Central depletion of catecholamines--importance of hypertension and anesthesia.

The importance of the brain noradrenergic sympathetic nervous system in blood pressure control during anesthesia with halothane and enflurane was investigated in normotensive and hypertensive rats. Central noradrenergic neurons were destroyed by instillation of 6-hydroxydopamine (6-OHDA) into the cerebral ventricle of both normotensive Wistar rats and spontaneously hypertensive rats (SHR). One week later, arterial and venous lines were placed in the rats under anesthesia; the rats were allowed to recover; and blood pressure and plasma renin activity were measured while the rats were awake. Anesthesia then was induced with 1.3 vol% halothane (Wistar n = 8, Wistar 6-OHDA n = 10, SHR n = 8, SHR 6-OHDA n = 6) or 2.2 vol% enflurane (Wistar n = 6, Wistar 6-OHDA n = 10, SHR n = 8, SHR 6-OHDA n = 6). A control group (Wistar n = 10, Wistar 6-OHDA n = 6, SHR n = 8, SHR 6-OHDA n = 6) was treated identically, but remained unanesthetized throughout the experiment. The untreated normotensive and hypertensive rats received no intraventricular injections. After 1 hr of stable anesthesia, plasma renin activity was measured again, and saralasin, a competitive inhibitor of angiotensin II, was infused to determine the importance of the renin--angiotensin system in blood pressure control. Treatment with 6-OHDA resulted in a 60-90% depletion of norepinephrine in the medulla and hypothalamus. Normotensive Wistar rats treated with 6-OHDA responded to halothane and enflurane anesthesia in a manner similar to untreated normotensive rats. In contrast, hypertensive animals treated with 6-OHDA and then anesthetized with halothane had a significantly greater decrease in blood pressure than untreated hypertensive rats (100 +/- 4 mm Hg vs 125 +/- 4 mm Hg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)