The role of α‐adrenergic receptors in mediating beat‐by‐beat sympathetic vascular transduction in the forearm of resting man

Key points Sympathetic support of blood pressure demands the efficient control of vascular tone; however, little is known regarding how spontaneously occurring bursts of muscle sympathetic nerve activity (MSNA) dynamically influence forearm vascular conductance. This study examined the extent to which spontaneous MSNA bursts evoke changes in forearm vascular conductance and blood pressure with and without local α‐adrenergic blockade in young healthy men during supine rest. We observed that under resting conditions, forearm vascular conductance increases briefly and then significantly decreases in association with the total amount of the preceding MSNA; however, during α‐adrenergic blockade the decrease in vascular conductance is eliminated. These results indicate that normal variations in spontaneous MSNA burst activity are systematically followed by transient and robust responses of forearm vasoconstriction and that this influence is mediated via α‐adrenergic receptor mechanisms. Abstract Sympathetic vascular transduction is commonly understood to act as a basic relay mechanism, but under basal conditions, competing dilatory signals may interact with and alter the ability of sympathetic activity to decrease vascular conductance. Thus, we determined the extent to which spontaneous bursts of muscle sympathetic nerve activity (MSNA) mediate decreases in forearm vascular conductance (FVC) and the contribution of local α‐adrenergic receptor‐mediated pathways to the observed FVC responses. In 19 young men, MSNA (microneurography), arterial blood pressure and brachial artery blood flow (duplex Doppler ultrasound) were continuously measured during supine rest. These measures were also recorded in seven men during intra‐arterial infusions of normal saline, phentolamine (PHEN) and PHEN with angiotensin II (PHEN+ANG). The latter was used to control for increases in resting blood flow with α‐adrenergic blockade. Spike‐triggered averaging was used to characterize beat‐by‐beat changes in FVC for 15 cardiac cycles following each MSNA burst and a peak response was calculated. Following MSNA bursts, FVC initially increased by +3.3 ± 0.3% ( P = 0.016) and then robustly decreased to a nadir of −5.8 ± 1.6% ( P < 0.001). The magnitude of vasoconstriction appeared graded with the number of consecutive MSNA bursts; while individual burst size only had a mild influence. Neither PHEN nor PHEN+ANG infusions affected the initial rise in FVC, but both infusions significantly attenuated the subsequent decrease in FVC (–2.1 ± 0.7% and –0.7 ± 0.8%, respectively; P < 0.001 vs . normal saline). These findings indicate that spontaneous MSNA bursts evoke robust beat‐by‐beat decreases in FVC that are exclusively mediated via α‐adrenergic receptors.