Drugs online research references
Behav Brain Res. 1996 Nov;81(1-2):199-205.
No evidence for involvement of angiotensin II in spatial learning in water maze in rats.
Chalas A, Conway EL.
University of Melbourne, Department of Medicine Hospital, Heidelberg, Victoria, Australia.
There is increasing evidence suggesting angiotensin II (AII) may inhibit memory formation in a range of conditioned avoidance and habituation learning tasks in rodents. We were interested to determine if AII might also play an inhibitory role in spatial learning. Angiotensin-converting enzyme (ACE) inhibitors, which block the formation of AII from AI, improve acquisition and/or retention of basal performance inhibited by the muscarinic receptor antagonist, scopolamine, in conditioned avoidance and habituation tasks. In hooded Wistar rats, over 5 days of training in a water maze neither the ACE inhibitor, ceranapril 5 and 50 micrograms/kg/day, nor the ACE inhibitor, ramipril 2 and 10 mg/kg/day, altered the increase in path length produced by administration of scopolamine 0.75 mg/kg/day. In probe trails (without platform), on the last day of training, ceranapril 50 micrograms/kg produced a 35% further deterioration in performance in the scopolamine-treated rats (P < 0.02). Administration of the substrate, renin, that leads to AII formation, did not alter water maze performance over 5 days of training. The angiotensin receptor antagonist, losartan, has been shown to improve basal and scopolamine-impaired performance in a habituation task and reverse the inhibition in long-term potentiation produced by diazepam. However, neither losartan 10 and 30 mg/kg/day nor ramipril 2 and 10 mg/kg/day reversed diazepam-impaired (3 mg/kg/day) acquisition of the spatial memory task over 5 days of training. These studies suggest AII does not inhibit spatial learning in rats in the constant platform position water maze task nor does it mediate the inhibitory effects of scopolamine or diazepam in this task.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8950017&dopt=Abstract
Ter Arkh. 1996;68(5):67-70.
[A comparison of the effect of Capoten (captopril) and ramipril on the circadian profile of the arterial pressure and peripheral hemodynamics in patients with hypertension combined with diabetes mellitus]
[Article in Russian]
Filatova EV, Vikhert OA, Rogoza AN, Arabidze GG, Kukharchuk VV.
20 patients with essential hypertension and diabetes mellitus (DM) type II were given Capoten (100-125 mg/day for 6 weeks) followed in a 2-week interval after its course termination by ramipril (10.0-12.5 mg/day). 50% of patients were sensitive to Capoten, 50% were resistance: 35 and 40% to ramipril, respectively. Ramipril was discontinued because of toxicity in 25% of patients. Hypotensive effects of ramipril were weaker than Capoten, though the former drug appeared more potent in lowering of peripheral vascular resistance at rest and at reactive hyperemia. Vasodilatation did not differ much.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9082606&dopt=Abstract
Immunopharmacology. 1997 Jun;36(2-3):185-91.
Possible protective effects of kinins and converting enzyme inhibitors in cardiovascular tissues.
Nolly H, Miatello R, Damiani MT, Abate CD.
Laboratory of Experimental Hypertension and Vasoactive Substances, School of Medicine and National Council of Research, Mendoza, Argentina.
The main objective of this study was to determine if the components of the kallikrein-kinin system are released into the venous effluent from isolated perfused rat hearts. To assess the contribution of kinins and the vascular and cardioprotective effects of the ACE inhibitor ramipril, we determined the status of cardiac kallikrein (CKK), potent kinin-generating enzyme, in rats with right ventricular hypertrophy induced by chronic volume overload and left ventricular hypertrophy by aortic banding. CKK was measured as previously described (Nolly, H.L., Carbini, L., Carretero, O.A., Scicli, A.G., 1994). Kininogen by a modification of the technique of Dinitz and Carvalho (1963) and kinins were extracted with a Sep-Pak C18 cartridge and measured by RIA. CKK (169 +/- 9 pg Bk/30 min), kininogen (670 +/- 45 pg Bk/30 min) and immunoreactive kinins (62 +/- 10 pg Bk/30 min) were released into the perfusate. The release was almost constant over a 120 min period. Pretreatment with the protein synthesis inhibitor puromycin (10 mg i.p.) lowered the release of kallikrein (42 +/- 12 pg Bk/30 min, p < 0.001) and kininogen (128 +/- 56 pg Bk/30 min, p < 0.001). Addition of ramiprilat (10 micrograms/ml) increased kinin release from 54 +/- 18 to 204 +/- 76 pg Bk/30 min (p < 0.001). Aortic banding of rats increased their blood pressure (BP) (p < 0.001), relative heart weight (RHW) (p < 0.001) and CKK (p < 0.001). Ramipril treatment induced a reduction in BP (p < 0.05) and RHW (p < 0.005) while CKK remained elevated. Aortocaval shunts increased their ANF plasma levels (p < 0.05), RHW (p < 0.001) and CKK (p < 0.01). Ramipril treatment induced a reduction in RHW (p < 0.05), while CKK and ANF increased significantly (p < 0.05). The present data show that the components of the kallikrein-kinin system are continuously formed in the isolated rat heart and that ramipril reduces bradykinin breakdown with subsequent increase in bradykinin outflow. The experiments with aorta caval shunt and aortic banding show that cardiac tissues increase their kinin-generating activity and this was even higher in ramipril-treated animals. This may suggest that the actual level of kinins is finely tuned to the local metabolic demands. In this experimental model of cardiac hypertrophy. ACE inhibitors potentiate the actions of kinins and probably try to normalise endothelial cell function.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9228545&dopt=Abstract
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