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Effect of endothelium removal on stimulatory and inhibitory modulation of rat aortic prostacyclin synthesis
Author(s) -
Jeremy J.Y.,
Dandona P.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb11806.x
Subject(s) - prostacyclin , inhibitory postsynaptic potential , endothelium , chemistry , pharmacology , aorta , endocrinology , medicine
1 Removal of the endothelium (DE) enhanced the in vitro release of prostacyclin (PGI 2 ) by rat aortae in response to adrenaline (Ad), noradrenaline (NA), thromboxane A 2 analogue U46619, phorbol dibutyrate (PDBU) and sodium fluoride (NaF) when assessed at 3 h post DE. At 6 h post DE, there were no differences between the dose‐response curves obtained from aortic rings with or without endothelium. 2 At 3 h post DE the antagonism of Ad‐ and NA‐stimulated PGI 2 synthesis by yohimbine and prazosin, and NA‐stimulated PGI 2 synthesis by nifedipine was markedly reduced in aortae without eudothelium when compared with controls. These effects were reversed by protracted incubation of aortic tissue post DE (6 h and 9 h). 3 Acetylcholine, carbachol, substance P and nitroprusside were without effect on de novo or NA‐stimulated PGI 2 synthesis, whether or not the endothelium was present and irrespective of incubation time, post‐DE. 4 These results indicate that: (a) PGI 2 synthesis linked to excitatory receptors (α‐adrenoceptors, thromboxane A 2 ) and associated systems (G proteins, protein kinase C) in the smooth muscle component of the rat aorta is not influenced by endothelium‐derived relaxing factor (EDRF); (b) the changes of response to stimulators and inhibitors of PGI 2 synthesis may be due to an increased reactivity of the vessels caused by the trauma of DE; and (c) vasodilators (parasympathomimetics, substance P and nitroprusside) that do not act directly on excitatory receptors do not influence PGI 2 synthesis.