Drugs online research references
J Ocul Pharmacol. 1985 Fall;1(3):245-54.
Effects of antiglaucoma drugs on [32P]orthophosphate incorporation into phospholipids of cat iris and ciliary process.
Yorio T, DeLoach G, Satumtira N.
Department of Pharmacology, Texas College of Osteopathic Medicine, Fort Worth.
The effects of antiglaucoma drugs on [32P]-orthophosphate incorporation into phospholipids of iris and ciliary process were investigated. Both iris and ciliary process rapidly incorporated 32Pi into the major phospholipids, with the acidic phosphoinositides demonstrating a greater labelling than phosphatidylcholine, indicating a greater turnover. The muscarinic agonists, carbachol and pilocarpine, stimulated 32Pi-labelling of phosphatidylinositol (PI) and phosphatidic acid (PA) in both iris and ciliary process. These effects were blocked by atropine, suggesting that the response was mediated through muscarinic receptors. The beta blocking ocular hypotensive drugs, propranolol, timolol and atenolol, produced varying effects on 32P incorporation into phospholipids of iris and ciliary process. Propranolol stimulated 32Pi-labelling into phosphatidylinositol 4', 5' bisphosphate (PIP2), phosphatidylinositol 4' phosphate (PIP), PI and PA. Timolol decreased 32Pi-incorporation into PIP2 and PI, whereas atenolol, a selective beta 1 antagonist, had no significant effect on 32Pi-labelling of phospholipids. The above findings on propranolol agree with previous observations which demonstrated that propranolol redirects glycerolipid metabolism through multiple effects on the enzymes in phospholipid biosynthesis, particularly in stimulating phosphatidylinositol kinases. The results with timolol suggest that this drug may decrease phosphoinositide hydrolysis. The effects of these ocular hypotensive, non-selective beta blocking drugs on phospholipid turnover may ultimately limit the accumulation of breakdown products which could serve as cellular messengers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3880077&dopt=Abstract
Cardiology. 1981;68 Suppl 2:190-4.
Evaluation of effect of drugs on the exercise ECG.
Sanchez-Cascos A.
The result of an exercise ECG can be represented on an XY chart by four monovariate (normal) distributions: heart rate (divided by X axis); blood pressure (divided by Y axis); Working time deficit (-X axis); ST depression (-Y axis); and two bivariate (elliptic) distributions: double product (divided by X divided by Y quadrant); ST X time-deficit index (-X -Y quadrant). Charts for 100 normal men, 100 normal women, 100 coronary men, and 100 coronary women were first of all built up. Charts of 100 patients under propanolol, 33 under atenolol, 47 under nidefipine, 13 under verapamil, and 44 under isosorbide dinitrate were then compared with those from coronary men. Beta blockers produced a shift in all six parameters; nifedipine modified blood pressure, double product, ST and time deficit; verapamil only changed blood pressure and time deficit; isosorbide changed ST, time deficit and the ST X time-deficit index.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7317897&dopt=Abstract
Eur J Pharmacol. 1994 Dec 12;271(1):1-8.
Effects of antiischemic drugs on veratridine-induced hypercontracture in rat cardiac myocytes.
Hashizume H, Akiyama K, Abiko Y.
Department of Pharmacology, Asahikawa Medical College, Japan.
The effects of different groups of substances (beta-adrenoceptor antagonists, Ca2+ channel blockers and vasodilators) which are known to have antiischemic properties were studied on veratridine-induced hypercontracture. Veratridine increases Na+ influx by slowing the inactivation process of the Na+ channel, thereby inducing a continuously increased Na+ entry in depolarized cells. Veratridine (6.3 x 10(-6) M) produced a change in cell shape from rod-shape to round, resulting from hypercontracture of cells. Before treatment with veratridine the proportion of rod-shaped cells was 70% and fell to 0% 5 min after the treatment with veratridine. dl-Propranolol, d-propranolol, l-penbutolol, d-penbutolol, nisoldipine, and dilazep all inhibited veratridine-induced hypercontracture dose dependently. In contrast, acebutolol, atenolol, timolol, nifedipine, diltiazem, and nitroglycerin did not inhibit the rounding of cells. Concomitantly with the rounding of cells, the [Ca2+]i was increased by veratridine. dl-Propranolol, d-propranolol and dilazep prevented the increase of [Ca2+]i induced by veratridine, whereas timolol and nitroglycerin did not. These results show that dl-propranolol, d-propranolol, l-penbutolol, d-penbutolol, nisoldipine, and dilazep possess Na+ channel blocking actions on the veratridine-modified Na+ channel, thereby preventing excessive Na+ influx and secondary Ca2+ overload.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7698192&dopt=Abstract
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