COMPARISON OF HEMODYNAMIC AND SYMPATHONEURAL RESPONSES TO ADENOSINE AND LOWER-BODY NEGATIVE-PRESSURE IN MAN

Citation
Ga. Rongen et al., COMPARISON OF HEMODYNAMIC AND SYMPATHONEURAL RESPONSES TO ADENOSINE AND LOWER-BODY NEGATIVE-PRESSURE IN MAN, Canadian journal of physiology and pharmacology, 75(2), 1997, pp. 128-134
Citations number
44
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
00084212
Volume
75
Issue
2
Year of publication
1997
Pages
128 - 134
Database
ISI
SICI code
0008-4212(1997)75:2<128:COHASR>2.0.ZU;2-E
Abstract
Adenosine increases heart rate and sympathetic nerve activity reflexiv ely in conscious humans through several mechanisms. The purpose of thi s study was to assess the relative contributions of arterial barorecep tor unloading, carotid chemoreceptor stimulation, and other adenosine- sensitive afferent nerves to these responses. In 12 healthy men. the e ffect on blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA; peroneal nerve) of lower body negative pressure (LBNP ; -15 mmHg (1 mmHg = 133.3 Pa)) was compared with the effect of intrav enous adenosine (35, 70, and 140 mu g.kg(-1).min(-1)). In eight subjec ts, the highest dose was reinfused during 100% oxygen to suppress arte rial chemoreceptors. Blood pressure reductions during LBNP and adenosi ne (140 mu g.kg(-1).min(-1)) were similar. HR did not change significa ntly during LBNP (+2 +/- 2 beats/min; mean +/- SE) but increased at th e highest adenosine dose (+25 +/- 3 beats/min; p < 0.05). MSNA increas ed significantly (p < 0.05) during both interventions (+255 +/- 82 and +247 +/- 58 units/100 beats for adenosine and LBNP, respectively), an d there was no difference in the MSNA response to these two stimuli (p > 0.1). Oxygen inhibited adenosine-induced increases in HR and MSNA ( from +305 +/- 99 to +198 +/- 75 units/100 beats and from +26 +/-4 to 18 +/- 3 beats/min; p < 0.05 for both comparisons). The MSNA response to these combined stimuli was similar to that observed during LBNP. In contrast, the residual HR response (+18 +/- 3 beats/min) was signific antly greater than the response to LBNP (+2 +/- 2 beats/min; p < 0.05) . These data indicate that arterial baroreceptor unloading cannot acco unt for the marked adenosine-induced increase in HR. but may be suffic ient to explain its effect on MSNA. The effect of 100% oxygen confirms that stimulation of carotid chemoreceptors accounts for approximately one-third of the HR and MSNA response to adenosine. However, other me chanisms, such as stimulation of adenosine-sensitive afferent nerves i n other vascular beds, are involved in the HR and possibly the MSNA re sponse.