By Peter Ramwell
There is far proof to indicate that prostaglandins can have a physiological position to play within the keep an eye on of thyroid gland metabolism, even supposing the appropriate nature of this function continues to be outlined. Prostaglandins were present in general thyroid tissue, and there's facts of elevated degrees in a few, yet no longer all, instances of medullary carcinoma of the thyroid. which could account for the linked diarrhea. Exogenous prostaglandins, like TSH, bind to thyroid plasma mem branes, stimulate the adenylate cyclase-cyclic AMP method, thyroid hormone secretion, iodide organification, colloid droplet formation, glucose oxidation, and 32p incorporation into phospholipids. Prosta glandins of the E sequence are the main powerful, even supposing their maximal results are quite often under the maximal results of TSH. The interrelationships current among TSH and prostaglandins were the topic of in depth research, yet as but not anyone uni fying suggestion has emerged. TSH and prostaglandins were proven to occupy assorted receptors at the thyroid plasma membrane. Al even though TSH can bring up intracellular prostaglandin degrees, most likely due to elevated synthesis, prostaglandins don't seem to be crucial intermediates in TSH motion on adenylate cyclase. The pos sibility that prostaglandins are a part of a detrimental suggestions procedure con trolling TSH motion is, as but, a tentative speculation, and extra paintings can be required to resolve the interrelationships among those sub stances that now seem to be way more complicated than has been envisaged therefore far.
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Extra resources for The Prostaglandins: Volume 2
1971). As could be predicted, in endotoxin shock there are increased levels of prostaglandins in venous blood: this has been shown by Collier et al. (1973), who measured prostaglandin-like activity in renal venous blood, and by Kessler et al. (1973), who found both prostaglandin E and prostaglandin A-like material in "plasma" from an unspecified vessel of dogs. Collier et al. (1973) showed that the output of prostaglandin-like material was abolished by indomethacin and, at the same time, the hypotension due to the endotoxin was reversed.
1971, Studies on prostaglandin antagonists, Brit. J. Pharmacol 42: 584. , Friedman, C. , and Vane, J. ) 216: 873. , Stamford, I. , and Unger, W. , 1973, Prostaglandin E2 and gastric acid secretion in man, J. Physiol. ) 229: 349. , von Euler, U. , 1959, Observations on the effects of infusions of prostaglandin E in man, Acta Physiol. Scand, 45: 145. , 1969, Effect of prostaglandin El on forearm blood flow, Scand. J. Clin. Lab. Invest. 3: 347. , 1972, Effect of prostaglandin biosynthesis of collagen, Nature New BioI.
E. Control of Release of the Sympathetic Mediator From his work on cat spleen, Hedqvist (1969a, b, 1970) proposed that prostaglandin release from splenic smooth muscle acts as a negative feed-back mechanism which attenuates the effects of nerve stimulation. This hypothesis, and its extension to other sympathetically innervated tissues, has been extensively reviewed in the first volume of this series (Hedqvist, 1973). Hedqvist and his colleagues used 5,8,1l,14-eicosatetraynoic acid (ETA) to inhibit prostaglandin biosynthesis in rabbit heart, cat spleen, and guinea pig vas deferens.
The Prostaglandins: Volume 2 by Peter Ramwell