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Postjunctional α1- and α2-Adrenoceptors
48
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0
References
1982
Year
Synaptic TransmissionAnesthetic MechanismExperimental PharmacologyPerfused SpleenSpleen Perfusion PressureMolecular PharmacologyAdrenal GlandSympathetic Nervous SystemNeuroendocrine MechanismAnesthetic PharmacologySodium HomeostasisBehavioral PharmacologyNeurotransmitter ReceptorsNeuropharmacologyNervous SystemPharmacologyNeurophysiologyPhysiologyMedicinePostsynaptic α2-AdrenoceptorsAlpha-adrenergic Pharmacology
Summary: Postsynaptic α2-adrenoceptors have been reported to mediate pressor responses in vivo in several species. It has been suggested that it is the presence of these receptors that renders the pressor response to injected noradrenaline resistant to the α1-adrenoceptor antagonist prazosin in these species. We have now investigated this phenomenon in the perfused cat spleen preparation in vitro. We find that the pressor responses to nerve stimulation and phenylephrine are blocked to a greater extent by prazosin than the responses to either noradrenaline or the selective α2-agonist M7. In the presence of cocaine the increases in spleen perfusion pressure induced by noradrenaline. phenylephrine, and nerve stimulation are equally blocked by prazosin. We conclude from these results that the responses of the perfused spleen to exogenous noradrenaline are resistant to prazosin because the access of noradrenaline to α1-adrenoceptors is limited by the neuronal uptake mechanism. The difference in the sensitivity of neuronally released and exogenously administrated noradrenaline to blockade by prazosin may be due to the preferential noradrenergic innervation of α1-adrenoceptors, and the predominant extrasynaptic location of α2-adrenoceptors in vascular smooth muscle.