Catecholamine-induced vasodilator metabolite release from guinea-pig hearts is not due to increased myocardial activity.

Guinea-pig isolated hearts were perfused in series, the donor heart perfusate supplying the recipient heart. Isoprenaline increased the rate and force of contraction and oxygen consumption of donor hearts and produced a coronary vasodilatation. This was accompanied by the release of vasodilator metabolite as demonstrated by vasodilatation of the recipient heart, the beta-adrenoceptors of which were antagonized by propranolol. During arrest of donor hearts by either carbachol or application of a fibrillating current, isoprenaline still released vasodilator metabolite and increased oxygen consumption but without changes in rate or tension. This release was prevented by beta-adrenoceptor blockade. It is concluded that the sympathomimetic-induced coronary vasodilatation is mediated via the release of a vasoactive metabolite, the trigger for which is not the concomitant mechanical hyperactivity.