Fosinopril improves the electrophysiological characteristics of left ventricular hypertrophic myocardium in spontaneously hypertensive rats.

This study investigated the effects of fosinopril on the electrophysiological characteristics of the left ventricular hypertrophic myocardium in spontaneously hypertensive rats (SHRs). Twenty-four 10-week-old male SHRs were divided into fosinopril and non-fosinopril groups (n = 12 each). Twelve 10-week-old Wistar-Kyoto rats were used a control group.

Valsartan improves the electrophysiological characteristics of left ventricular hypertrophic myocardium in spontaneously hypertensive rats.

The objective was to investigate the effects of valsartan on the electrophysiological characteristics of left ventricular hypertrophic myocardium in spontaneously hypertensive rats (SHR). A total of 24 10-week-old male SHR were divided into two groups: valsartan and non-valsartan groups (n=12 in each). Twelve 10-week-old Wistar-Kyoto rats were served as the control group.

Effect of fosinopril on the transient outward potassium current of hypertrophied left ventricular myocardium in the spontaneously hypertensive rat.

To investigate fosinopril's effect on the transient outward potassium current (Ito) of differing degrees of hypertrophied myocytes in the spontaneously hypertensive rat (SHR). Ten- and 24-week-old SHRs were used as models for cardiac hypertrophy. Hypertrophied ventricular myocytes were exposed to 1, 10, and 100 μmol/L fosinopril; the whole-cell patch-clamp technique was used to study the effects on the transient outward potassium current.

Association of higher resistin levels with inflammatory activation and endothelial dysfunction in patients with essential hypertension.

Background: Some studies have shown that serum resistin levels increase in hypertensive patients. Whether the increase of resistin is related to inflammatory or vascular endothelial function is still unknown. We investigated the relationship of increased resistin levels to inflammatory factors and circulating biomarkers of vascular endothelial function in hypertensive patients.

Increased level of soluble syndecan-1 in serum correlates with myocardial expression in a rat model of myocardial infarction.

A candidate marker for ventricular remodeling after myocardial infarction (MI), syndecan-1 (Sdc1), has been shown to be upregulated in myocardial tissues. However, the clinical potential of this marker depends on the ability to obtain samples safely and noninvasively. Therefore, we investigated the expression of soluble Sdc1 in the serum of rats after MI.

Blockades of angiotensin and aldosterone reduce osteopontin expression and interstitial fibrosis infiltration in rats with myocardial infarction.

Background: It has been reported that osteopontin has an important role in cardiac fibrosis and remodeling. However, its direct mechanisms remain unclear. The purpose of this study was to investigate the role of angiotensin and aldosterone blockades in cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted (MI) rats.