HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hall, W. J. Articles by Martin, J. D. G. Search for Related Content PubMed PubMed Citation Articles by Hall, W. J. Articles by Martin, J. D. G.

1. Prostaglandin E₁ increases sodium transport as measured by short circuit current (SCC) across isolated frog skin whereas calcium, added to the external Ringer fluid, decreases sodium transport. To help establish the site of action of prostaglandin the possible interaction of these two agents on sodium transport has been examined.

2. The effect of a standard dose of prostaglandin (0·5 x 10^-6 M) on the short circuit current was tested on paired skins with either zero or high calcium (22·4 mM) in the external Ringer fluid. In ten experiments the responses to prostaglandin (expressed in µA/cm²) were not significantly affected by external calcium.

3. In another series of experiments the chelating agent, EGTA, was included in calcium-free external Ringer in order to promote greater depletion of skin calcium. The response of these skins to the standard dose of prostaglandin was of the same order of magnitude as that of control skins. The response was not sustained in contrast to that of normal skins and skins in high-calcium fluids.

4. In a further series of experiments the reverse procedure was adopted whereby the response of the skin to low and high doses of calcium in the external Ringer was recorded in control conditions and when the skin had responded fully to twice the standard dose of prostaglandin. In addition, the calcium-sensitive current was calculated for each skin in both circumstances. The latter was unchanged on addition of prostaglandin, and graded doses of calcium caused the same degree of inhibition of the short circuit current.

5. The results show no interaction between external calcium and prostaglandin and also no need for external calcium in prostaglandin stimulation of sodium transport.

6. The findings do not support the concept of chelation by prostaglandin of calcium from critical sites on the skin as the primary mechanism of its action on sodium transport. The results closely parallel those of a similar type of study into the relationship between vasopressin and external calcium on frog skin also.

7. When frog skin has responded fully to either prostaglandin E₁ or vasopressin, it shows no response to the other, although removal of calcium from the external Ringer fluid causes a further increase in short circuit current.

8. Vasopressin causes a further increase in short circuit current in skins treated with prostaglandin F₁. Prostaglandin F₁ may be a weaker agonist on frog skin than either vasopressin or prostaglandin E₁.