EFFECT OF PROSTAGLANDIN (PGE-1) ON THE PERMEABILITY RESPONSE OF TOAD BLADDER TO VASOPRESSIN, THEOPHYLLINE AND ADENOSINE 3',5'-MONOPHOSPHATE.

Abstract

THE prostaglandins (PGE), a group of naturally occurring fatty acids, have been isolated from a number of sources including sheep vesicular glands and human vesicular plasma1,2. The chemical nature and separation of this series of related analogues have been reported in detail2–4. They have profound effects on blood pressure and on smooth muscle contractility, and are also known to interfere with the action of a variety of hormones on adipose tissue5–7. Because of the possibility that the prostaglandins may have other physiological effects of a more general nature, and perhaps serve as regulators of hormone action in certain tissues, the effect of one of them, PGEI, on the response of the toad bladder to vasopressin, theophylline and adenosine 3′,5′-monophosphate (cyclic-AMP) was examined. All three of the latter compounds, when added to the serosal surface of the isolated bladder of Bufo marinus, increase the osmotic flow of water across this membrane. It has been suggested that vasopressin exerts its permeability effects here and in the kidney by increasing the concentration of adenosine 3′,5′-monophosphate within the tissue8. The cyclic-AMP is presumed to be the intracellular mediator of the vasopressin effect. Theophylline mimics vasopressin in toad bladder, since it inhibits the degradation of cyclic-AMP to inactive 5′-adenosine monophosphate9.