Stimulation of Monovalent Cation Active Transport by Low Concentrations of Cardiac Glycosides: ROLE OF CATECHOLAMINES (original) (raw)
Free access | 10.1172/JCI110366
Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02115
Cardiology Department, Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Hougen, T. in:PubMed |Google Scholar
Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02115
Cardiology Department, Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Spicer, N. in:PubMed |Google Scholar
Cardiovascular Division, Brigham and Women's Hospital, Boston, Massachusetts 02115
Cardiology Department, Children's Hospital Medical Center, Boston, Massachusetts 02115
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115
Find articles by Smith, T. in:PubMed |Google Scholar
Published November 1, 1981 -More info
Published November 1, 1981 -Version history
The stimulatory effect of low concentrations of ouabain on the Na-K pump in isolated guinea pig left atria was studied in vitro by assessing active transport of the K+ analog Rb+. Active transport of Rb+ was stimulated 20±8% (SEM, P < 0.05) above control values by 3 nM ouabain, but was inhibited by concentrations >10 nM. Preincubation with the β-adrenergic antagonist propranolol (1 μM) completely blocked stimulation of active transport of Rb+ by 3 nM ouabain. Norepinephrine, 10 nM, increased Rb+ active transport 29±10% (P < 0.02) above control values. The β-adrenergic agonist l-isoproterenol, 10 nM, increased active transport of Rb+ by 33±10% (P < 0.01) above control levels. This stimulatory effect was abolished if tissues were first exposed to propranolol. Tyramine (0.1 μM), a stimulator of endogenous catecholamine release, increased active transport of Rb+ 26±12% (P < 0.05) above control values. Rb+ active transport was not significantly changed when left atrial tissues were incubated with α-adrenergic agonists or antagonists. Ouabain stimulation of Rb+ active transport was prevented by in vivo depletion of myocardial endogenous catecholamines by either reserpine or 6-hydroxydopamine. These findings indicated that in myocardial tissue, Na-K pump stimulation by low concentrations of ouabain is mediated at least in part through β-adrenergic effects of endogenous catecholamines.
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