Adrenaline-induced enhancement of the blood pressure response to sympathetic nerve stimulation in adrenal demedullated pithed rats

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Abstract
Summary The influence of the prejunctional β-adrenoceptor-mediated control mechanism of noradrenaline release on the cardiovascular response to preganglionic nerve stimulation (PNS) and the role of adrenaline as endogenous activator of this facilitatory mechanism were studied in pithed rats. The increases in mean arterial blood pressure and heart rate responses to eight PNS (0.8 Hz, 1 ms, 75 V, for 20 s at 12 min intervals) were measured in control, adrenal demedullated and sham-operated pithed rats, respectively. Repeated stimuli of the sympathetic outflow elicited similar blood pressure responses in control and sham-operated rats, whereas the blood pressure responses were attenuated in adrenal demedullated rats. Administration of the non-selective β-adrenoceptor antagonist propranolol (5 mg × kg−1, i.v.) decreased the blood pressure response in control, but not in adrenal demedullated rats. The increase in heart rate during PNS was abolished in both groups after administration of propranolol. Infusion of adrenaline (0.06 μg × kg−1 × min−1) increased the circulation levels of adrenaline from 0.4 nmol × 1−1 to 4.8 nmol × l−1, but did not modify the blood pressure response to PNS in control rats. In adrenal demedullated rats, however, the blood pressure response to PNS was enhanced during as well as after the infusion of adrenaline. This facilitatory effect of adrenaline on the blood pressure response in adrenal demedullated rats was blocked by pretreatment with propranolol (5 mg × kg−1, i.v.). Taken together the present findings give further support to the hypothesis that neuronal adrenaline of adrenal medullary origin is the endogenous agonist at prejunctional β-adrenoceptors mediating a facilitation of neuronal noradrenaline release.