Drugs online research references
J Hum Hypertens. 1994 Aug;8(8):565-9.
Evidence for stimulation of neutrophil degranulation by selected angiotensin converting enzyme inhibitors in vitro.
Miselis J, Siminiak T, Wysocki H.
Academy of Medicine, Department of Intensive Therapy, Poznan, Poland.
Polymorphonuclear neutrophils (PMN) participate in the development of myocardial injury during ischaemia/reperfusion and granules released by human neutrophils contain proteases capable of activating prorenin in human plasma and can cleave angiotensin II directly from angiotensin I and angiotensinogen. The purpose of the present study was to investigate whether angiotensin converting enzyme (ACE)-inhibitors exert an in vitro effect on PMN degranulation. Isolated neutrophils were incubated with captopril, lisinopril, enalaprilat or ramiprilat and release of lysozyme and myeloperoxidase was measured from unstimulated and opsonised zymosan stimulated cells. All ACE inhibitors increased neutrophil myeloperoxidase release and lysozyme release by both unstimulated and stimulated cells. In the presence of saline unstimulated PMN released 4.48 +/- 0.68% and zymosan-stimulated cells released 7.28 +/- 0.76% of myeloperoxidase content and the enzyme release increased after incubation with captopril (5.55 +/- 0.71 and 8.74 +/- 0.72%), lisinopril (5.43 +/- 0.57 and 9.02 +/- 0.7%), enalaprilat (6.05 +/- 0.67 and 9.20 +/- 0.82%) and ramiprilat (5.82 +/- 0.69 and 9.26 +/- 0.74%), respectively. In the presence of saline unstimulated PMN released 16.71 +/- 1.28% and zymosanstimulated PMN released 34.42 +/- 1.71% of lysozyme content and the release increased after incubation with captopril (21.15 +/- 1.36 and 42.75 +/- 1.95%), lisinopril (23.95 +/- 1.26 and 39.23 +/- 1.94%), enalaprilat (21.34 +/- 1.32 and 41.59 +/- 1.99%) and ramiprilat (20.88 +/- 1.35 and 37.53 +/- 1.95%) by unstimulated PMN, respectively. The ACE-inhibitory effect of these drugs may therefore be decreased by stimulation of PMN degranulation and neutrophil-dependent angiotensin II forming pathway.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7990082&dopt=Abstract
J Cardiovasc Pharmacol. 1998 Dec;32(6):1001-8.
Regulation of aortic atrial natriuretic factor and angiotensinogen in experimental hypertension.
Ogawa T, Linz W, Scholkens BA, de Bold AJ.
University of Ottawa Heart Institute at the Ottawa Hospital, Ontario, Canada.
We investigated the relation between atrial natriuretic factor (ANF) gene expression and the status of the renin-angiotensin system (RAS) in aortic tissue in rats made hypertensive by either aortic banding or by deoxycorticosterone acetate (DOCA)-salt administration. These experimental models of hypertension are known to have differences in terms of the status of RAS. ANF messenger RNA (mRNA) levels were measured in aortic tissue by using a newly developed quantitative competitive reverse transcription polymerase chain reaction (QC-RT-PCR) technique. Changes in the proportions of alpha1 and alpha2 isoforms of Na+K+-adenosine triphosphatase (ATPase) mRNA levels were used as indicators of aortic hypertrophy. Treatment with DOCA alone, salt alone, or DOCA-salt for 5 weeks increased aortic-weight/body-weight ratio and aortic angiotensinogen mRNA levels, but did not change alpha1 or alpha2 Na+K+-ATPase mRNA levels. Aortic ANF mRNA levels had a tendency to increase after treatment with DOCA, salt, or DOCA-salt, but this change did not reach statistical significance. Suprarenal aortic banding for 6 weeks or 12 weeks increased aortic-weight/body-weight ratio (12 weeks), decreased alpha2 Na+K+-ATPase and angiotensinogen mRNA levels, but did not affect alpha1 Na+K+-ATPase mRNA levels or ANF mRNA levels. Treatment with ramipril, an angiotensin-converting enzyme (ACE) inhibitor was carried out for 6 weeks just after aortic banding (prevention experiment) or after 6 weeks in rats that were banded for the previous 6 weeks (regression experiment). High-dose ramipril (1 mg/kg)--a treatment known to inhibit both tissue and circulating RAS--normalized aortic-weight/body-weight ratio, and also normalized alpha2 Na+K+-ATPase mRNA levels. Aortic angiotensinogen mRNA levels of banded rats treated with high-dose ramipril was higher than those of the normal control, sham operated, and banded rats. Treatment with high-dose ramipril did not affect alpha1 Na+K+-ATPase mRNA levels or ANF mRNA levels. Low-dose ramipril (10 microg/kg)--a treatment that selectively inhibits tissue RAS--normalized aortic-weight/body-weight ratio but did not normalize alpha2 Na+K+-ATPase mRNA levels (regression experiment) or angiotensinogen mRNA levels (prevention experiment) and did not change either alpha1 Na+K+-ATPase mRNA levels or ANF mRNA levels. The results suggest that, in contrast to previous findings in heart and kidney, the regulation of ANF mRNA levels in aortic tissue is largely independent of pressure load, volume load, and plasma or tissue RAS. It is suggested that any antihypertrophic actions of ANF may be mediated by the increased circulating ANF levels and its interaction with its receptor or through CNP.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9869508&dopt=Abstract
J Cardiovasc Pharmacol. 1992;20 Suppl 1:S1-6.
Development and modulation of experimental right ventricular hypertrophy in rats.
Zimmer HG.
Physiologisches Institut der Universitat Munchen, Germany.
Two models of right ventricular (RV) hypertrophy in rats have been created and characterized: chronic myocardial infarction and pulmonary artery stenosis. A Millar ultraminiature catheter pressure transducer designed specifically for right heart catheterization was used for the measurement of RV function in closed-chest, anesthetized rats. Four weeks after coronary artery ligation, left ventricular (LV) function was depressed as evidenced by the reduction of LV systolic pressure (LVSP), the maximal rate of rise in LV pressure (LV dp/dtmax), cardiac output, and by the elevation of LV end-diastolic pressure (LVEDP). There was an increase in RVSP and an elevation in RV dp/dtmax as well as an increase in the RV weight/body weight ratio. Myocytes isolated from the RV 4 weeks after coronary artery ligation had a greater volume and cross-sectional area. In addition, 14 days after pulmonary artery stenosis, there also was an elevation in RVSP and in RV dp/dtmax. In this model, the effect of angiotensin-converting enzyme (ACE) inhibition with ramipril (1 mg/kg daily) was examined. The increase in RVSP from 35 +/- 2 to 61 +/- 4 mm Hg after pulmonary artery stenosis was not influenced by ramipril (63 +/- 4 mm Hg), neither was the elevation of RV weight. However, the increase in cell volume and cross-sectional area of myocytes isolated from the RV was less pronounced in the ramipril-treated group (+27% compared with +58% in untreated animals). Thus, ACE inhibition with ramipril altered the hypertrophic response at the cellular level.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1380611&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||