Angiotensin-converting enzyme inhibition and vascular structure in hypertension.
The pathogenesis of hypertension is associated with a remodeling of vascular structure. Folkow has postulated that the decreased luminal area and thickened medial layer in hypertensive vessels enhance the vasoconstrictive response to vasoactive agents. It is hypothesized that this increase in vascular reactivity may serve to perpetuate hypertension. These same structural changes also predispose to the end-organ damage associated with hypertension. A growing body of evidence suggests that autocrine-paracrine vasoactive substances and growth factors modulate vascular structure in hypertension. It is speculated that therapeutic interventions that normalize blood pressure as well as reverse the vascular remodeling process may have special clinical value. The roles of the paracrine renin-angiotensin system and angiotensin-converting enzyme inhibitors in hypertension are discussed in this context.
Gibbons
G H
GH
Falk Cardiovascular Research Center, Stanford University School of Medicine, California.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001808:Blood Vessels / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D051381:Rats; D012084:Renin-Angiotensin System / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
D000806:Angiotensin-Converting Enzyme Inhibitors