J. Wattanapermpool, INCREASE IN CALCIUM RESPONSIVENESS OF CARDIAC MYOFILAMENT ACTIVATION IN OVARIECTOMIZED RATS, Life sciences (1973), 63(11), 1998, pp. 955-964
Citations number
31
Categorie Soggetti
Biology,"Medicine, Research & Experimental","Pharmacology & Pharmacy
To evaluate a possible role of ovarian sex hormones in the Ca2+ respon
siveness of cardiac myofilament activation, the relations of pCa (-log
Ca2+ molar concentration) to actomyosin adenosine triphosphatase (ATP
ase) activity of isolated myofibrillar preparations from 8-10 week ova
riectomized (Ovx) rat hearts were compared with those from sham-operat
ed hearts. Deficiency of ovarian sex hormones in plasma of ovariectomi
zed rats was indirectly verified by a significant reduction in uterine
weights. Body weights of the ovariectomized rats were significantly g
reater than those of sham-operated controls. Despite a significant inc
rease in heart weight of 10 week ovariectomized animals, the percent o
f heart weight-to-body weight ratio was not different from control gro
up. The maximum myofibrillar ATPase activity at pH 7.0 was significant
ly suppressed after ovariectomy in both eight and ten week groups. How
ever, the maximum ATPase activity at pH 6.5 was significantly suppress
ed only in 10 week ovariectomized hearts. Surprisingly, in every condi
tion with depressed maximum myofibrillar ATPase activity, the pCa-acto
myosin ATPase relationships of ovariectomized cardiac myofilaments dem
onstrated a significant leftward shift in pCa(50) (-log half-maximally
Ca2+ activation) from those of sham-operated controls. There was, how
ever, no change in the Hill-coefficient of these cardiac myofilaments
after ovariectomy. Analysis of myofilament proteins using gel electrop
horesis demonstrated neither change nor loss of any thin filament prot
eins. These results indicate a possible modulating effect of ovarian s
ex hormone deficiency on the Ca2+ responsiveness of cardiac myofilamen
t activation by induction of myofilament Ca2+ hypersensitivity but sup
pression of maximum myofibrillar ATPase activity.