Plasma renin activity during infusion of epinephrine into the carotid and vertebral arteries of anesthetized dogs.

Previous experiments have demonstrated that increments of epinephrine concentration within the physiological range elevate PRA when epinephrine is infused iv but not when it is infused directly into the renal artery. The present experiments examined whether an elevation of the circulating epinephrine concentration to the head could account for this elevation of PRA by epinephrine. Anesthetized dogs were surgically prepared for blood sampling and blood pressure recording and for the infusion of epinephrine into either a femoral vein (iv) or the carotid and vertebral arteries. After a control period, epinephrine was infused for 45 min at a total rate of 25 ng kg-1 min-1 either iv or into the head vasculature (3.5 ng kg-1 min-1 into each vertebral artery and 9 ng kg-1 min-1 into each carotid artery). PRA (in nanograms per ml h-1) rose from 1.8 +/- 0.5 to 5.9 +/- 1.2 (mean +/- SE) during iv epinephrine infusion. PRA rose similarly (from 1.5 +/- 0.4 to 4.8 +/- 1.8) during epinephrine infusion to the head. The arterial blood epinephrine concentration rose similarly in response to iv and head epinephrine infusions. Furthermore, the changes in hematocrit, heart rate, blood pressure, and plasma potassium concentration were identical regardless of the route of epinephrine infusion. In separate experiments, a smaller infusion of epinephrine infusion. In separate experiments, a smaller infusion of epinephrine directly into the head vasculature at a total rate of 2.5 ng kg-1 min-1 (0.35 ng kg-1 min-1 into each vertebral artery and 0.9 ng kg-1 min-1 into each carotid artery) was without effect on PRA. The data indicate that 1) epinephrine is apparently neither taken up nor degraded by the microcirculation of the head, and 2) the receptors mediating the stimulatory effect of epinephrine on PRA are not located in regions supplied by the carotid and vertebral arteries.