REFLEXES MEDIATED BY CARDIAC SYMPATHETIC AFFERENTS DURING MYOCARDIAL-ISCHEMIA - ROLE OF ADENOSINE

1. Myocardial ischaemia and infarction activate vagal and sympathetic sensory endings in the ischaemic myocardium, resulting in powerful ref lex effects. The vagal afferents are either mechano- or chemosensitive , whereas sympathetic afferents may be mechano-, chemosensitive or bot h. 2. Activation of vagal afferents results in sympathoinhibitory, car dioinhibitory, vasodepressor responses. Cardiac sympathetic afferents activated during myocardial ischaemia mediate sympathoexcitatory, vaso constrictor cardioaccelerator responses. 3. The focus of the present r eview is on the activation of sympathetic afferents by myocardial isch aemia and on the resulting reflex responses that they mediate. 4. Thes e endings are more likely to be activated as the degree of ischaemia p rogresses from subendocardial towards transmural. They are evenly dist ributed between the anterior and inferoposterior wall. Although it has been suggested that these endings are activated by bradykinin, recent evidence indicates that they are activated by adenosine released from the ischaemic myocardium. Results from our laboratory indicate that t his effect is due to the activation of adenosine A(1), but not adenosi ne A(2) receptors. 5. Activation of ventricular vagal and sympathetic afferent fibres during myocardial ischaemia in humans is responsible f or the autonomic changes observed and, in the case of the sympathetic afferents, for the sensation of angina pectoris.