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J Pharm Pharmacol. 2000 May;52(5):561-8.
Benidipine inhibits apoptosis during ischaemic acute renal failure in rats.

Yao K, Sato H, Ina Y, Nagashima K, Nishikawa S, Ohmori K, Ohno T.

Drug Development Research Laboratories, Pharmaceutical Research Institute, Kyowa Hakko Kogyo Co., Ltd, Japan.

We have investigated the effects of benidipine (hydrochloride), a calcium antagonist, against ischaemic acute renal failure in rats. Using histological examination, we studied whether the inhibition of apoptosis was associated with the protective effects of benidipine on the ischaemic renal injury. Acute renal failure was induced by the unilateral clamping of the left renal artery for 60 min, followed by reperfusion and contralateral nephrectomy. Drugs were given intravenously 5 min before the unilateral clamping. Prophylactic administrations of benidipine (10 microg kg(-1), i.v.) significantly ameliorated the development of renal failure as estimated by the measurements of serum creatinine and blood urea nitrogen 24 h after the reperfusion. Amlodipine (besilate, 100 and 300 microg kg(-1), i.v.) tended to attenuate renal dysfunction. Lisinopril (300 and 1000 microg kg(-1), i.v.), an angiotensin converting enzyme inhibitor, was ineffective in this acute renal failure model. Histological examination using the terminal transferase-mediated dUTP-biotin nick end-labelling (TUNEL) method to detect apoptotic cells revealed that the TUNEL-positive tubular epithelium was prominent in the renal cortex 24 h after the reperfusion. The TUNEL-positive cells were significantly reduced by pretreatment with benidipine. The results demonstrate that benidipine can ameliorate the ischaemic acute renal failure in rats and suggest that the renoprotective effect of benidipine was at least partly attributable to the reduction of apoptosis in tubular epithelial cells.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10864145&dopt=Abstract

mds.qmw.ac.uk

Angiotensin-converting enzyme (ACE) inhibitors reduce systemic and coronary vasoconstriction by modulating sympathetic neuroeffector function and by decreasing sympathetic activation. Here, blood pressure, and tissue concentrations of noradrenaline and neuropeptide Y (NPY) were studied in normotensive and spontaneously hypertensive rats (SHR) after 2 weeks treatment with lisinopril (0.3 mg/day; osmotic mini-pump). MAP was reduced in both normotensive rats and SHR after lisinopril by 32 mm Hg and 66 mm Hg respectively (P < 0.001 compared to corresponding control rats). NPY levels were significantly higher in extracts of atria, kidney, spleen and adrenal of normotensive rats compared to SHR. Lisinopril treatment increased NPY levels in atria and skeletal muscle extracts of SHR by 15% and 70% respectively (P < 0.05). Lisinopril also significantly increased noradrenaline content of the atria by 16% in SHR (P < 0. 05). The decrease in MAP and increase in tissue levels of sympathetic neurotransmitters provide further evidence that inhibition of ACE decreases sympathetic neurotransmission leading to accumulation of stored neurotransmitters. Journal of Human Hypertension (2000) 14, 381-384

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10878699&dopt=Abstract




Basic Res Cardiol. 2000 Jun;95(3):208-14.
Early rather than delayed administration of lisinopril protects the heart after myocardial infarction in rats.

Zornoff LA, Matsubara BB, Matsubara LS, Paiva SA, Spadaro J.

Departamento de Clinica Medica, Faculdade de Medicina de Botucatu, UNESP, Brazil.

BACKGROUND: ACE inhibitors have shown beneficial results in several studies after myocardial infarction (MI). However, these studies have shown conflicting results about the ideal starting time of the ACE inhibitors administration after MI and the importance of infarct size. OBJECTIVES: This study was designed to assess the long-term effects of lisinopril on mortality, cardiac function, and ventricular fibrosis after MI, in rats. METHODS: Lisinopril (20 mg/kg/day) was given on day 1 or 21 days after coronary occlusion in small or large infarctions. RESULTS: The mortality rate was reduced by 39 % in early treatment and 30 % in delayed treatment in comparison to the untreated rats. Early treatment reduced cardiac dysfunction in small MIs; however, delayed treatment did not. No statistical difference was observed among the groups for large MIs. No statistical difference was observed among the groups with large or small MIs on myocardial hydroxyproline concentration. CONCLUSIONS: Both early and delayed treatments with lisinopril increased survival. Treatment exerts no marked effects on fibrosis; early treatment has exerted beneficial influences on cardiac function whereas delayed treatment had no consistent effects. The protective effect of lisinopril is detectable only in small (< 40 % of LV) MIs.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10879622&dopt=Abstract












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