Drugs online research references
Circ Res. 1993 Jun;72(6):1202-10.
Role of kinins and nitric oxide in the effects of angiotensin converting enzyme inhibitors on neointima formation.
Farhy RD, Carretero OA, Ho KL, Scicli AG.
Hypertension and Vascular Research Division, Ford Hospital, Detroit, MI 48202.
Marked neointima formation occurs after balloon injury to the intima of rat arteries. Angiotensin II has been implicated as a growth factor in this process, since angiotensin converting enzyme (ACE) inhibitors block neointima formation after injury. However, ACE is an important kininase, and its inhibitors may act in part by a kinin-mediated mechanism. Kinins are also known to stimulate synthesis of endothelium-derived relaxing factor/nitric oxide (EDRF/NO) and prostacyclin, both of which have antigrowth effects. To determine whether the effect of ACE inhibitors on neointima formation is due to blockade of angiotensin II synthesis alone and/or inhibition of kinin inactivation, we followed two approaches. First, we compared the inhibition of neointima formation induced by the AT1-type angiotensin II receptor antagonist losartan with that caused by the ACE inhibitor ramipril. We also studied whether a kinin receptor antagonist, Hoe 140, blocks the effect of two different ACE inhibitors, ramipril and enalapril, on neointima formation. In addition, we studied whether the effect of ramipril is blocked by an NO synthesis inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME). Although both ramipril and losartan significantly reduced neointima formation, ramipril had a more marked effect (p < 0.05 for ramipril versus losartan). The kinin antagonist Hoe 140 reduced the inhibitory effect of ramipril and enalapril by 73% and 62%, respectively. The remaining effect of the ACE inhibitors was now similar to that of losartan. Inhibition of neointima formation by ramipril was also blocked by the NO synthesis inhibitor L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7684331&dopt=Abstract
Patol Fiziol Eksp Ter. 1997 Oct-Dec;(4):3-5.
[Effect of the angiotensin-converting enzyme inhibitor ramipril on the processes of lipid peroxidation on the status of the endogenous antioxidant system in patients with myocardial infarction]
[Article in Russian]
Davydov BV, Golikov PP, Marchenko VV, Riabinin VA, Golikov AP.
57 patients with macrofocal through-and-through myocardial infarction (MI) formed two groups. The control one (37 patients) received conventional treatment and the study one (20 patients) received adjuvant ramipril beginning from day 1 of MI and over the observation period. The patients were examined on day 1, 3, 10 and 20 from the moment of admission. MI patients of all the studied groups exhibited high level of lipid peroxidation (LP) products in the serum. Ramipril treatment produced marked correcting influence on conjugated dienes, malonic dialdehyde and degree of lipid oxidation. In MI patients on ramipril conjugated dienes level was the lowest on MI day 1-3, and malonic dialdehyde on MI day 10-20. Ramipril treatment limited alpha-tocopherol and ceruloplasmin increase in the serum. It is shown that in the mechanism of a positive effect of angiotensin-converting enzyme inhibitors in MI not only their direct pharmacological action can be involved but also a correction of LP processes and antioxidant system disturbances.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9471600&dopt=Abstract
Circulation. 1998 Feb 17;97(6):576-80.
Amlodipine releases nitric oxide from canine coronary microvessels: an unexpected mechanism of action of a calcium channel-blocking agent.
Zhang X, Hintze TH.
Department of Physiology, New York Medical College, Valhalla 10595, USA.
BACKGROUND: Recent studies suggest that amlodipine may reduce mortality in patients with heart failure, especially those with dilated cardiomyopathy. In general, drugs that release NO, such as organic nitrates and ACE inhibitors, have been shown to be of substantial benefit in the treatment of heart failure. METHODS AND RESULTS: We hypothesized that a portion of the beneficial actions of amlodipine may involve the release or action of NO. Coronary microvessels were isolated from the heart of normal dogs and incubated with increasing doses of the calcium channel blockers nifedipine, diltiazem, and amlodipine or the ACE inhibitors enalaprilat and ramiprilat. Neither nifedipine nor diltiazem increased nitrite production at any dose studied. In marked contrast, amlodipine caused a dose-dependent increase in nitrite production from 74+/-5 to 130+/-8 pmol/mg (by 85+/-21%,10(-5) mol/L, P<.05) that was similar in magnitude to that of either of the ACE inhibitors. Amlodipine also increased nitrite production in large coronary arteries and in aorta. N(omega)-Nitro-L-arginine methyl ester, HOE-140, and dichloroisocoumarin essentially abolished the increase in nitrite production, indicating that (1) nitrite production reflected NO formation, (2) nitrite production was dependent on stimulation of the kinin2 receptor, and (3) nitrite production is most likely secondary to the formation of local kinins. CONCLUSIONS: Thus, unlike nifedipine and diltiazem, amlodipine releases NO from blood vessels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9494028&dopt=Abstract
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