Pharmacologic regression of cardiac hypertrophy in experimental hypertension.
The normal heart has the capacity to either augment or reduce its mass in relation to long-term alterations in hemodynamic and metabolic demands. However, once cardiac hypertrophy is established, as in hypertensive heart disease, it is less clear whether the augmented mass can revert to normal with control of arterial pressure. In experimental models in which systemic hypertension is induced in genetically normotensive animals, left ventricular weight generally returns toward normal with the removal of the inciting stimulus for the hypertension. However, when arterial pressure control is achieved by pharmacologic therapy, and the inciting stimulus (mechanical or genetic) is intact, the results of pressure reduction on ventricular weight are much more variable than that observed with the removal of a mechanical stimulus for hypertension. It is hypothesized that pharmacologic pressure reduction elicits secondary adjustments in cardiorenal and neurohumoral function which have important influences on ventricular hypertrophy.
D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D006332:Cardiomegaly / Q000150:complications / Q000188:drug therapy*; D002908:Chronic Disease; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR
D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers