Drugs online research references
Naunyn Schmiedebergs Arch Pharmacol. 1997 May;355(5):566-70.
Involvement of 5-hydroxytryptamine and bradykinin in the hyperalgesia induced in rats by collagenase from Clostridium histolyticum.
Damas J, Liegeois JF, Bourdon V.
Departement de Physiologic humaine, Universite de Liege, Belgium.
The involvement of bradykinin, 5-hydroxytryptamine, substance P and prostanoids in the hyperalgesia elicited by collagenase in rat paw was investigated. Collagenase (100 micrograms) induced a slight hyperalgesia in kininogen deficient rats in comparison with the behavioural response obtained in normal rats. Lisinopril (10(-5) M), and angiotensin-converting enzyme inhibitor, increased the duration of the hyperalgesia elicited in normal rats. Ondansetron (0.5 to 5 mumol/kg), a 5-HT3 antagonist, suppressed the hyperalgesia as did methysergide (1.1 to 11 mumol/kg), a mixed 5-HT1 and 5-HT2 receptor antagonist. However, the hyperalgesia was not modified by RP 67580 (1.8 to 18 mumol/kg), a NK1 receptor antagonist, and was only slightly delayed by indomethacin (2 mg/kg), a cyclo-oxygenase inhibitor. The oedema-promoting effect of 5-HT (6 nmol) was inhibited by methysergide but not by ondansetron. The swelling induced by collagenase in rat paw was reduced by methysergide but not by ondansetron. We conclude that the behavioural response induced by collagenase depends on an interactions between bradykinin and 5-HT. Prostanoids play a minor role in the beginning of the reaction whereas substance P is not significantly involved in this hyperalgesia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9151293&dopt=Abstract
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Jpn J Pharmacol. 1997 Apr;73(4):337-45.
Dual effects of lisinopril on puromycin aminonucleoside nephrosis in unilaterally nephrectomized rats.
Shinosaki T, Takagawa I, Sunagawa N, Yonetani Y, Kurihara H.
Shionogi Discovery Research Laboratories II, Shionogi & Co., Ltd., Osaka, Japan.
The therapeutic effects of angiotensin converting enzyme inhibitor, lisinopril, on puromycin aminonucleoside (PAN)-induced nephrosis were investigated using unilaterally nephrectomized rats. Lisinopril showed potent dual effects on PAN nephrosis. Lisinopril treatment (50 mg/l in drinking water) from day 5 or day 9 reduced urinary protein excretion and suppressed the development of glomerular sclerosis at 8 weeks after PAN injection (150 mg/kg, i.p.), indicating a therapeutic effect on the nephrosis. Recovery of decreased anionic charge sites on the glomerular basement membrane was involved, at least in part, in the therapeutic action of lisinopril against proteinuria. On the other hand, oliguria and progressive azotemia derived from continuous deterioration of the renal function was induced if the treatment of lisinopril was started on the same day as PAN injection. The renal dysfunction induced by simultaneous administration of lisinopril with PAN could be abolished by combination dosing with sarcosine, an angiotensin II (AII)-receptor agonist. These results indicate that lisinopril treatment attenuates proteinuria by ameliorating the anionic charge barrier on the glomerular basement membrane and that it also protects against the development of chronic renal disease with segmental glomerular sclerosis, although AII depletion during the acute nephrotic stage exacerbates the renal damage in PAN nephrosis of unilaterally nephrectomized rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9165371&dopt=Abstract
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J Am Coll Cardiol. 1997 Jun;29(7):1599-606.
Angiotensin-converting enzyme inhibitors potentiate preconditioning through bradykinin B2 receptor activation in human heart.
Morris SD, Yellon DM.
The Hatter Institute, University College London Hospitals, England, United Kingdom.
OBJECTIVES: This study was designed to determine whether angiotensin-converting enzyme (ACE) inhibitors play a role in cardioprotection in a human model of preconditioning. BACKGROUND: Recent studies have suggested that bradykinin may contribute to the protective effects of preconditioning in animal models. ACE inhibitors are known to inhibit the degradation of bradykinin and hence may be able to potentiate the effect of preconditioning. METHODS: We examined the effects of the ACE inhibitors captopril and lisinopril in combination with a subthreshold preconditioning stimulus (i.e., insufficient to have any protective effects alone). Human atrial trabeculae were superfused with Krebs buffer and paced at 1 Hz. They were subjected to a full or subthreshold preconditioning stimulus consisting of either 3 or 1.5 min of simulated ischemia and 7 min of reoxygenation. In each instance, this stimulus was followed by 90 min of simulated ischemia and 2 h of reoxygenation. In addition, the subthreshold preconditioned group had 20 min of previous ACE inhibitor treatment. RESULTS: Recovery of contractile function (percent of baseline) was 22 +/- 1% (mean +/- SEM) in the control group versus 61 +/- 1% in the preconditioned group. The subthreshold preconditioned group and the ACE inhibitor-alone groups did not exhibit any protection; however, in combination, the protection was significant (71 +/- 4% in the captopril group, 58 +/- 8% in the lisinopril group, p < 0.005) compared with the control group. There was no significant difference between these values and recovery after the full preconditioning stimulus. Furthermore, Hoe 140, a specific bradykinin B2 receptor antagonist, abolished the protection. CONCLUSIONS: To our knowledge, these are the first results in human muscle to suggest that ACE inhibitors may augment ischemic preconditioning, possibly through B2 receptor activation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9180125&dopt=Abstract
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