Drugs online research references
Naunyn Schmiedebergs Arch Pharmacol. 2001 Feb;363(2):175-81.
Differences in electromechanical coupling between bradykinin and the nonpeptide kinin B2 receptor agonist, FR 190997, in the circular muscle of guinea-pig colon.
Santicioli P, Catalioto RM, Meini S, Maggi CA.
Pharmacology Department, Menarini Ricerche SpA, Florence, Italy.
We have compared the effect of bradykinin (BK) and the nonpeptide kinin B2 receptor agonist, FR 190997, in producing changes in membrane potential and tension in the circular muscle of guinea-pig colon by the sucrose gap technique. In the presence of atropine (1 microM), S-ketoprofen (3 microM) and apamin (0.1 microM), BK (1 microM for 20 s) induced a transient depolarization of the membrane with superimposed action potentials (spikes) and transient contraction. Nifedipine (1 microM) eliminated the spikes and markedly inhibited the BK-induced contractions. FR 190997 (3-10 microM for 20 s) induced a slowly developing sustained small depolarization associated with a slowly developing and sustained contraction but, contrary to BK, FR 190997 was unable to trigger spikes. Nifedipine had no effect on depolarization and contraction induced by FR 190997. In the presence of 1 microM nifedipine, the combined application of a blocker of receptor-operated cation channels, SKF 96365 (50 microM for 30 min), and of an inhibitor of sarcoplasmic reticulum calcium pump, cyclopiazonic acid (CPA 10 microM for 30 min), reduced the BK-induced depolarization and contraction by about 45%-60%. The same treatment induced about 40% reduction of the sustained contraction induced by FR 190997, whereas the concomitant depolarization was not significantly affected. The tyrosine kinase inhibitor genistein (40 microM for 20 min) had no effect on the BK- and FR 190997-induced depolarization and contraction in the presence of nifedipine. In radioligand binding experiments performed in membranes of colonic smooth muscle cells, both agonists displaced the [3H]BK specific binding with a pIC50 of 9.6 and 8.5 for BK and FR 190997, respectively. These findings indicate a substantial qualitative difference in mechanisms of excitation contraction coupling activated by BK and FR 190997 via B2 receptors in guinea-pig colon.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11218070&dopt=Abstract
Am J Physiol. 1998 Jun;274(6 Pt 2):H2018-24.
Oxygen induces electromechanical coupling in arteriolar smooth muscle cells: a role for L-type Ca2+ channels.
Welsh DG, Jackson WF, Segal SS.
The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519, USA.
We tested whether O2-induced vasomotor responses of arterioles correspond to changes in membrane potential (Em) of cells in the arteriolar wall. The cheek pouches of anesthetized male hamsters were prepared for intravital microscopy and intracellular recording. Microelectrodes containing Lucifer yellow dye were used to label smooth muscle cells (SMC) or endothelial cells (EC) during arteriolar responses to O2. During low- PO2 superfusion (approximately 20 Torr; arteriolar diameter 55 +/- 2 micron), Em of SMC and EC averaged -37 and -36 mV, respectively. High-PO2 superfusion ( approximately 150 Torr) depolarized SMC (to -15 +/- 1 mV) with vasoconstriction (to 24 +/- 2 micron) and diameter cycled with Em of SMC during vasomotion. In contrast, the Em of EC did not change with PO2 nor during vasomotion, yet Em depolarized by 21 +/- 2 mV when the extracellular K+ concentration ([K+]o) was raised to 55 mM. Superfusion with diltiazem (10 microM) or nifedipine (1 microM) abolished vasomotor and electrical responses to PO2 in SMC but did not eliminate depolarizations to elevated [K+]o. We conclude that, under physiological conditions, electrical and mechanical responses of arteriolar SMC to changes in PO2 are mediated through L-type Ca2+ channels without corresponding electrical activity in EC.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9841528&dopt=Abstract
Gen Pharmacol. 1988;19(6):759-66.
Comparative electrophysiological response of young and old rat myocardium to pharmacological agents.
Jullien T, Verdetti J.
Laboratoire de Physiologie Cellulaire Animale, Saint Martin d'Heres, France.
1. Age-related changes in electrophysiological and pharmacological properties of rat ventricular cells have been investigated. 2. As compared to adults, transmembrane action potential (TAP) of aged rat myocardium exhibits a prolonged phase of repolarization. 3. For both young and aged groups tetrodotoxin reduces TAP duration. 4. Nifedipine and isoproterenol induce more pronounced modifications of the TAP in aged subjects. 5. Amiloride and tetraethylammonium ions prolong, for both groups, phase 2 of repolarization. This effect is more marked in the aged group. 6. Our results suggest that the prolonged TAP in aged myocardium could result from an age-related increase in calcium current.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3229619&dopt=Abstract
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