Electromagnetic flow probes were used to measure regional blood flow responses to central injection of L-proline in conscious rats. Ten min after intracisternal injection of 10 mu mol of L-proline, arterial pressure increased from 113+/-1.6 (mean+/-SEM, n=23) to 142+/-2.9 mmHg, while the heart rate decreased from 383+/-9.6 (n=23) to 313+/-5.4 beats/min, vascular resistance increased an average of 239% in the superior mesenteric artery (n=8) and 72% in the renal artery (n=8), without change in the terminal aorta (-6%, n=7). However, 10 mu mol of D-proline induced neither blood pressure increase nor bradycardia 10 min after its injection. After sine-aortic denervation, the heart rate was not decreased by L-proline injection. Ganglionic blockade with chlori-sondamine evoked significantly greater presser action by L-proline injection than that without treatment, but intravenous injection of the vasopressin antagonist, (d(CH2)(5)(1), O-Me-Tyr(2), Arg(8))-vasopressin (10 mu g/kg), promptly dilated the superior mesenteric vascular bed and lowered the arterial pressure. In addition, pretreatment with the vasopressin antagonist alone almost abolished the presser and vasoconstrictor action induced by L-proline injection. These results indicate that intracisternal injection of L-proline specifically elicited an increase in arterial pressure mainly through marked vasoconstriction of the superior mesenteric artery bed, and that bradycardia was elicited via the baroreflex. Thus, vasopressin release in the blood-stream was involved in these hemodynamic actions.
