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Effect of epinephrine on norepinephrine release from rat kidney during sympathetic nerve stimulation



Effect of epinephrine on norepinephrine release from rat kidney during sympathetic nerve stimulation



European Journal of Pharmacology 93(3-4): 137-148



Experiments were performed to study presynaptic .beta.-adrenoceptor facilitation of sympathetic neurotransmitter release in the isolated perfused rat kidney and evaluate the effect of epinephrine on norepinephrine release during sympathetic nerve stimulation. The right kidney was isolated and perfused with Krebs-Ringer solution. Norepinephrine storage sites were labeled with [3H]norepinephrine. Increasing concentrations of isoproterenol and salbutamol when perfused through the kidney, caused an enhancement of the stimulus-induced release of [3H]norepinephrine at 0.5 and 2 Hz, with the maximum facilitatory effect being observed in 0.5 Hz. The effect of salbutamol on [3H]norepinephrine release was concentration-dependent and more pronounced than that of isoproterenol. While propranolol (10-9-10-5 M) by itself did not cause any significant changes in the stimulus-induced release of [3H]norepinephrine, it antagonized the facilitatory action of salbutamol on [3H]norepinephrine release during periarterial nerve stimulation. When epinephrine (10-10-10-7 M), was perfused through the kidney in the presence of cocaine, it caused a concentration-dependent inhibition of the stimulus-induced release of [3H]norepinephrine at 0.5 Hz. In the presence of cocaine plus phentolamine, epinephrine did not have any effect on [3H]norepinephrine release elicited during periarterial nerve stimulation. When epinephrine was perfused in the presence of cocaine, phentolamine and corticosterone it caused a slight but significant increase in the stimulus-induced release of [3H]norepinephrine; the highest concentration (10-7 M) still caused a decrease in the [3H]norepinephrine release. These results, while providing evidence for the existence of presynaptic facilitatory .beta.-adrenoceptors on renal sympathetic nerves, fail to support the hypothesis that these receptors have a physiological role in the regulation of sympathetic neurotransmitter release.

Accession: 005236493

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PMID: 6139283

DOI: 10.1016/0014-2999(83)90131-0

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