Regression of cardiac hypertrophy with drug treatment in spontaneously hypertensive rats.
Left ventricular hypertrophy is an important complication of essential hypertension. Some antihypertensive drugs have been shown to allow regression of cardiac hypertrophy, both in spontaneously hypertensive rats and in hypertensive patients. Recent results show that the agents which interfere with the functions of the sympathetic nervous system, converting enzyme inhibitors and calcium antagonists are effective in reducing arterial blood pressure and regression of left ventricular hypertrophy. The use of vasodilators and diuretics may under certain circumstances, however, even exacerbate cardiac hypertrophy. Regression of left ventricular hypertrophy in hypertension does not appear to depend solely on reduction of arterial blood pressure. Other factors seem to modulate the myocardial response to antihypertensive treatment. Included among these mechanisms are neural, humoral, haemodynamic and biochemical factors. The available experimental data further suggest that some functional derangements and biochemical changes associated with hypertrophy may be reversed by antihypertensive treatment. There is, however, insufficient experience with human subjects to determine whether a reduction in left ventricular mass is associated with lower incidences of heart failure or mortality than may be achieved by adequate blood pressure control alone.
D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D006332:Cardiomegaly / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D002395:Catecholamines / Q000502:physiology; D003094:Collagen / Q000032:analysis; D004232:Diuretics / Q000627:therapeutic use; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D008750:Methyldopa / Q000627:therapeutic use; D009206:Myocardium / Q000032:analysis; D009218:Myosins / Q000032:analysis; D009955:Ornithine Decarboxylase / Q000378:metabolism; D011073:Polyamines / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D014655:Vascular Resistance; D014665:Vasodilator Agents / Q000627:therapeutic use
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D002395:Catecholamines; D004232:Diuretics; D011073:Polyamines; D014665:Vasodilator Agents; D008750:Methyldopa; D003094:Collagen; D009218:Myosins; D009955:Ornithine Decarboxylase