Drugs online research references
Int J Sports Med. 1982 Feb;3(1):29-32.
Running performance as a function of the dose-response relationship to beta-adrenoceptor blockade.
Kaiser P.
There is a discrepancy between the effect of beta-blockade on exercise heart rate and the effect on exercise capacity. Thus, it was of interest to study the dose-response relationship between an unselective (propranolol) and a beta 1-selective (atenolol) blocker and endurance exercise performance. Nine habitually active males ran their own jogging route 10 times and the distances of the routes ranged between 4000 and 10000 m. Placebo (twice), 25, 50, 75, and 100 mg of atenolol and 40, 80, 120, and 160 mg of propranolol were administered orally with a double-blind, crossover procedure. After each experiment, running time and rate of perceived exertion (RPE) were registered. Small drug doses markedly affected exercise heart rates yet such doses minimally affected running performance when on the beta 1 selective blocker. With 160 mg propranolol, a greater exercise impairment occurred than with 100 mg atenolol (P less than 0.05). RPE data suggested that drug treatment induced an increased subjective feeling of fatigue in addition to the impaired performance, and these changes were positively related (r = 0.66, P less than 0.05). Impairment of exercise performance during acute beta-blockade is evidently not related solely to the effect on heart rate. The nature of other drug effects is presently unclear although there is evidence that the metabolic profile of the muscle is implicated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6121762&dopt=Abstract
Biochem Biophys Res Commun. 1995 Feb 6;207(1):13-9.
Beta-adrenergic receptor function in cultured AT-1 cardiomyocytes.
Drvota V, Wei H, Haggblad J, Carlsson B, Sylven C.
Karolinska Institute Dept. of Medicine, Huddinge University Hospital, Sweden.
AT-1 cells are highly differentiated, contracting cardiomyocytes derived from atrial tumours in transgenic mice. The aim of this study was to characterize beta-adrenergic receptor function and associated intracellular calcium regulation in AT-1 cells. Equilibrium binding experiments with [3H]-CGP-12177 showed a Kd = 0.30 +/- 0.08nM and a Bmax = 2.25 +/- 0.47 fmol/10(5) cells. Competition binding experiments with CGP-20712A showed presence of predominantly beta 1-adrenoreceptors. S-(-)propranolol, atenolol and R-(+)propranolol showed a competitive inhibition of binding with successively lower affinity. Isoproterenol, 2 microM, for 48 hours down-regulated the number (p < 0.05) of beta-adrenergic receptors/cell by about 50%; 10 microM for one hour increased the cAMP concentration (p < 0.05) by about 100%. Cytosolic [Ca2+] was measured flourimetrically in spontaneously and synchronously beating AT-1 cells. The resting cytosolic concentration was 94 +/- 10 nM. The observed sinusoidal Ca2+ oscillation frequency increased after addition of 10 microM isoproterenol (p < 0.02). This effect was antagonized by 10 microM alprenolol (p < 0.01). In conclusion, AT-1 cells have functional beta-adrenoreceptor signalling pathways and constitute an important tool in cardiac biology.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7857255&dopt=Abstract
J Am Coll Cardiol. 1992 Oct;20(4):864-8.
Preserved ventricular pump function after a marked reduction of left ventricular mass.
Ketelhut R, Franz IW, Behr U, Toennesmann U, Messerli FH.
Klinik Wehrawald, Todtmoos, Germany.
OBJECTIVES. This study was designed to evaluate the long-term effects of combination therapy with an angiotensin-converting enzyme inhibitor and a beta-adrenergic blocking agent on the relation between the decrease in arterial pressure at rest and during exercise and the decrease in left ventricular mass. BACKGROUND. A variety of antihypertensive drugs including angiotensin-converting enzyme inhibitors and beta-blockers have been shown to reduce ventricular hypertrophy, although little is known about combination therapy and the time course of such a reduction. METHODS. Twenty-one patients with previously untreated essential hypertension were treated with a low dose combination of 50 mg of atenolol and 10 mg of enalapril once daily for 39 months. Cardiovascular findings were assessed by two-dimensionally guided M-mode echocardiography in the pretreatment phase and after 6 and 39 months of combination therapy. RESULTS. Combination therapy reduced arterial pressure at rest from 161/108 to 130/86 mm Hg (p less than 0.001) and exercise arterial pressure at 100 W from 192/112 to 167/95 mm Hg (p less than 0.001). After 6 months of treatment, significant decreases in interventricular septal thickness (9%, p less than 0.001), posterior wall thickness (9%, p less than 0.001) and left ventricular mass index (16%, p less than 0.001) were demonstrated on the echocardiogram. After 39 months of therapy, reductions in these values were 28% (p less than 0.001), 29% (p less than 0.001) and 40% (p less than 0.001), respectively. CONCLUSIONS. Long-term treatment with combination therapy of atenolol and enalapril produced significant reductions in arterial pressure at rest and during exercise accompanied by a marked reduction of left ventricular mass. However, whereas arterial pressure decreased immediately and remained unchanged, left ventricular mass decreased more gradually and continued to decrease throughout the treatment period of greater than 3 years. Despite this marked reduction in left ventricular mass, left ventricular pump function was well preserved during rest and exercise.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1356116&dopt=Abstract
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