Publications by authors named "R Wahawisan"

Ileal villus and crypt cells exhibit morphological and biochemical differences which may be responsible for functional differences in relation to ion transport. Cholinergic agonists act directly on epithelial cell muscarinic receptors, but it is not known if these receptors exist on both villus and crypt cells. Using the potent muscarinic antagonist [3H](-)-quinuclidinyl benzilate (QNB) we have determined the distribution of muscarinic receptors in rat ileal villus and crypt cells.

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Isolated, intact epithelial cells from rat ileum synthesized a variety of radiolabeled compounds when 32Pi was added to the incubation medium. One of these, referred to as P-0.7 because of its Rf value in the thin layer chromatography system used to separate phosphorylated compounds, was found in the extracellular medium but not in extracts of cells.

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Muscarinic receptors on epithelial cells mediate intestinal secretion, while those in intestinal smooth muscle mediate motility. Experiments were carried out to determine whether the muscarinic receptors mediating each of these two functions in intestinal tissue might be associated with differences in the way agonist and antagonist drugs interact with the receptors. The inhibition constant (Kj) values for atropine, pirenzepine, and oxotremorine competition of specifically bound (3H)QNB were determined using membrane preparations from the muscular coat and from epithelial cells of rat jejunum, ileum, and colon.

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Clonidine, an alpha-adrenergic agonist, and apomorphine, a dopaminergic agonist, inhibit water secretion in rat intestine induced by dibutyryl cAMP (DBcAMP) in situ. Apomorphine reversed DBcAMP-induced secretion in ileum and jejunum with ED50 values of 90 and 200 nM, respectively. ED50 values for clonidine's antisecretory effect were 32 and 2 microM in ileum and jejunum, respectively.

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The hormonal regulation of uterine and oviductal cytoplasmic estrogen and progesterone receptors was studied in immature beagles that were untreated, treated with estradiol-17 beta, or treated sequentially with estradiol and progesterone. Estradiol treatment increased the concentration of estrogen receptors in both tissues. Progesterone receptors were not detectable in the reproductive tract of untreated animals, but increased dramatically under the influence of estradiol.

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