ABSTRACT
Objective To investigate the effect of hypert riglyceridemia on vascular endothelial function. Methods With high-resolution ultrasound, flow and nitroglycerin-induced dilatation of the brachial artery were determined in thirty hypertriglyceridemic patients and thirty healthy subjects as controls. Serum lipid and plasma endothelin (ET) were determined. Results In patients with hypertriglyceridemia,flow-induced vasodilatation was much reduced compared with that in the control subjects[(2.7±2.0)% vs (15.0±8.0)%, P<0.001］.However, vasodilatation in response to nitroglycerin were similar in both groups［(15.0±5.0)% vs (16.8±9.0)%, P>0.05].Plasma ET level in the hypertriglyceridemic group was significantly higher than that in the control group［(106.22±19.16) μg/L vs (72.37±14.06) μg/L, P<0.001].ConclusionEndothelium-dependent vasodilatation was impaired in patients with hypertriglyceridemia.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of micronized fenofibrate on vascular endothelial function in patients with hypertriglyceridemia.</p><p><b>METHODS</b>Using high-resolution ultrasound, we measured flow- and nitroglycerin-induced dilatation of the brachial artery in 30 patients with hypertriglyceridemia before and after treatment with micronized fenofibrate at a dose of 200 mg once daily for 4 weeks. Simultaneously, both serum lipid and plasma endothelin (ET) levels were determined.</p><p><b>RESULTS</b>After micronized fenofibrate therapy, serum triglyceride (TG) levels decreased significantly (P < 0.05). Plasma ET levels also decreased markedly [(82.66 +/- 15.46) microg/L vs. (106.22 +/- 19.16) microg/L, P < 0.001]. Flow-induced vasodilatation was much improved (11.0% +/- 9.0% vs 2.7% +/- 2.0%, P < 0.01). However, no significant changes in vasodilatation occurred in response to nitroglycerin (16.2% +/- 6.0% vs 15.0% +/- 5.0%, P > 0.05) in patients with hypertriglyceridemia.</p><p><b>CONCLUSIONS</b>Micronized fenofibrate can improve impaired endothelium-dependent vasodilatation in patients with hypertriglyceridemia. Improving endothelial function may also be the mechanism responsible for the beneficial effects of micronized fenofibrate.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Endothelium, Vascular , Physiology , Fenofibrate , Pharmacology , Therapeutic Uses , Hypertriglyceridemia , Drug Therapy , VasodilationABSTRACT
The effects and mechanism of long-term angiotensin converting enzyme inhibitor (ACEI) Forsinopril on left ventricular hypertrophy of spontaneous hypertension rat (SHR) and left ventricular pressure overloading rat were studied. The left ventricular index (left ventricle weight/body weight) was used to evaluate left ventricular hypertrophy and the in situ hybridization to investigate the TGF-beta 1 gene expression in left ventricle. The results showed that Forsinopril significantly decreased the left ventricular index of both SHR and left ventricle pressure overloading rat. Forsinopril reduced the integral photic density of TGF-beta 1 gene statement from 2.836 +/- 0.314 to 1.91 +/- 0.217 (P < 0.01, n = 8) of SHR rat and from 3.071 +/- 0.456 to 2.376 +/- 0.379 (P < 0.01, n = 8) of left ventricular pressure overloading rat respectively. It was concluded that Forsinopril could prevent the occurrence of left ventricular hypertrophy and reduce the TGF-beta 1 gene expression in left ventricle of both SHR and left ventricular pressure overloading rat significantly.
Subject(s)
Animals , Female , Male , Rats , Angiotensin-Converting Enzyme Inhibitors , Pharmacology , Fosinopril , Pharmacology , Hypertension , Hypertrophy, Left Ventricular , Myocardium , Metabolism , Random Allocation , Rats, Inbred SHR , Rats, Inbred WKY , Transforming Growth Factor beta , GeneticsABSTRACT
To explore the influence of angiotensinⅡ(AngⅡ) and aldosterone (Ald) on synthesis of collagen and activity of precollagenase secreted by cardiac fibroblasts.Sirus Red method was employed to evaluate collagen synthesis of cultured cardiac fibroblasts; typeⅠ collagen was measured by competitive ELISA; collagenase activity was tested by fluorescence spectrophotometry.At the doses of 10-9～10-7mol/L, AngⅡ could enhance gross and typeⅠ collagen production in a dose-dependent manner. Collagenase activity decreased with increasing concentration of AngⅡ. These effects of AngⅡcould be completely abolished by its receptor antagonist, saralasin. Ald might enhance gross and typeⅠ collagen production only at a higher concentration (10-7～10-8mol/L), whereas lower concentration (10-9mol/L) had no effect on it. These effects of Ald could be abolished by spironolactone,a specific Ald receptor antagonist. In addition, Ald could significantly decrease the activity of collagenase secreted from cultured cardiac fiboblasts at concentrations of 10-9～10-7mol/L within 24h，which could not be antagonized by 10-6mol/L spironolactone. The results suggested that AngⅡand Ald enhance cardiac fibroblasts collagen synthesis and inhibit collagenase activity ,resulting in net collagen accumulation resulted and acceleration of cardiac fibrosis.