Propranolol Accentuates the Cold Induced Fall in Skin Temperature and Elevation in Blood Pressure in 12 Normotensive Men: A Role for the Beta Receptor in Cold.

摘要

Exposure to cold air induces a rapid and characteristic rise in plasma norepinephrine and blood pressure. The mechanism of this cold induced hypertension, which is independent of renin, appears to be mediated by adrenergic receptors. To test this hypothesis, we administered propranolol (80mg/day: 1mg/kg), a beta adrenoreceptor blocker, and contrasted this response with the sympathomimetic drug ephedrine (60 mg/day: .9 mg/kg and placebo. We used a double blind cross over study. Twelve normotensive men entered a climatic chamber for a 30 minute exposure of either 4C or 25C. Fingertip capillary blood flow was estimated by a laser doppler technique, while fingertip skin and rectal temperatures were recorded. We serially measured brachial blood pressure/pulse and hematocrit. As indicators of sympathetic nervous system activity, venous plasma norepinephrine (NE) and epinephrine (EPI) were measured. These results suggest that cold rapidly evokes a fall in skin surface blood flow and elevates systemic blood pressure simultaneously as the distal extremity is cooled. We hypothesize that propranolol accentuates cold associated distal extremity cooling and blood pressure elevation by inhibiting the beta 2 medicated vasodilation and thus allows for alpha medicated vasodilation to be relatively unopposed. (KT)