Protein synthesis in pulmonary, cardiac, and skeletal muscle in acute hypertension induced by aortic constriction in the rat.
OBJECTIVE
The aim was to investigate nucleic acid composition and rates of protein synthesis in cardiopulmonary tissues and skeletal muscle in response to hypertension induced by aortic constriction.


METHODS
After five days of abdominal aortic constriction, protein, RNA, and DNA contents were measured in the lung, the left and right atria, the left and right ventricles, and gastrocnemius muscle from young male Wistar rats weighing 120-140 g. Rates of protein synthesis were also measured in these tissues with L[4-3H]phenylalanine.


RESULTS
Aortic constriction significantly increased the right atrial weight and in contrast reduced the lung weight, compared to pair fed and sham operated controls. The wet weights of all other tissues were unaffected. The concentrations of right atrial proteins, RNA, and DNA were also significantly reduced though total protein, RNA, and DNA contents were unaltered. The left ventricular RNA concentration increased and there were variable alterations in protein and DNA composition. The protein, RNA, and DNA compositions of the other tissues showed patterned responses, which included reductions in lung and skeletal muscle DNA concentrations, reductions in the skeletal muscle RNA/DNA ratio, and a decrease in the lung protein/DNA ratio. In response to aortic constriction there were increases in the left ventricular fractional rate of protein synthesis in mixed, high salt (myofibrillar), and low salt (sarcoplasmic) fractions. Rates of protein synthesis in all other regions of the heart, lung and skeletal muscle were not significantly changed.


CONCLUSIONS
We conclude that in abdominal aortic constriction, the left ventricles display early adaptive responses without any concomitant change in mass. Those regions of the rat cardiopulmonary system which are not directly exposed to the acute pressure overloading, ie, right atrium, lungs, and skeletal muscle, also show disturbances.
Siddiq
T
T
Cardiac Department, King's College School of Medicine and Dentistry, London, United Kingdom.
Richardson
P J
PJ
Sherwood
R A
RA
Preedy
V R
VR
D000208:Acute Disease; D000818:Animals; D001012:Aorta, Abdominal; D003250:Constriction; D004247:DNA / Q000032:analysis; D004195:Disease Models, Animal; D006325:Heart Atria / Q000033:anatomy & histology; D006973:Hypertension / Q000235:genetics / Q000378:metabolism*; D008168:Lung / Q000737:chemistry / Q000378:metabolism*; D008297:Male; D009132:Muscles / Q000737:chemistry / Q000378:metabolism*; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D009929:Organ Size; D014176:Protein Biosynthesis; D012313:RNA / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains
D012313:RNA; D004247:DNA