[Hypoxia/reoxygenation induced endoplasmic reticulum stress in cultured neonatal rat cardiomyocyte].

Objective: To investigate the effect of hypoxia/reoxygenation on endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes.

Methods: Neonatal rat cardiac myocytes in primary culture were exposed to hypoxia for 5.5 hours and subsequently reoxygenation for 2-24 hours.

[Mechanism of urotensin II-stimulated adrenomedullin secretion in human vascular endothelial cells].

Objective: To study the mechanism of urotensin II(U II)-stimulated adrenomedullin secretion in human vascular endothelial cells.

Methods: In cultured human vascular endothelial cells (HEVCs), different concentrations of U II was used to stimulate the secretion of Adm, and different inhibitors were used to study the changes in the secretion after block of different signal transduction pathways. The contents of Adm in the medium were detected with radioimmunoassay.

Intermedin 1-53 in central nervous system elevates arterial blood pressure in rats.

Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene-related peptide (CGRP) family identified from human and other vertebrate tissues. Preprointermedin can generate various mature peptides by proteolytic cleavage. Amino acid sequence analysis showed cleavage sites located between two basic amino acids at Arg93-Arg94 resulting in the production of prepro-IMD(95-147), namely IMD(1-53).

Dysfunction of myocardial sarcoplasmic reticulum in rats with myocardial calcification.

We investigated the relationship between cardiac dysfunction and Ca2+ transport in the myocardial sarcoplasmic reticulum (SR) during the pathogenesis of cardiovascular calcification in rats. The possible mechanism of SR dysfunction was explored by detecting the alteration of the nitric oxide/nitric oxide synthase (NO/NOS) pathway in the SR. Using the vitamin D plus nicotine (VDN treatment for 2 week and 6 week) experimental model of cardiac calcification, cardiac function and sarcoplasmic reticulum function were measured.

Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits.

Aim: To investigate effects of taurine on ischemia/reperfusion (I/R)-induced compartment syndrome in rabbit hind limbs.

Methods: Rabbits underwent femoral artery occlusion after ligation of branches from terminal aorta to femoral artery. After a 7-h ischemia, reperfusion was established with the use of heparinized polyethylene shunts.

Adrenomedullin induces heme oxygenase-1 gene expression and cGMP formation in rat vascular smooth muscle cells.

Adrenomedullin (ADM) is a potent vasodilatory peptide. It regulates blood pressure by increasing cyclic adenosine monophosphate (cAMP) and guanosine-3',5'-monophosphate (cGMP). We sought to investigate the effect of ADM on heme oxygenase-1 (HO-1) gene expression and cGMP formation in cultured rat vascular smooth muscle cells (VSMCs).

Ghrelin blunted vascular calcification in vivo and in vitro in rats.

Ghrelin is a new peptide with regulatory actions in growth hormone secretion in the anterior pituitary gland and in energy metabolism. Currently, ghrelin has potently protective effects in cardiovascular diseases. We used an in vivo model of rat vascular calcification induced by vitamin D3 and nicotine and one of cultured rat vascular smooth muscular cells (VSMCs) calcification induced by beta-glycerophosphate to study the possible mechanism in the regulatory action of ghrelin in vascular calcification.

Adrenomedullin(27-52) inhibits vascular calcification in rats.

Adrenomedullin (ADM) has the vasodilatory properties and involves in the pathogenesis of vascular calcification. ADM could be degraded into more than six fragments in the body, including ADM(27-52), and we suppose the degrading fragments from ADM do the same bioactivities as derived peptides from pro-adrenomedullin. The present study carries forward by assessing the effects on vascular calcification of the systemic administration of ADM(27-52).

Protective role of metallothionein in stress-induced gastric ulcer in rats.

Aim: To illustrate the pathophysiological role of metallothionein (MT) in gastric ulcer induced by stress.

Methods: Wistar rats underwent water-immersion-restraint (WIR) stress, ZnSO(4) (an MT inducer) treatment, WIR+ZnSO(4) or WIR+MT, and the ulcer index (UI) was estimated in excised stomach and liver tissues. The mRNA level of gastric MT was determined by semi-quantitative RT-PCR.

[A new strategy to treat hyperhomocysteinemia].

Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B(6), B(12) and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine.

HSP70 and GRP78 induced by endothelin-1 pretreatment enhance tolerance to hypoxia in cultured neonatal rat cardiomyocytes.

The heat shock protein 70 and glucose-regulated protein 78 have been shown to protect cells against deleterious stimuli. This study was performed to determine whether endothelin-1 pretreatment could increase cardiomyocyte tolerance to hypoxia and induce heat shock protein 70 and glucose-regulated protein 78 expression. Cultured cardiomyocytes were treated with endothelin-1 at doses of 0.

Plasma mitochondrial coupling factor 6 in patients with acute myocardial infarction.

Previous studies have shown that mitochondrial coupling factor 6 (CF6) is an endogenous peptide that inhibits prostacyclin (PGI2) synthesis in vascular endothelial cells. In this study, we measured the plasma CF6 level of patients with acute myocardial infarction (AMI) to observe dynamic changes of CF6. All patients showed elevated plasma CF6 levels upon admission for treatment of AMI.

Changes in production and metabolism of brain natriuretic peptide in rats with myocardial necrosis.

In this study, we employed rat model of acute myocardial necrosis induced by isoproterenol (ISO) to study the possible roles of corin, the protease uniquely distributing in myocardium to convert pro-brain natriuretic peptide (proBNP) to BNP, and neutral endopeptidase (NEP), the major enzyme to degrade BNP, in changing the levels of BNP. In rats with isoproterenol alone, the myocardium necrosis occurred and the cardiac function was inhibited; the BNP contents in plasma and myocardium were upregulated, so did the myocardial corin mRNA level; the NEP activity in plasma and myocardium were downregulated. Omapatrilat (OMA) treatment relieved myocardial lesions and improved cardiac function.

Protective effects of intermedin/adrenomedullin2 on ischemia/reperfusion injury in isolated rat hearts.

Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene-related peptide (CT/CGRP) family identified from human and other vertebrate tissues. Preprointermedin can generate a 47-amino acid mature peptide (IMD(1-47)) and a shorter 40-amino acid one (IMD(8-47)) by proteolytic cleavage. The present study was designed to determine the protective effect of IMD on cardiac ischemia/reperfusion (I/R) injury and its possible mechanism.

Effects of intermedin(1-53) on cardiac function and ischemia/reperfusion injury in isolated rat hearts.

Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene-related peptide (CT/CGRP) family identified from human and other vertebrate tissues. Preprointermedin (preproIMD) can generate a 47 amino acid mature peptide (IMD(1-47)) and a shorter 40 amino acid one (IMD(8-47)) by proteolytic cleavage. Amino acid sequence analysis showed that cleavage sites are located between two basic amino acids at Arg93-Arg94, resulting in the production of preproIMD(95-147), namely IMD(1-53).

[Promoting effect of hyperhomocysteinemia on vascular calcification in rats].

Aim: To explore the effect of hyperhomocysteinemia on vascular calcification and the underlying mechanism of it.

Methods: Arterial calcification of Sprague-Dawley rats was induced by vitamin D3 plus nicotine. Hyperhomocysteinemia was established by feeding high methionine diet for six weeks and was assessed b y plasma total homocysteine (tHcy) level detected by HPLC method.

Effects of adrenomedullin on aldosterone-induced cell proliferation in rat cardiac fibroblasts.

Aldosterone induces cardiac remodeling in cardiovascular diseases by stimulating the proliferation, production and secretion of collagen in fibroblasts. It also stimulates vascular smooth muscle cells to produce and secrete adrenomedullin (ADM), which has a cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion in rat cardiac fibroblasts, and the effect of ADM on aldosterone-stimulated fibroblast proliferation to observe the interaction between endogenous ADM and aldosterone.

Urotensin-II activates L-arginine/nitric oxide pathway in isolated rat aortic adventitia.

Urotensin-II (U-II), a cyclic peptide widely expressed in blood vessels, has diverse vascular actions that range from potent vasoconstriction to vasodilation. Although, U-II-induced vasodilation has been shown to be partially dependent on nitric oxide (NO), the involvement of vascular adventitia-derived NO, remains unknown. The present study aimed to elucidate the activation of U-II on L-arginine/NO pathway in isolated rat aortic adventitia.

Electrophysiological evidences for the contribution of NMDA receptors to the inhibition of clonidine on the RVLM presympathetic neurons.

The main objective of this study is to test the hypothesis that N-methyl-D-aspartate (NMDA) receptors within the rostral ventrolateral medulla (RVLM) are involved in the inhibition of clonidine on the RVLM presympathetic neurons. Totally, 22 presympathetic neurons were recorded in anesthetized and paralyzed rats. The majority of these neurons (n=16 of 22) were significantly inhibited by iontophoretic (30 nA) clonidine, the other 6 neurons were insensitive to clonidine.

Effects of adrenomedullin on cell proliferation in rat adventitia induced by aldosterone.

Objective: Aldosterone is involved in cardiovascular diseases such as hypertension and heart failure by inducing sodium retention and vascular remodeling, which is characterized by fibroblast proliferation and migration in adventitia. It is well known that aldosterone stimulates vascular smooth muscle cells and fibroblasts to produce and secrete adrenomedullin (ADM), a multiple functional peptide with an important cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion and its mRNA expression in rat aortic adventitia to study the paracrine/autocrine interaction between endogenous ADM and aldosterone.

Ghrelin protects myocardium from isoproterenol-induced injury in rats.

Aim: To investigate the cardiac protective effects of ghrelin in rat with myocardial injury induced by isoproterenol (ISO).

Methods: Rats were subcutaneously injected ISO 40 mg/kg/d with or without ghrelin 1 or 10 nmol/kg/d for 2 d. Hemodynamic parameters including mean arterial blood pressure and left ventricular pressure were measured at 12 h after the last injection with ISO and/or ghrelin.

[Changes and significance of hydrogen sulfide/cystathionine gamma-lyase system in hypertension: an experimental study with rats].

Objective: To explore the significance of hydrogen sulfide/cystathionine gamma-lyase (H(2)S/CSE) system in the development of hypertension and the effects of H(2)S/CSE system on the modulation of aortic remodeling process of hypertension.

Methods: Eight 4-week-old male WKY rats were used as WKY control group, and another sixteen SHR rats at the age of 4 weeks were randomly divided into SHR control group (n = 8) and SHR + NaHS (H(2)S donor) group (n = 8). The rats of SHR control and WKY control were injected with normal saline and the rats of the SHR + NaHS group were injected with NaHS each day.

[Effect of hydrogen sulfide, a new gaseous signal molecule, on pulmonary vascular smooth muscle cell apoptosis in rats].

Objective: To explore the effects of hydrogen sulfide (H(2)S) on hypoxic pulmonary vascular smooth muscle cell (VSMC) apoptosis in rats.

Methods: Twenty-four Wistar rats were divided into 3 groups: control group (n=8), hypoxia group (n=8), and hypoxia +NaHS group (n=8). The plasma level of H(2)S was determined by methylene blue spectrophotometric method.