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  • Title: In vivo labelling of alpha-adrenoceptor-binding sites and membrane-bound extraneuronal transport sites in the urinary bladder of the rat by 3H-ST-1059 and 3H-phentolamine. An autoradiography study.
    Author: Jonas D, Moritz F, Jenner S, Baumgarten HG.
    Journal: Urol Int; 1980; 35(1):47-62. PubMed ID: 6102423.
    Abstract:
    An attempt was made to trace alpha-adrenoceptor-binding sites in the lower urinary tract tissue of the rat by means of analyzing the distribution of radioactivity in autoradiograms of freeze-dried or glutaraldehyde-fixed tissue following intravenous injection of an alpha-agonist, 3H-ST-1059, or an alpha-antagonist, 3H-phentolamine. Both drugs were rapidly excreted into the urine and reabsorbed by the bladder mucosa. This is evidenced by the presence of high amounts of silver grains superimposed onto the epithelium and bordering the lamina propria structures 10-30 min after intravenous injection of 3H-ST-1059 or 3H-phentolamine in rats not subjected to ligation of their ureters. In rats that underwent ligation of their abdominal ureters prior to intravenous injection of 3H-ST-1059 or 3H-phentolamine, silver grains were preferentially localized over the plasmalemmata of smooth muscle cells and fibroblasts of the detrusor and trigonum of the urinary bladder. Phentolamine and phenoxybenzamine but not propranolol counteracted the labelling of the plasma membranes of smooth muscle cells, fibroblasts and striated muscle fibres of the pelvic floor by low doses of 3H-ST-1059 and 3H-phentolamine, suggesting that both drugs have affinity to alpha-adrenoceptor-agonist and alpha-adrenoceptor-antagonist binding sites. Since phentolamine and phenoxybenzamine as well as hydrocortisone pretreatment also attenuated the accumulation of radiolabel in the perikarya of the three types of cells mentioned, both drugs--at the concentration used--are also substrates for membrane-bound carriers, such as uptake two according to Iversen. A more selective in vivo demonstrationof alpha-agonist-binding and alpha-antagonist-binding sites requires drugs of higher specific activity than available at present.
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