Presynaptic α-adrenoceptor regulation of transmitter release in the conscious rat

Abstract

1. 1. Blood pressure (BP) and heart rate (HR) were recorded in conscious, adrenal demedulated rats. The rats were subjected to a 1-min period of mild “stress”, induced by jet-air directed into the experimental cage. The plasma content of noradrenaline (NA), dopamine (DA) and 3, 4-dihydroxy-phenylacetic acid (DOPAC) was determined 1 min after termination of “stress”. 2. 2. The presynaptic α 2-adrenoceptor antagonist yohimbine (YOH) (10 −7 − 10 −6 mol/kg, given 5 min prior to “stress”) did not alter the increase in BP and HR, induced by “stress”, when compared to control rats (receiving NaCl instead of YOH at the corresponding time). 3. 3. Pre-treatment with atropine (ATR) (2.5 mg/kg) 5 min before YOH (10 −6 mol/kg) or NaCl increased HR but not BP significantly in both groups of rats. “Stress”, as above, gave a significant prolongation of the increase in HR in rats receiving YOH, when compared to control rats. The increase in BP was not significantly altered, compared to controls. 4. 4. The neuronal re-uptake inhibitor desroethylimipramine (DMI) (0.1 mg/kg) was given together with ATR (2.5 mg/kg) 5 min before YOH (10 −6 mol/kg) or NaCl in one group of rats. This treatment induced a significant increase in HR but did not affect BP. “Stress”, induced as above, extended the duration of the increase in HR in the YOH-treated rats, compared to controls. The increase in BP was not significantly different between the YOH-treated rats and the controls. 5. 5. Plasma levels of NA, DA and DOPAC were measured 1 min after termination of “stress” in rats pre-treated with ATR (2.5 mg/kg) and DMI (0.1 mg/kg) 10 min before “stress”. Five minutes prior to “stress”, the animals received YOH (10 −6 mol/kg) or NaCl. The group receiving YOH showed significantly higher plasma levels of NA, compared to controls. DA and DOPAC levels were not affected. 6. 6. Our findings support the theory that presynaptic α 2-adrenoceptor modulation of sympathetic transmitter release exists in vivo. It is also indicated that maintenance of homeostasis is more dependent on other mechanisms, such as vagal influence.