Search

Your search keyword '"Lewis, Stephen J"' showing total 47 results
Start Over Author "Lewis, Stephen J" Publisher wiley
47 results on '"Lewis, Stephen J"'

15. Localization and induced release of potentially therapeutic components of the rat submandibular salivary gland

Author

Watanabe, Michiko, primary, Lin, Amy, additional, Doughman, Yong Qiu, additional, Al‐Adhami, Omar, additional, Getsy, Paulina, additional, Coffee, Gregory, additional, Giarola, Alessandra S, additional, Sridhar, Arun, additional, Siegel, Ruth, additional, Liu, Yehe, additional, Jenkins, Michael W, additional, Befus, Dean, additional, and Lewis, Stephen J, additional

Published
2019
Full Text
View/download PDF

46. L-beta,beta-dimethylcysteine attenuates the haemodynamic responses elicited by systemic injections of peroxynitrite in anaesthetized rats.

Author

Graves JE, Kooy NW, and Lewis SJ

Subjects
Anesthesia, Animals, Blood Pressure, Cromakalim pharmacology, Dose-Response Relationship, Drug, Injections, Intravenous, Male, Peroxynitrous Acid administration & dosage, Rats, Rats, Sprague-Dawley, Splanchnic Circulation, Vascular Resistance, Vasodilator Agents administration & dosage, Free Radical Scavengers pharmacology, Muscle, Skeletal blood supply, Penicillamine pharmacology, Peroxynitrous Acid pharmacology, Vasodilation drug effects, Vasodilator Agents pharmacology
Abstract

1 There is direct chemical evidence that L-beta,beta-dimethylcysteine (L-penicillamine (L-PEN)) is a scavenger of peroxynitrite. The aim of this study was to determine whether L-PEN attenuates the haemodynamic responses elicited by peroxynitrite in pentobarbital-anaesthetized rats. 2 Peroxynitrite (1-20 micromol kg(-1), i.v.) elicited dose-dependent reductions in mean arterial blood pressure (MAP) and mesenteric and hindquarter vascular resistances. 3 L-PEN (2 mmol kg(-1), i.v.) elicited relatively minor but significant increases in MAP and vascular resistances. The initial reductions in MAP and vascular resistances elicited by peroxynitrite were not diminished after administration of L-PEN whereas they were much shorter in duration. As such, the total reductions in MAP and vascular resistances were markedly reduced by L-PEN. 4 The finding that L-PEN (2 mmol kg(-1), i.v.) did not affect the hypotensive or vasodilator responses elicited of the ATP-dependent potassium-channel agonist, cromakalim (3-18 microg kg(-1), i.v.), suggests that this dose of L-PEN is not a nonselective inhibitor of vasodilation. 5 These findings suggest that L-PEN may effectively scavenge peroxynitrite in vivo and/or interfere with the mechanisms by which peroxynitrite elicits its vasodilator responses.

Published
2006
Full Text
View/download PDF

47. Downregulation of propranolol-sensitive beta-adrenoceptor signaling after inhibition of nitric oxide synthesis.

Author

Whalen EJ, Bates JN, Johnson AK, and Lewis SJ

Subjects
Adrenergic beta-Agonists pharmacology, Animals, Blood Pressure drug effects, Down-Regulation drug effects, Enzyme Inhibitors pharmacology, Heart Rate drug effects, Hemodynamics drug effects, Hindlimb blood supply, In Vitro Techniques, Isoproterenol antagonists & inhibitors, Isoproterenol pharmacology, Male, NG-Nitroarginine Methyl Ester pharmacology, Nitric Oxide Synthase metabolism, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, alpha-2 drug effects, Receptors, Adrenergic, beta-1 drug effects, Regional Blood Flow drug effects, Splanchnic Circulation drug effects, Vascular Resistance drug effects, Adrenergic beta-Antagonists pharmacology, Nitric Oxide biosynthesis, Nitric Oxide Synthase antagonists & inhibitors, Propranolol pharmacology, Signal Transduction drug effects
Abstract

The beta-adrenoceptor agonist, isoprenaline, elicits vasodilation and tachycardia in anesthetized rats via activation of propranolol-sensitive beta1- and beta2-adrenoceptors and also by propranolol-insensitive beta1- and beta3-adrenoceptors. The aim of this study was to determine whether the relative contribution of propranolol-sensitive and -insensitive beta-adrenoceptors to the changes in heart rate (HR) and vascular resistances elicited by isoprenaline is altered after blockade of nitric oxide (NO) synthase, in pentobarbital-anesthetized rats. The hemodynamic responses elicited by isoprenaline (0.1 and 0.5 microg kg(-1), i.v.) were determined before and after injection of saline or the NO synthase inhibitor, N(G)-nitro-L-arginine methylester (L-NAME, 50 micromol kg(-1), i.v.), and again after injection of the beta1- and beta2-adrenoceptor antagonist, propranolol (1 mg kg(-1), i.v.). The responses elicited by the above doses of isoprenaline were also determined before and during infusion of the alpha1-adrenoceptor agonist, phenylephrine (3 microg kg(-1) min(-1), i.v.), and again 15-20 min after injection of propranolol (1.0 mg kg(-1), i.v.). Both doses of isoprenaline elicited tachycardia and reductions in vascular resistances. Propranolol eliminated the responses elicited by the lower dose of isoprenaline and substantially diminished the responses elicited by the higher dose of the beta1-, beta2- and beta3-adrenoceptor agonist. The maximal vasodilator responses elicited by both doses of isoprenaline were not diminished whereas the maximal increases in HR were higher after injection of L-NAME. The ability of propranolol to diminish the hemodynamic actions of isoprenaline was substantially diminished in L-NAME-treated rats, whereas propranolol retained its potency in rats that received an equi-pressor infusion of the alpha1-adrenoceptor agonist, phenylephrine. The finding that the maximal vasodilator responses elicited by isoprenaline were not diminished by L-NAME suggests that the vasodilation elicited by this drug was due to direct activation of beta-adrenoceptors on vascular smooth muscle and that the full compliment of isoprenaline-sensitive receptors was not changed after inhibition of NO synthesis. However, these results suggest that the activities of propranolol-sensitive beta-adrenoceptors are downregulated, whereas propranolol-insensitive beta-adrenoceptors are upregulated upon the loss of exposure to endothelial nitrosyl factors.

Published
2006
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results