Renin-angiotensin system modulates neurotransmitters in the paraventricular nucleus and contributes to angiotensin II-induced hypertensive response.

Angiotensin II (ANG II)-induced inflammatory and oxidative stress responses contribute to the pathogenesis of hypertension. In this study, we determined whether renin-angiotensin system (RAS) activation in the hypothalamic paraventricular nucleus (PVN) contributes to the ANG II-induced hypertensive response via interaction with neurotransmitters in the PVN. Rats underwent subcutaneous infusion of ANG II or saline for 4 weeks.

[Effects of selenium and/or iodine deficiency on chondrocyte apoptosis in rats].

Objective: To explore the effects of selenium and/or iodine deficiency on chondrocyte apoptosis in articular cartilage in rats.

Methods: Forty-eight Sprague-Dawley rats were randomly divided into selenium deficiency group, iodine deficiency group, combined selenium and iodine deficiency group, and control group. Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) method, and Bcl-2 and Bax in articular cartilage were stained by immunohistochemistry in F3 generation of rats.

[Angiotensin II increases ROS production in cardiac fibroblasts by inducing p22phox over-expression].

Objective: To investigate the changes in the reactive oxygen species (ROS) in rat cardiac fibroblasts exposed to angiotensin II (Ang II) treatment and explore the possible pathways that mediate ROS production.

Methods: In vitro cultured fetal rat cardiac fibroblasts treated with apocynin (APO, 100 micromol/L), Ang II (10(-7) mol/L), or APO+Ang II (10(-7) mol/L Ang II was added 1 h after 100 micromol/L APO), and the ROS levels and p22phox expression in the cells were detected using fluorescent microscope and immunohistochemistry, respectively.

Results: Compared with the normal control cells, Ang II treatment of the cardiac fibroblasts resulted in significantly increased ROS production, the effect of which was inhibited by the application of APO.

[Angiotensin II type 2 receptors participate in the regulation of inflammatory cytokine secretion in adult rat hypertrophied cardiomyocytes].

Objective: To investigate the effect of angiotensin II (AngII) type 2 (AT2) receptors on pressure overload-induced inflammatory cytokine secretion in adult rat hypertrophied cadiomyocytes.

Methods: Rat models of left ventricular hypertrophy induced by pressure overload was established by placing a band around the abdominal aortic of the rats, from which the hypertrophied cadiomyocytes were isolated and purified 8 weeks later. The isolated cardiomyocytes were treated with AngII plus losartan or AngII plus PD123319, and 36 h after the treatments, the expression levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-6 in the supernatant were detected using radioimmunoassay.

[Epimedium alleviates chemotherapy-induced damage to the ultrastructure and function of rat epididymides].

Objective: To investigate the protective action of Epimedium against chemotherapy-induced damage to rat epididymides.

Methods: Fifty 60-day-old male rats were divided into a control, a model and a treatment group. Procarbazine was injected into the abdominal cavity of the model rats at the dose of 30 mg/(kg x d).

The signalling of AT2 and the influence on the collagen metabolism of AT2 receptor in adult rat cardiac fibroblasts.

Objectives: Angiotensin (Ang) II exerts its roles on cardiac fibroblasts by two receptors: type I (AT1) and type 2 (AT2). The role of AT1 has been well known, but less is known about AT2. The present study was designed to explore signal pathways of AT2 and observe whether AT2 is involved in the collagen metabolism of cardiac fibroblasts.

Angiotensin II receptors subtypes mediate diverse gene expression profile in adult hypertrophic cardiomyocytes.

1. Although the systemic and cardiac renin-angiotensin systems are known to be activated in the setting of pressure overload, the actions and signaling mechanisms of angiotensin (Ang) II via AT(1) and AT(2) receptors in hypertrophic cardiomyocytes (CM) remain largely unclear. 2.

[Alteration of signal transduction-associated gene expression in rat cardiac fibroblasts induced by blocking angiotensin II receptors].

To investigate the molecular mechanism of angiotensin II (Ang II) receptor activation in adult rat cardiac fibroblasts, the expressions of cell signal transduction-associated genes were studied by using cDNA microarray. Cardiac fibroblasts of adult Sprague-Dawley rats (230~250 g) were isolated and cultured. The cells were divided into 4 groups: Ang II, Ang II + losartan, Ang II + PD123319, Ang II + losartan + PD123319.

The protective effect of captopril on nicotine-induced endothelial dysfunction in rat.

This study was designed to examine the in vivo and in vitro effects of captopril, an angiotensin-converting enzyme inhibitor, on nicotine-induced endothelial dysfunction in rats. Endothelial dysfunction was induced by exposing isolated rat mesenteric arteries to nicotine (0.01, 0.