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The role of α‐adrenergic receptors in mediating beat‐by‐beat sympathetic vascular transduction in resting humans
Author(s) -
Fairfax Seth T,
Credeur Daniel P,
Holwerda Seth W,
Zuidema Mozow Y,
Medley John H,
Dyke Peter C,
Wray D Walter
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1119.2
Subject(s) - microneurography , medicine , endocrinology , phentolamine , adrenergic , brachial artery , vasodilation , sympathetic nervous system , receptor , cardiology , blood pressure , baroreflex , heart rate
Sympathetic vascular transduction is commonly understood to act as a basic relay, 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). In 7 young men, MSNA (microneurography) and brachial artery blood flow (duplex Doppler ultrasound) were continuously measured during 20 minute infusions of intra‐arterial saline (control), phentolamine (PHEN), and PHEN with angiotensin II (PHEN‐ANG). The latter was used to control for increases in resting blood flow with a‐adrenergic blockade. Signal averaging was used to characterize beat‐by‐beat changes in FVC for 15 cardiac cycles following each individual MSNA burst and a peak response was calculated. During saline, FVC initially increased by +3.3±0.3% following MSNA bursts (P=0.016) and then robustly decreased to a nadir of −5.8±1.5% (P<0.001). PHEN and PHEN+ANG infusion did not alter the initial rise in FVC, but significantly attenuated the ensuing decrease in FVC (−2.1±0.7% and −0.7±0.8%, respectively; P<0.001 vs. saline). These findings indicate that spontaneous MSNA bursts are capable of evoking robust decreases in FVC that are exclusively mediated via α‐adrenergic receptors. Supported by RO1 HL093167