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THE INFLUENCE OF PROSTAGLANDINS ON NORADRENALINE‐INDUCED VASOCONSTRICTION IN ISOLATED PERFUSED MESENTERIC BLOOD VESSELS OF THE RAT
Author(s) -
COUPAR I.M.,
MCLENNAN P.L.
Publication year - 1978
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.1476-5381.1978.tb07005.x
Subject(s) - phentolamine , medicine , endocrinology , vasoconstriction , prostaglandin , prostaglandin e , perfusion , chemistry , receptor , norepinephrine , dopamine
1 The report of the depression by indomethacin of vasoconstrictor responses to noradrenaline and their partial restoration by prostaglandin E 2 (PGE 2 ) and PGE 1 in rat isolated perfused mesenteric blood vessels was investigated. The further suggestion that prostaglandins may be necessary for the combination of noradrenaline with the α‐adrenoceptor in this tissue was also studied. 2 The reported depression by indomethacin was confirmed and was further shown to be in the form of a concentration‐dependent flattening of the noradrenaline concentration‐effect curve. 3 A concentration‐dependent restorative effect was observed for all prostaglandins studied. The decreasing order of potency for the restoration towards normal of the indomethacin‐depressed responses to noradrenaline was: PGE 2 , PGE 1 , PGA 1 , PGF 2α , PGA 2 . 4 The prostaglandins studied were not uniform in their restorative actions and could be separated into two groups. PGE 2 and PGE 1 restored responses towards the control level whereas PGA 1 , PGA 2 and PGF 2α increased responses to an above control level and did so over a smaller concentration range. The possibility of several prostaglandin receptors is discussed. 5 At concentrations equi‐effective in restoring depressed responses to control levels PGA 1 but not PGE 2 , caused a parallel shift of the noradrenaline concentration‐effect curve to the left and a small, gradual rise in the basal perfusion pressure. 6 The reason for the differing effects remains obscure but does not seem to involve a change in the α‐adrenoceptor as indicated by the pA 2 of phentolamine. Furthermore, the restorative and potentiating effect of PGA 1 is not mediated by blockade of neuronal uptake of noradrenaline. 7 It appears that prostaglandins are required for the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels and that this effect is distal to the drug‐receptor interaction. The possible involvement of prostaglandins with intracellular calcium ions is discussed.