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PubMed1998

[Effect of eggplant on plasma lipid levels, lipidic peroxidation and reversion of endothelial dysfunction in experimental hypercholesterolemia].

PURPOSE: To study the effect of egg plant on endothelium-dependent relaxation, and plasma lipids in hypercholesterolemic rabbits, and to assess influence of this plant on the malondialdehyde (MDA) content of LDL particles and the arterial wall. METHODS: Thirteen male rabbits were randomly assigned to control (C), hypercholesterolemic (H) and egg plant (E) treated groups (n = 10 each). The H and E rabbits were fed a diet supplemented with cholesterol (0.5%) and coconut oil (10%) for 4 weeks. In addition, group E received 10 mL of the fruit juice/day during the last 2 weeks. The animals were killed and the aorta removed to measure MDA content and the endothelium dependent relaxation responses. Total plasma cholesterol, VLDL, LDL, HDL and triglyceride levels were determined using commercial kits. MDA was quantified in native and oxidized LDL and in the arterial wall. RESULTS: After 4 weeks, the E group rabbits had a significantly lower weight, plasma cholesterol, LDL, triglyceride and aortic cholesterol content than group H(p < 0.05). The MDA content that was significantly increased in the LDL particles and in the arterial wall of H rabbits was reduced in the E group (p < 0.05). Endothelium-dependent relaxation were significantly higher in the E group compared H group rabbits (p < 0.05). CONCLUSION: In hypercholesterolemic rabbits egg plant juice significantly reduced weight, plasma cholesterol levels, aortic cholesterol content and the MDA concentrations in native-oxidized LDL and in the arterial wall and increased the endothelium-dependent relaxations.

Animals↗
PubMed2002

Endothelial dysfunction, hypertension and atherosclerosis. A review of the effects of lacidipine.

Lacidipine, a third generation dihydropyridine calcium antagonist, has demonstrated pronounced anti-atherosclerotic activity in preclinical studies. The drug can act at several stages within the atherosclerotic process, utilising its antihypertensive and antioxidant properties to protect hypertensive animals against mortality and vascular damage, to reduce cholesterol levels from the vessel wall of hypercholesterolaemic animals, and to reduce the progression of existing atherosclerotic lesions. The clinical benefit of lacidipine in atherosclerosis has recently been confirmed in humans in a large, multicentre, comparative, 4-year clinical trial involving patients with mild to moderate hypertension. The European Lacidipine Study on Atherosclerosis (ELSA) showed that lacidipine was able to slow the progression of atherosclerosis, measured as carotid intimato-media thickness, by 40% compared with atenolol (p = 0.0073). Although further comparative trials are needed, based on the results of ELSA, lacidipine is likely to become a promising therapeutic agent for atherosclerosis.

Animals↗
PubMed1999

Endothelial dysfunction in the aorta of transgenic rats harboring the mouse Ren-2 gene.

The renin-angiotensin system plays an important role in the pathophysiology of hypertension. We studied vascular function in the aorta of mouse Ren-2 transgenic rats (TGR(mRen2)27). Changes in isometric tension of isolated aorta of TGR(mRen2)27 and Sprague-Dawley rats (SD) were recorded in organ chambers. Contractions to angiotensin II (AII), big-endothelin and endothelin-1 (ET-1), but not KCl were decreased in TGR. Blockade of nitric oxide (NO)-synthase by L-NAME or removal of the endothelium did not alter these decreased contractions to ET-1 and AII in TGR, suggesting that receptors or signaling pathways of these two agonists are downregulated during hypertension. Contractions to norepinephrine (NE) were also lower in TGR, however blockade of NO-synthase by L-NAME or removal of the endothelium evoked similar contractions to NE in both strains, suggesting that basal release of NO reduces contractions to NE to a greater extent in transgenic than control rats. In the presence of L-NAME, acetylcholine evoked endothelium-dependent contractions (EDCF) in TGR, which were blocked by the thromboxane/prostaglandin H2 receptor antagonists SQ 30741, and partially by the thromboxane synthase inhibitor CGS 13080, suggesting that prostaglandin H2 is the mediator. Endothelium-dependent relaxation to acetylcholine was decreased in TGR, while endothelium-independent relaxations to sodium nitroprusside were similar in both strains. SQ 30741 did not improve relaxations to acetylcholine in TGR indicating that impaired relaxations to acetylcholine are due to a decreased acetylcholine-receptor mediated release of NO rather than increased release of EDCF. Thus, Ren-2 hypertension leads to marked alterations of vascular functions in the aorta. These changes could contribute to hypertension and its vascular complications in TGR(mRen2)27 rats.

Acetylcholine↗

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