Drugs online research references
Pharm Res. 1997 Jun;14(6):767-73.
Influence of morphometric factors on quantitation of paracellular permeability of intestinal epithelia in vitro.
Collett A, Walker D, Sims E, He YL, Speers P, Ayrton J, Rowland M, Warhurst G.
Department of Medicine (University of Manchester School of Medicine), Hope Hospital, Salford, UK.
PURPOSE: The relative contribution of the small and large intestine to paracellular absorption is a subject of some controversy. Direct comparison of paracellular permeability in different epithelia is complicated by variations in junctional density and/or the absorptive surface area. METHODS: This study used a combination of morphometric analyses and in vitro absorption studies to define permeability characteristics in relation to the amount of paracellular pathway present in rat ileum, colon and the model epithelium, Caco-2. RESULTS: Mucosal to serosal amplification was higher in ileum (3.9) than colon (1.9) or Caco-2 (1). Tight junctional density (lp) of ileal crypts was approximately 3 fold greater (91 m/cm2) than that measured in ileal villi, colonic surface and crypt cells or Caco-2 monolayers (34-37 m/cm2). However, when the relative contributions of the crypts and villi was taken into account there was no significant difference in the mean lp per mucosal area for the three epithelia studied. Using these data to correct for morphometric differences the permeabilities of a range of small hydrophilic molecules (atenolol, D-PheAsp and PEG oligomers MW 282-634) was measured. Permeability of rat ileum and colon were virtually identical for all compounds studied. In contrast, Caco-2 monolayers showed a significantly lower permeability than intestinal tissues with the difference increasing markedly with molecular size. CONCLUSIONS: These studies suggest the importance of accounting for morphological variation when comparing the permeability characteristics of different epithelial systems.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9210195&dopt=Abstract
J Auton Pharmacol. 1985 Dec;5(4):307-16.
Influence of urapidil on alpha- and beta-adrenoreceptors in pithed rats.
Sanders KH, Kilian U, Kolassa N, Schoetensack W.
The interaction of urapidil with pre- and postsynaptic alpha-adrenoreceptors and with postsynaptic beta-adrenoreceptors was studied in pithed normotensive rats and compared to the effects of clonidine, prazosin, and atenolol. I.v. injection of urapidil did not substantially change blood pressure, while clonidine raised blood pressure. Urapidil dose-dependently antagonized the pressor effects of the alpha 1-agonist L-phenylephrine (pDR2 6.8) and of the alpha 2-agonist azepexole (pDR2 5.2). Compared to urapidil, prazosin was a more potent antagonist of phenylephrine at postsynaptic vascular alpha 1-adrenoreceptors (pDR2 8.7) and of azepexole at alpha 2-adrenoreceptors (pDR2 5.6). Urapidil inhibited the tachycardia produced by discontinuous or continuous electrical stimulation of the thoracic spinal outflows (ID50 4.8 and 27.2 mumol/kg, respectively). In contrast to the inhibitory action of clonidine (ID50 0.039 and 0.023 mumol/kg, respectively), the inhibition by urapidil was not reversed by the selective alpha 2-antagonist rauwolscine (10 mumol/kg). Prazosin did not change stimulation-evoked tachycardia but atenolol caused pronounced inhibition (ID50 0.158 mumol/kg, discontinuous stimulation). Urapidil dose-dependently antagonized the tachycardic effect of isoprenaline at beta 1-adrenoreceptors (pDR2 5.1) but also exhibited intrinsic activity by increasing basal heart rate (maximum effect of urapidil was 30% of that of isoprenaline). Urapidil did not change the vasodilatory beta 2-adrenoreceptor-mediated effect of isoprenaline. The results suggest that urapidil is an antagonist at postsynaptic vascular alpha 1- and alpha 2-adrenoreceptors, with a greater potency against alpha 1-adrenoreceptors. An agonistic interaction of urapidil with presynaptic alpha 2-adrenoreceptors could not be demonstrated in pithed rats. Instead, the inhibition by urapidil of stimulation-evoked tachycardia could be accounted for by its beta 1-adrenoreceptor antagonistic effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3005330&dopt=Abstract
J Pharmacol Exp Ther. 1988 Sep;246(3):935-40.
Sympathetic denervation fails to produce beta adrenergic supersensitivity in adult rat parotid gland.
Melvin JE, He XJ, Baum BJ.
Clinical Investigations and Patient Care Branch, National Institute of Dental Research, Bethesda, Maryland.
Parotid acinar cells, prepared from pharmacologically sympathectomized adult rats (reserpine, 0.1 mg/kg/day for 1 week), display decreased responsiveness to beta adrenergic stimulation in vitro compared to cells from control and surgically sympathectomized rats. Both methods of denervation increase amylase content (amylase activity per microgram of DNA). Percent release of amylase activity and percent release of CCl3COOH-precipitable [14C]leucine were used as indicators of protein secretion. Exposure of cells from pharmacologically sympathectomized rats to the beta adrenergic agonist, isoproterenol, resulted in a marked reduction in receptor-coupled secretion (67% and 75% relative to controls, respectively). 8-Bromo-cyclic AMP, like isoproterenol, was unable to surmount this reserpine-induced inhibition of stimulated secretion, suggesting that an alteration in receptor-adenylate cyclase coupling is not responsible for the observed secretion defect. Cells prepared from surgically sympathectomized rats displayed modest decreases in stimulated secretion when the same secretory markers were monitored (30% and 25% relative to controls, respectively). The number of beta adrenoreceptors [( 3H]dihydroalprenolol binding sites) increased (35%), with no change in binding affinity, in membrane preparations from reserpine-treated rats. Thus, the observed inhibition of beta adrenergic agonist-induced secretion is not likely the result of alterations in beta adrenergic receptor characteristics. Short-term (1 week) surgical denervation had no effect on the number of beta adrenergic receptor sites; however, an increase in ligand binding affinity was noted. The decrease in the apparent Kd (30%) was not the result of a shift in receptor subtype as determined by competition studies with specific beta-1 (atenolol) and beta-2 (ICI 118,551) receptor antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2843635&dopt=Abstract
online pharmacies ||
Hair Million herbal formula for hair loss and hair growth ||
Amoxicillin ||
Tramadol ||
Paxil ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Zithromax ||
online pharmacy ||
Antibiotics and prescription medications online literature ||
Antibiotics