Titlebook: Cardiac Glycoside Receptors and Positive Inotropy; Evidence for more th E. Erdmann Conference proceedings 1984 Dr. Dietrich Steinkopff Verl

Pert敏捷

Nonradioactive Analysis of Biomoleculesh the increase in the intracellular Na. concentration. It is suppressed in Na. free medium or when Na. is replaced by Li. suggesting that the increase is due to the indirect activation of the Na./Ca. exchange system in the plasma membrane. Dose-response curves for the inotropic effects of ouabain on

玉米

Nonradioactive Analysis of Biomoleculeseems to correlate with the inotropic action, whereas the low affinity ouabain binding is more related to NaK-ATPase inhibition..To further discriminate the two cardiac glycoside binding sites operative in guinea pig heart muscle, erythrosin B, shown to be an inhibitor of the high affinity ouabain bi

incision

Nutrient

Contractility of isolated bovine ventricular myocytes is enhanced by intracellular injection of car

輕彈

The electrogenic Na-K pump current and actions of the cardiac glycosides,

intangibility

Monocle

Cardiac glycosides with different effects in the heart,

Electrolysis

Cardiac glycoside receptors and positive inotropy Evidence for more than one receptor?, the latter 3. would cause an increase of intracellular Ca., which in turn would 4. stimulate the contractile proteins to a larger extent than before addition of the drugs. This hypothesis seemed to explain the increase in force of contraction rather well and also the clinically important arrhythmia

有幫助

Binding sites for ouabain in human and rat erythrocytes and in rat heart cells,s only the bond between C-2 and C-3 of the rhamnose without affecting the steroid moiety. The periodate oxidation provided additional information for assigning a distorted chair conformation or a transient boat conformation for rhamnose in ouabain. It was also established by .H NMR spectroscopy that

容易做

Cardiac glycosides and intracellular Na+, K+, Ca2+,hythmias are present. The increase of intracellular free and bound calcium, which manifests itself functionally as contracture, is believed to be caused at least by two mechanisms: a stimulation of the Na-Ca-exchange and an inhibition of the specific Ca.-activated ATPase in the plasma membrane catal