Neurogenic-nitric oxide interactions affecting brachial artery mechanics in humans: roles of vessel distensibility vs. diameter.
The purpose of this investigation was to assess the interactive influence of sympathetic activation and supplemental nitric oxide (NO) on brachial artery distensibility vs. its diameter. It was hypothesized that 1) sympathetic activation and NO competitively impact muscular conduit artery (brachial artery) mechanics, and 2) neurogenic constrictor input affects conduit vessel stiffness independently of outright changes in conduit vessel diastolic diameter. Lower body negative pressure (LBNP) and a cold pressor stress (CPT) were used to study the changes in conduit vessel mechanics when the increased sympathetic outflow occurred with and without changes in heart rate (LBNP -40 vs. -15 mmHg) and blood pressure (CPT vs. LBNP). These maneuvers were performed in the absence and presence of nitroglycerin. Neither LBNP nor CPT altered brachial artery diastolic diameter; however, distensibility was reduced by 25 to 54% in each reflex (all P < 0.05). This impact of sympathetic activation on brachial artery distensibility was not altered by nitroglycerin supplementation (21-54%; P < 0.05), although baseline diameter was increased by the exogenous NO (P < 0.05). The results indicate that sympathetic excitation can reduce the distensibility of the brachial artery independently of concurrent changes in diastolic diameter, heart rate, and blood pressure. However, exogenous NO did not minimize or reverse brachial stiffening during sympathetic activation. Therefore, sympathetic outflow appears to impact the stiffness of this conduit vessel rather than its diastolic diameter or, by inference, its local resistance to flow.
Salzer
Deborah A
DA
Neurovascular Research Laboratory, School of Kinesiology, Rm. 3110 Thames Hall, The Univ. of Western Ontario, London, ON, Canada N6A 3K7.
Medeiros
Philip J
PJ
Craen
Rosemary
R
Shoemaker
J Kevin
JK
D000328:Adult; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001916:Brachial Artery / Q000033:anatomy & histology / Q000294:innervation / Q000502:physiology*; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D003080:Cold Temperature; D005260:Female; D005542:Forearm / Q000098:blood supply; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008150:Lower Body Negative Pressure; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology; D009619:Nociceptors / Q000502:physiology; D012018:Reflex / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
D020030:Nitric Oxide Donors; D009569:Nitric Oxide; D005996:Nitroglycerin