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THE INCREASE IN TESTICULAR VASCULAR PERMEABILTY INDUCED BY HUMAN CHORIONIC GONADOTROPHIN INVOLVES 5‐HYDROXYTRYPTAMINE AND POSSIBLY OESTROGENS, BUT NOT TESTOSTERONE, PROSTAGLANDINS, HISTAMINE OR BRADYKININ
Author(s) -
Sowerbutts SF,
Jarvis LG,
Setchell BP
Publication year - 1986
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1986.15
Subject(s) - endocrinology , medicine , histamine , aromatase , aminoglutethimide , chemistry , biology , cancer , breast cancer
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 (1,4,6‐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 H1 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.