title: ATPase activity of sulfhydryl-modified cardiac myosin from normal and isoproterenol-treated rats.
abstract: The possible role of sulfhydryl groups in the adaptation of cardiac myosin to work overload has been examined. The functional integrity of sulfhydryl groups was evaluated by measurement of Ca2+- and K+-(EDTA)-ATPase activities of myosins following sulfhydryl modification. No activation of Ca2+-ATPase of normal rat cardiac myosin was observed after pMB or NEM pretreatment. The decrease in Ca2+-ATPase of myosin from hypertrophied hearts was eliminated following sulfhydryl modification: moreover, slight stimulation of Ca2+-ATPase was observed. An increase in KCl concentration did not stimulate the Ca2+-ATPase of NEM-modified myosins obtained from either control or hypertrophied hearts. The sulfhydryl content of rat cardiac myosin expressed as moles of SH per 10(5) g of myosin was 6.99 +/- 0.30 and in IPR-induced hypertrophy did not change it significantly. In the authors' opinion an alteration in the integrity of the sulfhydryl groups may be responsible for the functional partition (decreased Ca2+-ATpase with unchanged K+-[EDTA]-ATPase activity) of myosin from hypertrophied hearts.
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D006332:Cardiomegaly; D005033:Ethylmaleimide / Q000494:pharmacology; D006902:Hydroxymercuribenzoates / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D013439:Sulfhydryl Reagents / Q000494:pharmacology*
chemical_list: D006902:Hydroxymercuribenzoates; D013439:Sulfhydryl Reagents; D011189:Potassium Chloride; D000251:Adenosine Triphosphatases; D009218:Myosins; D000252:Calcium-Transporting ATPases; D007545:Isoproterenol; D005033:Ethylmaleimide