Pathophysiology of genetic and experimental hypertension.
Evidence is summarized that some structural changes in resistance arteries (hyperplasia of smooth muscle and others) precede the development of vessel changes in genetic hypertension. Additional changes, such as hypertrophy of vascular muscle and altered collagen and elastin, accompany hypertension and contribute to its maintenance. Furthermore, some membrane defects, including reduced Ca2+-pumping by sarcolemma of vascular smooth muscle, contribute to the causation of genetic and experimental hypertension, as well as to some changes in hypertension associated with volume expansion. Analysis of these causative factors may aid in treatment and, ultimately, allow the prevention of hypertension.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006965:Hyperplasia; D006973:Hypertension / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D007473:Ion Channels; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012964:Sodium / Q000378:metabolism; D014655:Vascular Resistance; D014661:Vasoconstriction
D007473:Ion Channels; D012964:Sodium; D002118:Calcium