| Autor: |
van Mil ACCM; Department of Physiology, Radboudumc, Nijmegen , The Netherlands.; Research Institute for Sport and Exercise Sciences, Liverpool John Moores University , Liverpool , United Kingdom., Tymko MM; Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Science, University of British Columbia , Kelowna , Canada., Kerstens TP; Department of Physiology, Radboudumc, Nijmegen , The Netherlands., Stembridge M; Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Science, University of British Columbia , Kelowna , Canada.; Cardiff School of Sport, Cardiff Metropolitan University , Cardiff , United Kingdom., Green DJ; School of Sports Science, Exercise and Health, the University of Western Australia , Nedlands , Australia., Ainslie PN; Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Science, University of British Columbia , Kelowna , Canada., Thijssen DHJ; Department of Physiology, Radboudumc, Nijmegen , The Netherlands.; Research Institute for Sport and Exercise Sciences, Liverpool John Moores University , Liverpool , United Kingdom. |
| Abstrakt: |
Carotid artery (CCA) dilation occurs in healthy subjects during cold pressor test (CPT), while the magnitude of dilation relates to cardiovascular risk. To further explore this phenomenon and mechanism, we examined carotid artery responses to different sympathetic tests, with and without α 1 -receptor blockade and assessed similarity to these responses between carotid and coronary arteries. In randomized order, 10 healthy participants (25 ± 3 yr) underwent sympathetic stimulation using the CPT (3-min left-hand immersion in ice-slush) and lower-body negative pressure (LBNP). Before and during sympathetic tests, CCA diameter and velocity (Doppler ultrasound) and left anterior descending (LAD) coronary artery velocity (echocardiography) were recorded across 3 min. Measures were repeated 90 min following selective α 1 -receptor blockade via oral prazosin (0.05 mg/kg body wt). CPT significantly increased CCA diameter, LAD maximal velocity, and velocity-time integral area-under-the-curve (all P < 0.05). In contrast, LBNP resulted in a decrease in CCA diameter, LAD maximal velocity, and velocity time integral (VTI; all P < 0.05). Following α 1 -receptor blockade, CCA and LAD velocity responses to CPT were diminished. In contrast, during LBNP (-30 mmHg), α 1 -receptor blockade did not alter CCA or LAD responses. Finally, changes in CCA diameter and LAD VTI responses to sympathetic stimulation were positively correlated ( r = 0.66, P < 0.01). We found distinct carotid artery responses to different tests of sympathetic stimulation, where α 1 receptors partly contribute to CPT-induced responses. Finally, we found agreement between carotid and coronary artery responses. These data indicate similarity between carotid and coronary responses to sympathetic tests and the role of α 1 receptors that is dependent on the nature of the sympathetic challenge. NEW & NOTEWORTHY We showed distinct carotid artery responses to cold pressor test (CPT; i.e., dilation) and lower-body negative pressure (LBNP; i.e., constriction). Blockade of α 1 -receptors significantly attenuated dilator responses in carotid and coronary arteries during CPT, while no changes were found during LBNP. Our findings indicate strong similarity between carotid and coronary artery responses to distinct sympathetic stimuli, and for the role of α-receptors. |
