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Inhibition of prostaglandin effects by ouabain in the canine vascular tissue
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1969
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Spontaneous ContractionsPharmacotherapyExperimental PharmacologyThrombosisMolecular PharmacologyCanine Vascular TissueProstaglandin E 1Animal PhysiologyVeterinary PhysiologyMolecular PhysiologyProstaglandin EffectsVascular PharmacologySmall Animal Internal MedicineVascular BiologyEndocrinologyPharmacologyPotassium HomeostasisPhysiologyPge 1Veterinary ScienceEndothelial DysfunctionMedicine
The effects of prostaglandins on the isolated mesenteric vein and artery of the dog were investigated. Prostaglandin E 1 (PGE 1 ) inhibited spontaneous contractions of the tissue whereas prostaglandin F 1α (PGF 1α ) and prostaglandin F 2α (PGF 2α ) stimulated them. The effects of prostaglandins were not influenced by pretreatment with atropine, phenoxybenzamine, propranolol, or tetrodotoxin. The norepinephrine-induced contractions were inhibited by PGE 1 and enhanced by PGF 1α and PGF 2α Both these contrasting effects were enhanced in a low concentration of K + (1.2 mM) and diminished when the media contained K + in high concentration (23.2 mM). Pretreatment of the tissue with ouabain in sufficiently high concentration (1.5 × 10 −5 M) produced an initial contracture followed by relaxation. PGE 1 and PGF 1α had no effect on the ouabain-treated tissue but PGF 2α still induced dose-dependent contractions. In the ouabain-treated tissue the effects of PGE 1 and PGF 1α on the norepinephrine-induced contraction were also absent. From these experiments it is concluded that the transport enzyme (Na + + K + )-dependent ATPase is necessary for PGE 1 and PGF 1α to elicit their action on vascular tissue. The PGF 2α effect is probably mediated by an enzyme which is not sensitive to ouabain.