Prostaglandin-mediated Inhibition of Noradrenaline Release: Its Resistance to Variations in Rate of Prostaglandin Synthesis

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Abstract
Isolated rabbit hearts were perfused according to Langendorff. The bilateral sympathetic nerve supply to the organ was stimulated at intervals, and the overflow of noradrenaline [NA] and of prostaglandins [PG] of the E series in the effluent was assayed, using fluorimetric and bioassay methods, respectively. The synthesis of PG in the organ was stimulated, either by perfusing the heart at a low PO2, or by infusing nicotinic acid. Hypoxia increased the coronary flow, provided the PG synthesis was not inhibited, probably as a consequence of hypoxia stimulation of the endogenous formation of PG. The release of NA in response to nerve stimulation was, however, unaffected by hypoxia. Nicotinic acid also stimulated PG formation, doubling the overflow of the lipid and response to nerve stimulation. In this series, too, the release of NA induced by nerve stimulation was unaffected by stimulation of PG synthesis. Local variations in the rate of PG synthesis are unable to change the degree to which the release of sympathetic neurotransmitter is inhibited. Furthermore, it is suggested that the PG synthesis in rabbit heart takes place in compartments, separated functionally or morphologically.