Abstract
1. The dog isolated sphincter pupillae contracted in response to acetylcholine, angiotensin II (AII), bradykinin, prostaglandins F2 alpha, D2, E2 and I2, and thionate thromboxane A2 (sTXA2) in a concentration-dependent manner. 2. AII-induced contractions were suppressed by treatment with saralasin, indomethacin, aspirin and diphloretin phosphate (DPP), a prostaglandin receptor antagonist. Contractions induced by bradykinin were also attenuated by indomethacin, aspirin and DPP. The amount of prostaglandin F2 alpha (PGF2 alpha) in the bathing media was increased approximately 41% following stimulation of the preparations by bradykinin. 3. The potency of contractile responses was in the order of PGF2 alpha greater than PGD2 = sTXA2 greater than PGE2 greater than arachidonic acid greater than PGI2. Contractions induced by PGF2 alpha were not significantly affected by treatment with indomethacin and ONO3708, an antagonist of the vasoconstrictor effect of prostaglandins, but appreciably attenuated by DPP. Arachidonic acid-induced contractions were inhibited by indomethacin. 4. Contractions of dog iris sphincter muscle in response to AII and bradykinin may be mediated via substances synthesized by cyclo-oxygenase from arachidonic acid. The distribution and nature of the prostaglandin receptors appear to differ markedly in iris sphincter and vascular smooth muscles.
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