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Clin Chim Acta. 2001 Feb;304(1-2):85-90.
Captopril inhibits the production of tumor necrosis factor-alpha by human mononuclear cells in patients with congestive heart failure.

Zhao SP, Xie XM.

Department of Cardiology, Second Affiliated Hospital of Human Medical University, ChangSha 410011, China.

To study the effects of captopril on tumor necrosis factor-alpha produced by peripheral blood mononuclear cells (PBMC) of patients with congestive heart failure (CHF), we determined the TNF-alpha concentrations of culture supernatants of PBMC with and without catopril in 74 CHF patients with various heart diseases. The results showed that the supernatants concentrations of TNF-alpha in cultured PBMC (PBMC-TNF-alpha) were significantly increased in non-cachetic and cachetic CHF patients, and even higher in cachetic CHF patients, as compared with the controls (i.e., patients with New York Heart Association CHF classification I). The PBMC-TNF-alpha was significantly inhibited by captopril. These results demonstrate that the expression of TNF-alpha in PBMC is increased and can be inhibited by captopril in patients with CHF, especially in those accompanied by cachexia. This suggests that the immunomodulatory effects of captopril may contribute to its beneficial effects in heart failure patients.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11165202&dopt=Abstract

em.agr.ca

Angiotensin converting enzyme (ACE) inhibitory peptides prepared from soy protein by the action of alcalase enzyme was tested for its hypotensive effect on spontaneously hypertensive rats (SHR). Captopril, an ACE inhibitor used widely for hypertension treatment, was also applied in comparison. A significant (p < 0.05) decrease in systolic blood pressure of SHR was observed when soy ACE inhibitory peptides were orally administrated at three different dose levels (100, 500, and 1000 mg/kg of body weight/day), whereas little change occurred in the blood pressure of normotensive rats even at the highest dose. After a month-long feeding, blood pressure readings of SHR fell by approximately 38 mmHg from the original level at the lowest dose; a steadily and progressively hypotensive effect existed for these soy ACE inhibitory peptides administration groups. An obvious fluctuation was observed at the third week, although Captopril had a stronger hypotensive effect. The ACE activity of serum, aorta and lung, and lipid content of serum of SHR upon administration of soy ACE inhibitory peptides did not show a significant difference from that of the control group, whereas the serum ACE activity increased and the aorta ACE activity decreased significantly (p < 0.05) for the Captopril group. Serum Na(+) concentration decreased significantly in both the peptides-treated groups and the Captopril-treated group in comparison with the control group, whereas no lowering effect was observed for serum K(+) and serum Ca(2+) concentrations. These results suggested that the hypotensive effect of ACE inhibitory peptides derived from soy protein could be at least partly attributed to the action on salt/water balance.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11170618&dopt=Abstract

Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R822-30.
Effects of converting enzyme inhibitors on renal P-450 metabolism of arachidonic acid.

Ito O, Omata K, Ito S, Hoagland KM, Roman RJ.

Department of Nephrology, Endocrinology, and Hypertension, Tohoku University Graduate School of Medicine, Sendai 980 - 8574, Japan.

The effects of blockade of the renin-angiotensin system on the renal metabolism of arachidonic acid (AA) were examined. Male Sprague-Dawley rats were treated with vehicle, captopril (25 mg x kg(-1) x day(-1)), enalapril (10 mg x kg(-1) x day(-1)), or candesartan (1 mg x kg(-1) x day(-1)) for 1 wk. The production of 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) by renal cortical microsomes increased in rats treated with captopril by 59 and 24% and by 90 and 58% in rats treated with enalapril. Captopril and enalapril increased 20-HETE production in the outer medulla by 100 and 143%, respectively. In contrast, blockade of ANG II type 1 receptors with candesartan had no effect on the renal metabolism of AA. Captopril and enalapril increased cytochrome P-450 (CYP450) reductase protein levels in the renal cortex and outer medulla and the expression of CYP450 4A protein in the outer medulla. The effects of captopril on the renal metabolism of AA were prevented by the bradykinin-receptor antagonist, HOE-140, or the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester. These results suggest that angiotensin-converting enzyme inhibitors may increase the formation of 20-HETE and EETs secondary to increases in the intrarenal levels of kinins and NO.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11171663&dopt=Abstract

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