Cell membrane in hypertension.
Several alterations in membrane transport systems are observed in rat and human hypertension. Na+ flux changes are numerous, and cellular homeostasis to Na+ loading is impaired. Transmembrane Ca2+ movements are also numerous but clearly defined by a reduction in Ca2+ binders, a hypersensitivity of membrane phospholipase C, possible increased Ca2+ leak and reduced sensitivity of the Ca2+-pump to calmodulin. The resulting Ca2+ increase within arterial cells can be responsible for increased contractility and tone, leading to hypertension. These functional alterations in membrane transport can be secondary to a few well-defined membrane defects of genetic origin or to a diffuse structural perturbation in membranes involving lipid changes.
Meyer
P
P
Department of Pharmacology, Hospital Necker, Paris, France.
Marche
P
P
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D012964:Sodium / Q000378:metabolism*
D012964:Sodium; D002118:Calcium