Study of the effects of neurotransmitters on the hypothalamus-pituitary-testis function in in vitro cell suspension system

Vermes, I.; Várszegi, M.; Tóth, Emese; Telegdy, Gyula

doi:10.3109/01485017908985059

Cited by 4 publications

(1 citation statement)

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“…High doses cause testicular atrophy, presumably by virtue of the resulting ischaemia (Boccabella, Salgado and Alger, 1962;O'Steen, 1963;Kormano, Karhunen and Kahanpaa, 1968), but effects, particularly on the endocrine function of the testis, can also be demonstrated with implants of much smaller amounts (Kinson and Liu, 1973;Liu and Kinson, 1973;Niaraki, Subramanian and Moghissi, 1982). Direct effects on the Leydig cells in vitro have also been reported (Ellis, 1972;Vermes et aL, 1979;Kalla, 1979). It was necessary to add a 5HT inhibitor to the blood used to perfuse ram and goat testes for adequate perfusion rates to be achieved (Linzell and Setchell, 1969) and injections of 5HT into the testicular vein reduce blood flow through the testis, suggesting that the site of action of the 5HT may be in the pampiniform plexus, not in the testis itself (Free and Nguyen Due Kien, 1973).…”

Section: Discussionmentioning

confidence: 99%

The Increase in Testicular Vascular Permeabilty Induced by Human Chorionic Gonadotrophin Involves 5‐hydroxytryptamine and Possibly Oestrogens, but Not Testosterone, Prostaglandins, Histamine or Bradykinin

Sowerbutts

Jarvis

Setchell

1986

Aust J Exp Biol Med

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Summary. Possible intermediates in the response of the rat testicular vasculature to human chorionic gonadotrophin (hCG) have been investigated. Ketanserin, an antagonist of 5-hydroxytryptamine, significantly reduced the increase in 1-h albumin space seen 20 h after hCG, as did one aromatase inhibitor (l,4,6-androstatriene-3, 17-dione), but the effect of another (testolactone) did not reach significance. Aminoglutethimide, which inhibits overall steroid synthesis as well as aromatase, reduced the albumin space in both control and hCG-injected rats but the hCG response, as judged by the ratio between treated and control rats, was unaffected. Inhibitors of overall steroid synthesis (WIN 32,729), prostaglandin synthesis (meclofenamic acid or indomethacin) and angiotensin converting enzyme (captopril) and blockers of HI and H2 histamine receptors (mepyramine, cimetidine or ranitidine) were without effect. The time course of the vascular response to hCG is quite different from the response in testosterone secretion by the testis. Considerable numbers of mast cells were found in the vicinity of the testicular artery in the testicular capsule, and these may be a source of 5-hydroxytryptamine. INTRODUCTIONRecently, it was shown that a single injection of hCG into a male rat produced a striking increase in the permeability of the testicular blood vessels to albumin, in the amount of extracellular fluid in the testis and in testicular lymph flow (Setchell and Sharpe, 1981). For several reasons, it was suggested in that paper that hCG was not acting directly on the blood vessels, but rather that the effect was due to some testicular product whose formation was increased by hCG. Two obvious possibilities were oestrogens and prostaglandins. The present paper reports the results of a series of experiments designed to establish whether these or other possible vasoactive substances are involved in the hCG effect. While this paper was being written, the results of an independent study were published (Veijola and Rajaniemi, 1985), confirming our observations on the lack of effect of indomethacin and aminoglutethimide.

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