Please use this identifier to cite or link to this item:
|Title:||Adrenaline in the peripheral regulation of blood pressure.|
|Presented at:||University of Leicester|
|Abstract:||Majewski, Tung and Rand (1981) have suggested a role for adrenaline in the development and maintenance of a raised blood pressure in rats, presumably by an activation of pre-junctional B-adrenoceptors which facilitate sympathetic neurotransmission. The present study attempts to investigate the effect of acute alterations in circulating adrenaline upon vasoconstrictor responses in the pithed rat and the isolated perfused rat kidney, where an attempt was also made to correlate responses with transmitter overflow, and also attempts to elucidate the receptor mechanisms involved. The role of adrenaline in the development of blood pressure in young SHR rats was also investigated. In pithed rats, depleting plasma adrenaline levels by acute bilateral adrenal demedullation, reduced neurogenic pressor responses and those due to bolus injections of a-agonists. Adrenaline infusion selectively enhanced neurogenic pressor responses an effect inhibited by ?2-adrenoceptor antagonism but not by ?1-antagonism. The facilitatory effect of adrenaline was mimicked by infusions of ?2-agonists. Similar effects were observed in the isolated perfused kidney when adrenaline was added to the perfusate. The persistent nature of adrenaline's effect was abolished by cocaine, indicating that adrenaline is subject to neuronal uptake and facilitates sympathetic activity long after the amine has been removed from the circulation. Correlating changes in end-organ responses with changes in transmitter overflow proved more difficult and requires further work. Bilateral adrenal demedullation of young SHR rats attenuated their development of hypertension, an effect reversed with slow release implants of adrenaline and ?2-adrenoceptor agonists. The effect of adrenaline implants was antagonised by treatment with ICI 118551, which was not itself acutely hypotensive but was chronically effective in attenuating hypertension development in whole animals. It is concluded that adrenaline can facilitate sympathetic neurotransmission by an activation of pre-junctional ?2-adrenoceptors and so enhance end-organ responses to sympathetic nerve stimulation. Since adrenaline is subject for neuronal uptake, its effect persists long after its removal from the circulation. Such a long lasting facilitation of sympathetic activity may be the mechanism by which adrenaline exerts its pro-hypertensive effect in the SHR rat.|
|Rights:||Copyright © the author. All rights reserved.|
|Appears in Collections:||Theses, Dept. of Cell Physiology and Pharmacology|
Items in LRA are protected by copyright, with all rights reserved, unless otherwise indicated.