[The role of calcium in the regulation of normal vascular tone and in arterial hypertension].
The vascular tone depends on periarterial neurogenic nerve stimulus and endothelial substances release. The most evident biochemical cause of the vascular smooth muscle contraction-relaxation process lies in the changing concentration of cytosolic Ca2+. Intracellular free calcium is the major determinant of vascular tone. The depolarization wave opens the slow calcium channels, which permit Ca2+ to enter in small quantities into the interior of the cell triggering the release of much larger quantities of calcium from the sarcoplasmic reticulum. The flux of Ca2+ to and from the cytosol is regulated by three principle mechanisms. The calcium voltage sensitive Ca2+ channel that are opened by the depolarization wave. The potassium channels (CK+) and the Na+/K(+)-ATPase pump. The CK+ opening permits the exit of potassium from the interior of the cell which tends to hyperpolarize the smooth muscle cell membrane and closes the calcium channel avoiding the entry of Ca2+. The activity of the sodium pump also produces membrane hyperpolarization. Thus, the activity of these two mechanisms counter-regulates the voltage dependent calcium channel. The massive release of Ca2+ from intracellular stores of the sarcoplasmic reticulum is done through two classes of channels. One is ryanodine sensitive, the other is the inositol 1,4,5-trisphosphate receptor. The endothelial cell dysfunction is accompanied by a decrease in the production and/or the release of nitric oxide and the increase of contracting factors. That induce a Ca2+ mobilization of extracellular and intracellular stores. Contraction of smooth muscle to hypoxia is mediated by an accumulation of intracellular Ca2+. The relaxant substances of vascular smooth muscle inhibit activation of the phospholipase C and open Ca2+ channels, or produce a stimulus to the exit of the Ca2+ through the plasmatic membrane, with a decrease of intracellular calcium. An endothelial dysfunction with decrease of nitric oxide release exists in different types of hypertension. Pregnancy-induced hypertension is associated with low calcium levels in the diet, improving with the treatment of calcium supplements.
Ramón de Berrazueta
J
J
Catedrático de Cardiología, Hospital Universitario Marqués de Valdecilla, Santander. jrberrazueta@mundivia.es
D000328:Adult; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology*; D002462:Cell Membrane / Q000378:metabolism; D004730:Endothelium, Vascular / Q000502:physiology / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009129:Muscle Tonus; D009131:Muscle, Smooth, Vascular / Q000502:physiology* / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000502:physiology; D011225:Pre-Eclampsia / Q000503:physiopathology; D011247:Pregnancy; D014661:Vasoconstriction; D014664:Vasodilation
D015220:Calcium Channels; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D002118:Calcium