Contribution of sympathetic activation to coronary vasodilatation during the cold pressor test in healthy men: effect of ageing

Key points The sympathetic nervous system is an important regulator of coronary blood flow. How ageing may effect sympathetic nervous system regulation of coronary blood flow during physiological stress is unknown. We measured coronary vascular responses to sympathetic activation before and during systemic α‐ and β‐adrenergic receptor blockade in young and older healthy men. Our results indicate that the normal coronary vascular response to sympathetic activation in young men is pronounced vasodilatation and that this effect is lost with advancing age, as the result of an apparent adrenergic mechanism. These findings may help explain how acute sympathetic activation may trigger angina and coronary ischaemic events, particularly in older adults. Abstract The sympathetic nervous system is an important regulator of coronary blood flow. The cold pressor test (CPT) is a powerful sympathoexcitatory stressor. We tested the hypotheses that: (1) CPT‐induced sympathetic activation elicits coronary vasodilatation in young adults that is impaired with advancing age and (2) combined α‐ and β‐adrenergic blockade diminishes/abolishes these age‐related differences. Vascular responses of the left anterior descending artery to the CPT were determined by transthoracic Doppler echocardiography before (pre‐blockade) and during (post‐blockade) systemic co‐administration of α‐ and β‐adrenergic antagonists in young ( n = 9; 26 ± 1 years old, mean ± SEM) and older healthy men ( n = 9; 66 ± 2 years old). Coronary vascular resistance (CVR; mean arterial pressure/coronary blood velocity) was used as an index of vascular tone. CPT decreased CVR (i.e. coronary vasodilatation occurred) in young (Δ–33 ± 6%), but not older men (Δ–3 ± 4%; P 0.05 compared to young pre‐blockade). Impaired CPT‐induced coronary vasodilatation could not be explained by a reduced stimulus for vasodilatation as group and condition effects persisted when CVR responses were expressed relative to myocardial oxygen demand (rate–pressure product). These data indicate that the normal coronary vascular response to sympathetic activation in young men is pronounced vasodilatation and this effect is lost with age as the result of an adrenergic mechanism. These findings may help explain how acute sympathoexcitation may precipitate angina and coronary ischaemic events, particularly in older adults.