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Y S Reddy

Publications and source records attributed to Y S Reddy.

26 records · Page 2Linked to original sources
PubMed1975

Calcium, tropomyosin, and actomyosin as controls of calcium binding by troponin.

A nonlinear least squares analysis of Scatchard plots of Ca++ binding to troponin, native tropomyosin, and myosin B demonstrates that troponin does not possess two classes of independent binding sites. Since the data cannot be accounted for by assuming more than two classes of independent sites, we conclude that binding of one Ca decreases the affinity of troponin for binding the next. Negative interaction is increased in the presence of tropomyosin and further increased by actomyosin. The maximal Ca++ affinity of troponin at low fractional occupancy is not affected by tropomyosin but may be significantly reduced by actomyosin. Because of negative interaction, troponin's Ca++ affinity should vary during the course of contraction. This variation could profoundly affect translocations of Ca between troponin and reticulum and the time course of the active state.

Actomyosin↗
PubMedDate not supplied

Myocardial contractile protein ATPase activities in adrenalectomized and thyroidectomized rats.

This report compares the effects of adrenalectomy and thyroidectomy, with and without hormone replacement, on loss of contractile protein ATPase activities. The rationale for this study was derived from the similarities in their intracellular receptors, mechanisms of action, and the large number of proteins regulated by both hormones. Rats were adrenalectomized, thyroidectomized, or both, and were subsequently treated for 6 weeks with hydrocortisone, triiodothyronine, or saline. Sham-operated rats were given saline for the same period of time. Six weeks of adrenal insufficiency resulted in diminished enzymatic activity of myofibrillar, Ca(2+)-activated myosin ATPase, and actin-activated myosin ATPase fractions. Treatment with hydrocortisone prevented the decline in enzymatic activity due to adrenalectomy. Likewise, thyroidectomy caused a loss of enzymatic activity which was prevented by treatment with triiodothyronine. The full deleterious effect of combined ablation could be partially prevented by treatment with either hydrocortisone or triiodothyronine, but the latter was most effective. The results suggest that hydrocortisone and triiodothyronine each had significant positive effects in the presence of the other, but not in its absence, on the activity of myofibrillar Ca(2+)-dependent Mg-ATPase and Ca(2+)-activated myosin ATPase. The effects of these two hormones on actin-activated myosin ATPase activity were more independent of each other. We conclude that the actions of thyroid and glucocorticoid hormones on the heart are interrelated and that optimum myocardial function results from their combined action.

Adenosine Triphosphatases↗
PubMedDate not supplied

Effects of riboflavin analogues and diuretics on the spontaneously hypertensive rat heart.

The chronic treatment of spontaneously hypertensive rats (SHR) with 7,8-dimethyl-10-(3-chlorobenzyl) isoalloxazine [CBI], 7,8-diethyl-10-aminol isoalloxazine [DEAI], enduron (methyclothiazide) and amiloride were studied for their effects on blood pressure and cardiac contractile protein ATPase activities. After 35 weeks of treatment all the above antihypertensive agents showed a decrease in blood pressure in the SHR (p less than 0.01). Chronic treatment with CBI, DEAI, enduron, and amiloride significantly improved the myofibrillar ATPase activity at all pCa2+ concentrations (p less than 0.01). Furthermore, CBI, DEAI, enduron, and amiloride drug treatments enhanced actin-activated myosin ATPase activity (p less than 0.01). The Ca2(+)-activated myosin ATPase activity was significantly elevated after treating with CBI and DEAI (p less than 0.01). These results suggest that the antihypertensive agents used in this study helped in reducing the blood pressure with a subsequent increase in myocardial contractile protein ATPase activity.

Actins↗