellular. Influxes of Ca2+ across the membrane are enhanced by the calcium spike and electrical and chemical depolarizations or activations of autonomic receptors.l However, the Ca2+ influx during the generation of action potential does not directly increase the free Ca2+ in the cell; rather, this ion is sequestered in the storage site and activates the calcium-induced calcium-release mechanism in the storage sites with a subsequent increase in the levels of free Ca2+. In some vascular tissues depolarizations induced by activations of autonomic receptors are not a prerequisite for generation of the contraction, as these mechanical responses appear with hyperpolarization of the membrane or without a change in the membrane potential. Possible functional links between the myoplasmic membrane where the receptors are distributed and the Ca2+ storage and releasing sites (mainly sarcoplasmic reticulum) in the cell are discussed. In addition, small arteries possess possibly more than three subtypes of alpha-adrenoceptors, including the presynaptic alpha 2-adrenoceptor. The roles of sarcoplasmic reticulum and the calcium receptor of contractile proteins (calmodulin or leiotonin C) from the chemically skinned muscles of vascular tissues were compared with those of intact muscles. The relaxation of vascular tissues as induced by activations of beta-adrenoceptors, nitrites, and other chemicals is also briefly introduced.


2013 ◽  
Vol 50 (1) ◽  
pp. 69-87 ◽  
Author(s):  
Vladimir V. Matchkov ◽  
Vibeke Secher Dam ◽  
Donna M. Briggs Bødtkjer ◽  
Christian Aalkjær

1986 ◽  
Vol 23 (3) ◽  
pp. 113-124 ◽  
Author(s):  
Tomoko Shimada ◽  
Keiichi Shimamura ◽  
Satoru Sunano

PAMM ◽  
2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Klemens Uhlmann ◽  
Daniel Balzani

2021 ◽  
Vol 11 (01) ◽  
pp. e120-e124
Author(s):  
Duaa M. Raafat ◽  
Osama M. EL-Asheer ◽  
Amal A. Mahmoud ◽  
Manal M. Darwish ◽  
Naglaa S. Osman

AbstractDilated cardiomyopathy (DCM) is the third leading cause of heart failure in pediatrics. The exact etiology of DCM is unknown in more than half of the cases. Vitamin D receptors are represented in cardiac muscles, endothelium, and smooth muscles of blood vessels suggesting that vitamin D could have a vital cardioprotective function. This study aimed to assess serum level of vitamin D in children with idiopathic DCM and to correlate the serum level of vitamin D with the left ventricular dimensions and function. This study is a descriptive cross-sectional single-center study, includes 44 children of both sexes, diagnosed as idiopathic DCM. Serum level of vitamin D was assessed and correlated with the left ventricular dimensions and function. Mean age of studied children was 6.08 ± 4.4 years. Vitamin D deficiency was found in 90.9% of children with idiopathic DCM with a mean level 13.48 ng/mL. There was a negative correlation between vitamin D level and fraction shortening and left ventricular end-diastolic diameter in children with DCM. Vitamin D level is not only significantly low in children with idiopathic DCM but it is also significantly correlated with the degree of left ventricular dysfunction.


Sign in / Sign up

Export Citation Format

Share Document