MECHANISMS OF UPTAKE AND RELEASE OF NOREPINEPHRINE IN ADRENERGIC NERVE ENDINGS

点击翻译按钮获取中文摘要

Accumulating evidence continues to be supportive of our hypothesis that Ch+-Ca++-stimulated neurosecreton by adrenergic nerve endings is mediated by outward transport of NE in vesicles fused or attached to the plasmalemma. The overall plan is and has been to induce Ca++ dependent neurosecretion by rat heart ventricle slices incubated in a Na+ deprived Krebs bicarbonate medium containing choline Cl as the replacement for NaCl. The integrity of the plasmalemma was shown by a Ca++-dependent, secretion induced by K+ after secretion was slowed by appropriate modification of experimental conditions. Biochemical evidence of vesicles fusion was the demonstration of reactions known to characterize vesicle membranes. Inhibition of secretion by the impermeable ATP is such a reaction. Depending upon the concentration, chlorpromazine, a drug known to have a variety of effects on biological membranes, and to inhibit H+ transport, may increase or decrease Ch+-Ca++ stimulated neurosecretion. Yohimbine had little effect in specific alpha receptor blocking concentrations. Established secretion was reversible by the ommission of extracellular Ca++.