Abstract
This chapter discusses the effect of prostacyclin on the sympathetically mediated nociceptive cardiovascular reflex. Coronary vessels convert arachidonic acid into prostacyclin. When released into the coronary blood stream, prostacyclin may cause vasodilatation, prevent platelet aggregation, and reduce sympathetic discharge to the heart. Results suggest that prostacyclin, when released from the extravascular tissues, can act to sensitize sympathetic chemosensitive nerve endings to bradykinin and thereby contribute to the signaling of pain and initiation of the reflex hypertension and tachycardia that may accompany anginal attacks. However, when released into the coronary or systemic circulation, prostacyclin can act to sensitize vagal receptors in the heart to chemical and possibly mechanical stimulation. Hence, it facilitates the reflex depressor mechanisms. This action of circulating prostacyclin, in addition to its direct vasodilator and anti-aggregatory effects, may be of special importance in ischaemic heart disease, because the predominance of vagal over sympathetically mediated reflex activity would result in reduction of workload and oxygen demand by the heart.
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