Subcellular distribution of catecholamines in the dog heart Effects of reserpine and norepinephrine administration

Campos, H. A.; Shideman, F. E.

doi:10.1016/0028-3908(62)90004-7

Cited by 36 publications

(10 citation statements)

References 15 publications

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“…This suggests that 70 to 75% of the endogenous noradrenaline in the rat heart is present in a third intracellular pool which exchanges at a negligible rate with exogenous noradrenaline or with either of the other two intracellular pools during the limited duration of these experiments. These findings are consistent with the growing evidence that the noradrenaline store in sympathetically innervated tissues cannot be considered to be a single homogenous entity (Trendelenburg, 1961(Trendelenburg, , 1963Campos & Shideman, 1962 ;Kopin et al, 1962;Potter, Axelrod & Kopin, 1962;Iversen & Whitby, 1963), but it will require more experiments to delineate the characteristics of the various intracellular pools more precisely. I am grateful to the Medical Research Council for a scholarship and for a grant for animals and materials, to Dr E. Muscholl, University of Mainz, and to Dr J. Raventos, of I.C.I., for their generous gifts of (+)-noradrenaline, and to Professors L. G. Whitby and A. S. V. Burgen for much helpful advice and criticism.…”

Section: Discussionsupporting

confidence: 85%

The Uptake of Noradrenaline by the Isolated Perfused Rat Heart

Iversen

1963

British Journal of Pharmacology and Chemotherapy

240

172

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The uptake of noradrenaline by the isolated perfused rat heart was studied after perfusion with a medium containing various concentrations of (+)‐[3H]‐noradrenaline. Simultaneous measurement of the uptake of [3H]‐noradrenaline and of the net increase in the noradrenaline content of the heart showed that [3H]‐noradrenaline entering the heart both increased the tissue content and exchanged with endogenous noradrenaline. A large part (about 75%) of the endogenous noradrenaline pool, however, exchanged very slowly if at all with exogenous noradrenaline. The initial rates of noradrenaline uptake satisfied Michaelis‐Menten kinetics with a Km for (±)‐noradrenaline of 6.64times10−7 μM. Further analysis of the uptake process indicated that noradrenaline entered into at least two intracellular pools at different rates. Measurement of the initial rates of noradrenaline uptake during perfusion with various concentrations of nonradioactive (+)‐ and (−)‐noradrenaline showed that the uptake process exhibited stereochemical specificity. The Km values for (+)‐ and (−)‐noradrenaline were 13.9times10−7 and 2.66times10−7 μM respectively. Cocaine acted as a potent competitive inhibitor of noradrenaline uptake. This finding suggested that diffusion did not play any significant role in the entry of noradrenaline into the tissue.

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Section: Discussionsupporting

confidence: 85%

The Uptake of Noradrenaline by the Isolated Perfused Rat Heart

Iversen

1963

British Journal of Pharmacology and Chemotherapy

240

172

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“…8 The homogenate was centrifuged in the cold at 2000 X g for five minutes and the supernatant fluid containing the contents of the cells ruptured by homogenization was separated from the pellet, which is considered to consist of intact cells. This initial supernatant fluid was then fractionated into a pellet of subcellular particles and a second supernatant portion containing the cell fluid, by centrifugation at 100,000 X g for one hour.…”

mentioning

confidence: 99%

Mechanism of Norepinephrine Depletion in Experimental Heart Failure Produced by Aortic Constriction in the Guinea Pig

Spann

Chidsey

Pool

et al. 1965

Circulation Research

144

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The present study was undertaken to evaluate the influence of heart failure on the cardiac stores of norepinephrine, and to elucidate the mechanisms responsible for the changes observed. Congestive heart failure was produced in the guinea pig by supravalvular aortic constriction. Significant reductions in both the concentration and content of norepinephrine in the ventricles were observed, the magnitude of changes being related to the severity of the constriction. The renal concentration of norepinephrine was not usually affected. Infusions of large quantities of norepinephrine produced elevations of ventricular norepinephrine concentrations which were significantly less in guinea pigs with heart failure than in normal animals. Injections of lesser quantities of radioactive norepinephrine also resulted in smaller amounts of this material in the hearts of animals with failure. Measurement of the decay of specific activity indicated that heart failure did not alter the net turnover of norepinephrine in the left ventricle. From these findings it has been concluded that a defect in the uptake and/or retention of norepinephrine exists in these hearts and that this defect may be responsible for the depletion of norepinephrine.

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“…After reserpine, however, the uptake of noradrenaline by subcellular granules in the heart (Campos & Shideman, 1962) and the brain (Mirkin, Giarman & Freedman, 1963) is markedly diminished, suggesting that uptake after reserpine occurs mainly in other cellular constituents. It has also been shown recently that pre-treatment with reserpine prevents the selective concentration of tritium in the microsomal fraction (granule) of rat brain homogenates following incubation with H3-noradrenaline (Mirkin & Gillis, 1963).…”

Section: Discussionmentioning

confidence: 98%