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Eksp Klin Farmakol. 1997 May-Jun;60(3):6-8.
[Pharmacological correction of behavioral and memory disorders in rats with vasorenal arterial hypertension given propranolol]

[Article in Russian]

Petrov VI, Grigorev IA, Gorbunov SG.

It was established that propranolol in a daily dose of 2 mg/kg causes disturbance of behavior of rats with arterial hypertension in the open field, deteriorates retention of memory traces in passive avoidance paradigm, and leads to the development of depression in the test for zoosocial interrelation. Administration of nootropic piracetam (200 kg/mg/24 h). as well as the original compounds ACP-94 (20 mg/kg/24 h) and PIR-87--6-0 (50-mg/kg/24 h) facilitates the correction of negative changes in the behavior and memory of hypertensive rats.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9324403&dopt=Abstract




Nippon Yakurigaku Zasshi. 1993 Aug;102(2):141-51.
[Effect of arotinolol on the incomplete tetanic contractions of the cat soleus muscle--relation to its anti-tremorgenic action]

[Article in Japanese]

Hara Y, Sugimoto S, Ono H.

Research Laboratories, Sumitomo Pharmaceuticals Co., Ltd., Osaka, Japan.

The effect of arotinolol on the incomplete tetanic contractions of the cat soleus muscle was studied. Isoproterenol and epinephrine injected intravenously decreased the tension and degree of fusion of incomplete tetanic contractions of the soleus muscle in anesthetized cats. Intravenous arotinolol (> 3 micrograms/kg), propranolol (> 30 micrograms/kg) and pindolol (> 3 micrograms/kg) blocked the effects of isoproterenol and epinephrine, but atenolol (-300 micrograms/kg), prazosin (0.1-10 micrograms/kg) and phentolamine (10, 30 micrograms/kg) did not block them. These results indicate that the receptors involved can be classified as of the beta 2-type. It is proposed that arotinolol may inhibit beta 2-adrenoceptors in the extrafusal muscle fibers of slow muscle, and thereby reduces the amplitude of tremor by changing the incomplete tetanic contractions of the muscle to the complete ones.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7690340&dopt=Abstract




Am Rev Respir Dis. 1993 Oct;148(4 Pt 1):902-8.
Effect of thiazide diuretics against neurally mediated contraction of guinea pig airways. Contribution of carbonic anhydrase.

Sun J, Elwood W, Barnes PJ, Chung KF.

Department of Thoracic Medicine, National Heart and Lung Institute, London, England.

The effect of thiazide diuretics on neurally and agonist-induced contractile responses of guinea pig airways in vitro were investigated. Tracheal or bronchial strips were suspended in organ baths and isometric tension recorded. Chlorothiazide (CTZ, 10(-4) to 3 x 10(-3) M), hydrochlorothiazide (HCTZ, 10(-3) M), and dichlorphenamide (DCPM, 10(-3) M) significantly potentiated contraction of tracheal strips induced by electrical field stimulation (EFS). They also increased acetylcholine (ACh)- but not carbachol-induced tracheal contraction. In the presence of atropine and propranolol, on the other hand, CTZ and DCPM but not HCTZ significantly inhibited EFS-induced contraction in bronchial strips. We determined whether carbonic anhydrase inhibition could mimic the effects of CTZ and DCPM. Acetazolamide (ATZ), an inhibitor of carbonic anhydrase, had no effect on either EFS- or ACh-induced contraction in tracheal strips but significantly inhibited nonadrenergic, noncholinergic (NANC) contractile responses induced by EFS in bronchial strips. CTZ, DCPM, and ATZ did not affect substance P-induced contractile responses in the bronchi. We conclude that CTZ, DCPM, and ATZ attenuate NANC neurally mediated bronchial contraction by preventing the release of contractile neuropeptides from sensory nerve endings. This effect may occur through inhibition of carbonic anhydrase activity. In addition, thiazide diuretics potentiate contractile responses to ACh in the trachea, probably through inhibition of acetylcholinesterase activity.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7692774&dopt=Abstract













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