Drugs online research references
Hypertension. 1993 Oct;22(4):513-22.
Nephrectomy, converting enzyme inhibition, and angiotensin peptides.
Campbell DJ, Kladis A, Duncan AM.
St Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia.
To determine the contribution of kidney-derived renin and angiotensin converting enzyme to circulating and tissue levels of angiotensin peptides, we measured angiotensin (Ang)-(1-7), Ang II, Ang-(1-9), and Ang I in plasma, kidney, lung, heart, aorta, brown adipose tissue, adrenal, pituitary, and brain of five groups of male Sprague-Dawley rats: control rats, rats given the converting enzyme inhibitor ramipril (10 mg/kg), rats nephrectomized 24 hours, rats nephrectomized 48 hours, and rats nephrectomized 48 hours and given ramipril. Plasma and tissues, apart from adrenal, showed a 63% to 98% reduction in Ang II, the ratio of Ang II to Ang I, or both after ramipril administration, indicating a major role for converting enzyme in Ang II formation. Nephrectomy caused a more than 95% decrease in plasma renin levels and a fourfold to eightfold increase in plasma angiotensinogen levels. Apart from plasma and brain, tissues showed a 59% to 78% decrease in Ang II levels after nephrectomy, indicating a major role for kidney-derived renin in Ang II formation. The persistence of Ang II in plasma and tissues of anephric rats indicates that Ang II may be formed by a process independent of kidney-derived renin; this process may be amplified by the increased plasma angiotensinogen levels that accompany nephrectomy. For lung, adrenal, and aorta, Ang II levels showed a further decrease when nephrectomized rats were given ramipril. However, for plasma and the other tissues, ramipril produced little or no decrease in Ang II levels of anephric rats, suggesting that Ang II may be formed by a pathway independent of converting enzyme. Such a pathway may involve the direct formation of Ang II from angiotensinogen by a non-renin-like enzyme.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8406656&dopt=Abstract
Ugeskr Laeger. 1997 Mar 24;159(13):1945-9.
[Angiotensin-converting enzyme inhibitor in the treatment of epirubicin-induced dilated cardiomyopathy]
[Article in Danish]
Jensen BV, Nielsen SL, Jensen TS.
Klinisk fysiologisk nuklearmedicinsk afdeling, Amtssygehuset i Herlev.
Anthracycline chemotherapy of cancer can cause severe, frequently fatal congestive heart failure (CHF), the first line treatment for which is diuretics and digoxin. We have studied the use of an ACE-inhibitor added as a third agent. Of 85 patients evaluable for cardiotoxicity after treatment with a median of 1000 mg/m2 of epirubicin for metastatic breast cancer, nine developed CHF at 1.5 to 13 months after therapy. Left ventricular ejection fraction decreased from normal to 18 to 35%. All patients received digitalo-diuretic therapy and after a transient clinical relief enalapril or ramipril increasing from 1.25 mg orally daily to 10-15 mg after 4-6 weeks. Eight of the nine patients deteriorated while on digitalo-diuretic therapy. Within three months of starting the ACE-inhibitor in these patients, LVEF increased to normal or near normal. Only one patient died in heart failure. Follow-up ranged from 11-42 months (median 26) and survival in the nine patients was similar to that of those who did not develop CHF. We suggest that treatment of anthracycline-induced CHF with an ACE-inhibitor should start within one to two weeks after digitalo-diuretic therapy regardless of the severity of symptoms rather than waiting for clinical deterioration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9123633&dopt=Abstract
J Cardiovasc Pharmacol. 1989;14 Suppl 4:S32-6.
Inhibition of converting enzyme in brain tissue and cerebrospinal fluid of rats following chronic oral treatment with the converting enzyme inhibitors ramipril and Hoe 288.
Gohlke P, Scholkens B, Henning R, Urbach H, Unger T.
Department of Pharmacology, University of Heidelberg, F.R.G.
A direct central nervous system (CNS)-related component of the cardiovascular actions of converting enzyme (CE) inhibitors will be governed by the ability of these drugs to gain access to the brain. We investigated the inhibitory effect of the two CE inhibitors ramipril and Hoe 288 on CE activity in different brain regions and in the cerebrospinal fluid of rats. One-week oral gavage treatment with ramipril (10 mg/kg/day) and Hoe 288 (10 mg/kg/day) resulted in a marked inhibition of CE activity in the brain cortex (90 and 91%, respectively), the hypothalamus (78 and 82%, respectively), and in the brainstem (67 and 66%, respectively). The complete blockade of plasma CE activity was paralleled by a 84% inhibition of CE activity in cerebrospinal fluid. Both CE inhibitors failed significantly to inhibit CE activity in the striatum. Our results demonstrate that the CE inhibitors Hoe 288 and ramipril were able to pass the blood-brain barrier (BBB) to inhibit central CE activity. The penetration of CE inhibitors into the CNS appears to depend on the lipophilicity of the drugs and on the mode of drug application. The possibility that an inhibition of CE activity in circumventricular organs outside the BBB such as the subfornical organ and the organum vasculosum of the lamina terminalis may be sufficient to explain the central effects of orally applied CE inhibitors is discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2483426&dopt=Abstract
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