EFFECTS OF BROMOCRIPTINE ON CARDIOVASCULAR REGULATION IN HEALTHY HUMANS

Citation
Hp. Schobel et al., EFFECTS OF BROMOCRIPTINE ON CARDIOVASCULAR REGULATION IN HEALTHY HUMANS, Hypertension, 25(5), 1995, pp. 1075-1082
Citations number
33
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0194911X
Volume
25
Issue
5
Year of publication
1995
Pages
1075 - 1082
Database
ISI
SICI code
0194-911X(1995)25:5<1075:EOBOCR>2.0.ZU;2-X
Abstract
Bromocriptine, a dopamine agonist with central nervous system actions, may reduce sympathetic nervous system activity. We tested this hypoth esis by measuring arterial blood pressure, central venous pressure, he art rate, muscle sympathetic nerve activity, and forearm blood flow be fore and after unloading the arterial baroreceptors with sodium nitrop russide (0.5 to 1.5 mcg/kg per minute IV), before and after unloading the cardiopulmonary baroreceptors with incremental lower body negative pressure (0 to -15 mm Hg), and before and after immersion of the hand in ice-cold water for 2 minutes (cold presser test). After obtaining basal responses to provocative maneuvers, we gave 20 healthy subjects either 5 mg oral bromocriptine (n=10) or placebo (n=10) in a randomize d, double-blind fashion. Bromocriptine did not affect resting mean art erial pressure, heart rate, or forearm blood flow. Bromocriptine decre ased resting central venous pressure by 1.2 mm Hg (P<.05) and tended t o increase total integrated muscle sympathetic nerve activity (from 15 1+/-44 to 212+/-82 U/min, P=NS). The reflex increases in muscle sympat hetic nerve activity to nitroprusside infusion and lower body negative pressure were unchanged by bromocriptine; however, vascular responsiv eness to both maneuvers was impaired after bromocriptine administratio n compared with control. Without bromocriptine, the reflex increase in muscle sympathetic nerve activity after nitroprusside-induced hypoten sion maintained forearm blood flow at a constant level, whereas with b romocriptine the forearm blood flow increased from 1.9+/-0.3 to 2.8+/- 0.6 mL/min per 100 mt (P<.05). Similarly, the forearm blood flow respo nse to lower body negative pressure at -15 mm Hg was decreased with br omocriptine (+0.0+/-0.4 mL/min per 100 mt) compared with control value s (-0.4+/-0.3 mL/min per 100 mt, P<.05). Responses to the cold presser test were not altered by bromocriptine. We conclude that bromocriptin e inhibits catecholamine release in peripheral nerves. However, we wer e unable to substantiate a central effect of bromocriptine on either s ympathetic outflow or baroreflex sensitivity.