Mechanisms behind myocardial depression in rat renal hypertension.
Cardiac function in rat renal hypertension has been shown repeatedly to be depressed. The reason for this impairment has not been fully understood, although cardiac hypertrophy and increased collagen content have been claimed as possible causes. To further unravel the mechanisms underlying the deterioration of left ventricular function in rat renal hypertension, we investigated cardiac function, myocardial morphology, myosin iso-enzymes, plasma renin activity and levels of myocardial high-energy compounds in hearts from rats exposed to renal and reversed renal hypertension. Maximal cardiac function was unaltered in hearts exposed to antihypertensive therapy from the time of renal artery clipping compared with untreated hypertensive rats. The observed alterations of iso-enzyme pattern, plasma renin activity levels and myocardial morphology among the groups showed to be of less importance with respect to cardiac performance. Together with previous results from our laboratory, the present findings suggest that some negative inotropic agent of renal or non-renal origin is released during two-kidney, one clip renal hypertension, which counteracts the enhanced left ventricular performance induced by cardiac hypertrophy.
Friberg
P
P
Department of Physiology, University of Gothenburg, Sweden.
Nordlander
M
M
Rupp
H
H
D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000473:pathology / Q000503:physiopathology; D003326:Coronary Circulation; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology*; D006977:Hypertension, Renal / Q000503:physiopathology*; D007527:Isoenzymes / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009218:Myosins / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D000227:Adenine Nucleotides; D007527:Isoenzymes; D009218:Myosins