Adrenergic stimulation induces contraction of hypertrophied prostatic tissue via the alpha 1 adrenoceptor, and the results of pharmacological studies suggested the existence of adrenoceptor subtypes. Recently three subtypes (alpha 1a, alpha 1b, and alpha 1d) were cloned. Using probes for these subtypes, we demonstrated their expression in the tissues of ten cases of benign prostatic hypertrophy, using in situ hybridization. To determine the ratio between these subtypes, an RNase protection assay was also performed in three cases. Expression of the alpha 1a and alpha 1d adrenoceptors was diffuse in the smooth muscles of the interstitium, but was absent in glandular epithelial cells. On the contrary, the alpha 1b adrenoceptor was hardly detectable. The RNase protection assay confirmed the absence of the alpha 1b adrenoceptor, the ratio of alpha 1a and alpha 1d being 4:1. These results supported the idea that the differences in prostatic contractile response to several adrenergic drugs are based on the affinities of these drugs for the different subtypes.
Epidermal growth factor (EGF), in addition to its effects on cell growth, has a suppressive effect on gastric hydrochloride secretion. We recently demonstrated EGF‐receptor (EGF‐R)‐like immunoreactlvity on human gastric parietal cells by light microscopy. To reveal further the localization of this reaction an immuno‐electron microscopical study was performed. 5281gG, an anti‐EGF‐R murine monoclonal antibody and a polyclonal anti‐EGF antibody were employed for immunostaining using the avidin‐biotin method. Positive reaction against 5281gG was shown mostly on the outer membrane of parietal cells, except in the apical portion. No reaction was observed on most of the intracytoplasmic membranes including intracellular canaliculi, endoplasmic reticulum and other membranous components. In the basillar portion, the 5281 gG‐positive parietal cell membrane formed labyrinthine interdigitations. No reaction against anti‐EGF was demonstrated in any of the gastric mucosal cells, although a reaction was clearly shown on salivary gland cells. These findings suggest a blood‐mediated direct action of EGF on parietal cells.
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