Drugs online research references
Hypertens Res. 2002 Jan;25(1):109-15.
Novel mechanisms of the antiproliferative effects of amlodipine in vascular smooth muscle cells from spontaneously hypertensive rats.
Lai YM, Fukuda N, Su JZ, Suzuki R, Ikeda Y, Takagi H, Tahira Y, Kanmatsuse K.
Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
The calcium channel blocker amlodipine continues to be of interest due to its potential proven ability to hinder the progression of atherosclerosis and reduce the number of clinical ischemic events. Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) are useful in the study of atherosclerosis because they show exaggerated growth with production of angiotensin II (Ang II) by conversion to the synthetic phenotype. To clarify mechanisms of the antiproliferative effects of amlodipine, we evaluated effects of the expression of growth factors, the changes in phenotype, and the proliferation of VSMC from SHR. Amlodipine significantly inhibited basal DNA synthesis and proliferation of VSMC from SHR. Amlodipine also inhibited expression of platelet-derived growth factor (PDGF) A-chain, transforming growth factor beta1 (TGF-beta1) and basic fibroblast growth factor (bFGF) mRNAs in VSMC from SHR. Decreases in levels of PDGF A-chain and bFGF mRNAs in VSMC from SHR were greater with amlodipine than with nifedipine. Amlodipine significantly inhibited expression of the synthetic phenotype markers osteopontin and matrix Gla mRNAs, indicating that it inhibited the exaggerated growth of VSMC from SHR and suppressed the change from the contractile phenotype to the synthetic phenotype. Thus, amlodipine may be a beneficial therapeutic agent for patients with hypertensive vascular diseases.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11924715&dopt=Abstract
Biull Eksp Biol Med. 1992 Apr;113(4):381-3.
[Pharmacokinetics of antipyrine, nifedipine and diazepam in experimental myocardial infarct]
[Article in Russian]
Sharapov VI, Grek OR, Anan'ev EA, Kolpakov MA.
It has been shown, that antipyrine, nifedipine, diazepam pharmacokinetics changes in different ways after myocardial infarction. On day 7, 14, and 21 after myocardial ischemia antipyrine T1/2 increased considerably, and antipyrine Cl and Kel decreased. Nifedipine T1/2 increased on day 7 only. There were no diazepam pharmacokinetic changes during restoration period. However, microsomal diazepam metabolism changed significantly. Diazepam hydroxylation increased on day 7 of myocardial infarction, and on day 14 and 21 did not differ from the control. Diazepam metabolites content changed considerably during restoration period. Under myocardial infarction cytochrome P-450 isoenzymes, oxidizing present substances seem to be altered to different extent.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1391895&dopt=Abstract
Res Commun Mol Pathol Pharmacol. 1994 Nov;86(2):235-44.
Mechanisms of gastric antisecretory action of pentylenetetrazol in rats.
Lin WC.
Department of Pharmacology, China Medical College, Taichung, Taiwan.
The present study investigated the mechanisms of gastric antisecretory action of pentylenetetrazol (PTZ) in pylorus-ligated rats. Pretreatment with indomethacin, phentolamine, propranolol, 6-hydroxydopamine, flunarizine and nifedipine, which were reported to antagonize seizures induced by PTZ, did not influence the gastric antisecretory action of PTZ. In contrast, pentobarbital and phenobarbital reverse the action of PTZ. These results suggest that prostaglandins production, adrenoceptors and calcium entry are not involved in the gastric antisecretory action of PTZ, and that the GABAA receptor complex plays an important role in the action induced by PTZ.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7881872&dopt=Abstract
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