1. The autonomic and local control of the circumflex coronary bed evoked through acute rises in aortic pressure (aortic balloon inflation) was analysed in conscious, normotensive and hypertensive dogs in complete heart block with ventricles paced at 100 beats/min.
2. In normotensive dogs there was an initial rise (6–12 s) in circumflex conductance preceding a fall in conductance as aortic pressure increased and was sustained. The initial rise, but not the later fall, in circumflex conductance was partly due to a cholino-receptor and partly due to α-adrenoreceptor mechanisms. Local constrictor mechanisms were responsible for the later fall in conductance.
3. The initial cholinoreceptor component of the rise in circumflex conductance is initiated through arterial baroreflex mechanisms.
4. The initial autonomic mechanisms regulating circumflex conductance appear to be absent in renal hypertension.
5. The absence of the transient autonomic rise in circumflex flow and conductance in response to rapid elevations in aortic pressure in certain forms of hypertension, e.g. during tachyarrhythmias and behavioural disturbances, may result in myocardial ischaemia when it is least appropriate.