Drugs online research references
J Cardiovasc Pharmacol. 1991 Aug;18(2):207-11.
Effect of ramipril, an inhibitor of angiotensin converting enzyme, on the response of rat thoracic aorta to injury with a balloon catheter.
Capron L, Heudes D, Chajara A, Bruneval P.
Centre de Recherches sur les Maladies Vasculaires Peripheriques, Association Claude Bernard, Paris, France.
We have studied the effect of ramipril (10 mg/kg daily by gastric gavage) on the development of neointima 2 and 14 days after injury to rat aorta with a balloon catheter. In treated animals, there was no significant inhibition of the early mitotic reaction after injury (synthesis of DNA, as reflected by aortic thymidine incorporation on the second day): the mean (95% confidence interval) was 3,553 (892) in the control group vs. 2,853 disintegrations/min/micrograms of DNA (555) in the treated group, 2 p greater than 0.15. However, ramipril decreased the amount of neointima formed 14 days after injury, as characterized by (a) a highly significant decrease of the intima to intima + media areas ratio [21.1 (2.4) vs. 13.7% (2.2), 2 p less than 10(-4]); (b) a significant decrease of intima-media wet weight [35.4 (1.0) vs. 30.9 mg (0.9), 2p less than 0.005]; and (c) without any significant effect on intima-media DNA content [96.3 (7.9) vs. 91.7 micrograms (5.7), 2p greater than 0.3]. These observations suggest that angiotensin converting enzyme inhibitors may not act mainly through an inhibition of smooth muscle cell proliferation. Other effects, such as inhibition of migration, hypertrophy, and matrix synthesis, should also be considered.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1717780&dopt=Abstract
Basic Res Cardiol. 1991;86 Suppl 3:149-56.
Does converting enzyme inhibition change the neuronal and extraneuronal uptake of catecholamines?
Dominiak P, Blochl A.
Department of Pharmacology, Medical University of Lubeck, FRG.
In previous studies concerning the sympathetic outflow during converting enzyme inhibition, no significant changes after chronic treatment could be observed. Therefore, we investigated the effects of the long-acting converting enzyme inhibitor ramipril on the neuronal and extraneuronal uptake of SHR. Ramipril was administered either i.v. or orally to SHR, whereas desipramine or corticosterone were additionally infused to block the neuronal or extraneuronal uptake of catecholamines. As an index of sympathetic outflow, plasma noradrenaline and adrenaline concentrations were determined during preganglionic stimulation of the spinal cord using HPLC and ELCD. Blood pressure of SHR was measured in a carotid artery and was significantly decreased in the ramipril treated group under resting and stimulating conditions. Ramipril did not influence stimulated sympathetic outflow. However, in acute and chronic experiments ramipril led to an additive effect to desipramine concerning stimulated circulating catecholamines. Similar results could be obtained after blocking the uptake-2 with corticosterone. 3H-NA-uptake into the hearts of SHR was significantly diminished by about 10% after chronic ramipril administration. It is suggested that ramipril is able to decrease the neuronal and extraneuronal uptake of catecholamines by an unspecific effect due to the comparably high lipophilicity. The blood pressure lowering effect of ramipril is not supported by an inhibition of presynaptic noradrenaline release.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1838245&dopt=Abstract
Br J Pharmacol. 1994 Jan;111(1):238-44.
Potentiation by ACE inhibitors of the dilator response to bradykinin in the coronary microcirculation: interaction at the receptor level.
Hecker M, Porsti I, Bara AT, Busse R.
Center of Physiology, JWG-University Clinic, Frankfurt/Main, Germany.
1. To examine the possibility that angiotensin-converting enzyme (ACE) inhibitors modulate the action of bradykinin at the receptor level, their effect on the dilator response to bradykinin was studied in the isolated saline-perfused heart of the rabbit. 2. Continuous infusion of bradykinin (10 nM) elicited a transient decrease in coronary perfusion pressure (CPP) and increased prostacyclin (PGI2) release which returned to baseline values within 30 min. 3. Subsequent co-infusion of ramiprilat (> or = 10 nM) or moexiprilat, but not of the less potent ACE inhibitor n-octyl-ramipril (RA-octyl), caused another fall in CPP and an increase in PGI2 release, the magnitude and time course of which were almost identical to the first response to bradykinin. No change in CPP or PGI2 release was observed when the ACE inhibitors were administered in the absence of exogenous bradykinin. 4. Infusion of D-Arg[Hyp3]-bradykinin (10 nM), a specific B2-receptor agonist which was significantly more resistant to degradation by ACE than bradykinin, produced virtually identical changes in CPP and PGI2 release when compared to bradykinin. Subsequent co-infusion of ramiprilat was similarly effective in restoring the fall in CPP and increase in PGI2 release elicited by D-Arg[Hyp3]-bradykinin as in the presence of bradykinin. 5. In concentrations which should block the degradation of bradykinin by ACE in the coronary vascular bed, two ACE substrates, hippuryl-L-histidyl-L-leucine (0.2 mM) and angiotensin I (0.3 microM), were unable to elicit a significant change in CPP or PGI2 release while ramiprilat and another ACE inhibitor, quinaprilat, were still active in the presence of these substrates.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8012702&dopt=Abstract
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