Biomedical subjects

Shanjun Zhu

Publications and source records attributed to Shanjun Zhu.

10 recordsLinked to original sources

PubMed2006

Association of angiotensin-converting enzyme 2 gene A/G polymorphism and elevated blood pressure in Chinese patients with metabolic syndrome.

To establish whether angiotensin-converting enzyme 2 (ACE2) gene A/G single nucleotide polymorphism is associated with hypertension in Chinese patients with metabolic syndrome. The study was conducted in 353 patients with metabolic syndrome. The alleles of the ACE2 A/G polymorphism, which is located on the X chromosome, were detected using polymerase chain reaction and subsequent cleavage by Alu I restriction endonuclease. G allele frequencies in patients with metabolic syndrome were 36.6% in female subjects and 43.4% in male subjects, respectively. Female patients with metabolic syndrome who carry the GG genotype had a significantly higher diastolic blood pressure compared with other genotypes. Multivariate logistic regression showed that female gender (P = 0.019) and carrying only the G allele (odds ratio 2.83 [95% CI 1.36 to 5.91]; P = 0.005) were significantly associated with increased diastolic blood pressure. It is concluded that the ACE2 A/G polymorphism is associated with hypertension in patients with metabolic syndrome.

Angiotensin-Converting Enzyme 2↗

PubMed2005

GATA4-mediated cardiac hypertrophy induced by d-myo-inositol 1,4,5-tris-phosphate.

We evaluated the effects of d-myo-inositol 1,4,5-tris-phosphate on cardiac hypertrophy. d-myo-inositol 1,4,5-tris-phosphate augmented cardiac hypertrophy as evidenced by its effects on DNA synthesis, protein synthesis, and expression of immediate-early genes c-myc and c-fos, beta-myosin heavy chain, and alpha-actin. The administration of d-myo-inositol 1,4,5-tris-phosphate increased the expression of nuclear factor of activated T-cells and cardiac-restricted zinc finger transcription factor (GATA4). Real-time quantitative RT-PCR showed that d-myo-inositol 1,4,5-tris-phosphate-induced GATA4 mRNA was significantly enhanced even in the presence of the calcineurin inhibitor, cyclosporine A. The effect of d-myo-inositol 1,4,5-tris-phosphate was blocked after inhibition of inositol-trisphosphate receptors but not after inhibition of c-Raf/mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (ERK) or p38 mitogen-activated protein kinase pathways. The study shows that d-myo-inositol 1,4,5-tris-phosphate-induced cardiac hypertrophy is mediated by GATA4 but independent from the calcineurin pathway.

Animals↗

PubMed2004

Thiazide-like diuretics attenuate agonist-induced vasoconstriction by calcium desensitization linked to Rho kinase.

Lowering blood pressure using thiazide-like diuretics, including chlorthalidone and hydrochlorothiazide, has been proven to be effective in clinical studies. However, the mechanisms by which thiazide-like diuretics lower blood pressure are still poorly understood. To evaluate whether thiazide-like diuretics cause calcium desensitization in smooth muscle cells, we measured their effects on agonist-induced increase of blood pressure in Wistar rats in vivo and on agonist-induced vasoconstriction of aortic rings, DNA synthesis, and protein synthesis, RhoA, Rho kinase, and intracellular calcium in vascular smooth muscle cells in vitro. Thiazide-like diuretics significantly attenuated angiotensin II-induced or norepinephrine-induced increase of systolic blood pressure in rats. Thiazide-like diuretics inhibited agonist-induced vasoconstriction of aortic rings in a concentration-dependent manner in the presence and absence of endothelium. The inhibitory effects of thiazide-like diuretics were similar to that of the specific Rho kinase inhibitor Y27632. RT-PCR and immunoblotting showed that RhoA and Rho kinase were significantly reduced in vascular smooth muscle cells after administration of thiazide-like diuretics. In contrast, thiazide-like diuretics did not affect protein tyrosine phosphatase-2 (SHP-2) expression. Agonist-induced changes of intracellular calcium were not affected by thiazide-like diuretics. The study indicates that thiazide-like diuretics inhibit agonist-induced vasoconstriction by calcium desensitization in smooth muscle cells linked to the Rho-Rho kinase pathway.

Acute-Phase Proteins↗

PubMed2004

Differentially expressed genes in hypertensive rats developing cerebral ischemia.

The molecular events occurring after cerebral ischemia in hypertension may include de novo expression of numerous genes. Receptor genes are predominantly involved in the process of cell death, neuroprotection and reconstruction after ischemic injury. Ischemic stroke was observed in the non-genetic, non-surgical model of hypertension, the cold-induced hypertensive rat. In hypertensive rats suppression subtractive hybridization analysis was used to identify differentially expressed receptor genes in stroke-tissue compared to normal rat brain. We found 76 genes predominantly expressed in hypertensive rat stroke-tissue. These predominantly expressed genes included genes involved in energy metabolism, signal transduction/cell regulation, and replication/transcription/translation. For example, the T3 receptor alpha was predominantly expressed in stroke-tissue, indicating that regeneration of nerves in stroke tissue may be facilitated by increased T3 receptor alpha expression.

Animals↗

PubMed2004

Effect of sodium on blood pressure, cardiac hypertrophy, and angiotensin receptor expression in rats.

BACKGROUND: Sodium-induced hypertensive cardiac hypertrophy is related to pressure and volume overload. METHODS: Wistar rats were exposed to low and high sodium diet for 8 weeks. Angiotensin II receptor mRNA, abundance of p38 mitogen-activated protein kinase (p38MAPK), vasoconstriction of aortic rings, and angiotensin II-induced calcium increase were investigated. RESULTS: Rats on high sodium diet showed significantly elevated blood pressure. Heart weight, AT1 receptor mRNA in cardiac and aortic tissues, and abundance of p38MAPK were significantly increased in rats on high sodium diet. CONCLUSIONS: Increased AT1 receptor expression and angiotensin II-induced calcium increase are compensatory effects in sodium-induced hypertension.

Animals↗

PubMed2004

Effect of sodium on vasoconstriction and angiotensin II type 1 receptor mRNA expression in cold-induced hypertensive rats.

Angiotensin II and sodium play an important pathogenetic role in several models of hypertension. Now, we investigated the effects of sodium on vasoconstriction and angiotensin II type 1 (AT1) and type 2 (AT2) receptor mRNA expression in aortic vessels from cold-induced hypertensive rats. Wistar rats on low sodium and high sodium diet were exposed to cold-stress for 8 weeks. The effects of angiotensin II infusion on mean arterial blood pressure were investigated in these rats. In addition, angiotensin II induced contraction was measured using aortic rings. Expression of AT1 receptor mRNA and AT2 receptor mRNA was assessed in aortic vessels by reverse transcription polymerase chain reaction. After infusion of angiotensin II mean arterial blood pressure in cold-induced hypertensive rats on high sodium diet was significantly higher compared to cold-induced hypertensive rats on low sodium diet (p < 0.05). Angiotensin II-induced contraction of aortic rings was significantly higher in cold-induced hypertensive rats on high sodium diet compared to cold-induced hypertensive rats on low sodium diet (2.39 +/- 0.03 g vs. 2.21 +/- 0.04 g, n = 12, p < 0.01). Angiotensin AT1 receptor mRNA was significantly higher in cold-induced hypertensive rats on high sodium diet compared to cold-induced hypertensive rats on low sodium diet (p < 0.05). It is concluded that in this nongenetic, nonsurgical animal model of cold-induced hypertension increased vasoconstriction and increased AT1 receptor mRNA expression in aortic vessels are dependent on sodium intake.

Animals↗

PubMed2003

[Change of expression of cell/organs defense genes in brain tissue of rats with stroke-like episodes induced by complex environmental factors].

OBJECTIVE: To investigate the effect of environmental risk factors on the development of stroke. METHODS: With the use of cold-stimuli plus high-salt intake as environmental risk factors, a hypertension model with the complication of stroke was established in rats, then, a new technique, suppression subtractive hybridization (SSH), was used to identify the differential genes which specifically expressed in total cerebrum tissue of rat in each group. Comparison was made between control group and stroke group. RESULTS: By the application of SSH, a total of 576 clones were generated in this study from two subtractive libraries, among them 456 clones were usable and were analyzed. Genes for cell/organs defense were down-regulated in stroke group and metabolism transcripts were shown to be up-regulated (P<0.01). CONCLUSION: Cell/organs defense genes may play important roles in the development of stroke. The above findings suggested that environmental risk factors could genetically alter individual sensitivity to stroke.

Animals↗

PubMed2002

Endothelial dysfunction in cold-induced hypertensive rats.

Endothelial dysfunction can be observed in preatherosclerotic conditions. However, its pathogenetic role in hypertension is still controversial. Endothelial-dependent changes of blood pressure (BP) and expression of endothelial nitric oxide synthase (eNOS) were evaluated in cold-induced hypertensive rats. Wistar rats were exposed to cold stress for 8 weeks. Exposure to cold stress significantly increased the systolic BP in rats. The infusion of acetylcholine significantly lowered mean arterial BP in control rats by 48 +/- 2% and by 32 +/- 1% in cold-induced hypertensive rats. The acetylcholine-induced reduction of mean arterial BP was significantly attenuated in cold-induced hypertensive rats (control rats, 45 +/- 2 mm Hg; cold-induced hypertensive rats, 34 +/- 3 mm Hg; P < .05). Administration of N(G)-nitro-L-arginine-methyl ester for 1 week significantly increased BP in control rats, whereas no effect could be observed in cold-induced hypertensive rats. In cold-induced hypertensive rats eNOS in aortic vessels was significantly reduced compared to control rats. In this nongenetic, nonsurgical animal model of cold-induced hypertensive rats an endothelial dysfunction can be observed due to reduced eNOS.

Acetylcholine↗

PubMed2002

Angiotensin-(1-7) inhibits angiotensin II-induced signal transduction.

The inhibitory effects of angiotensin-(1-7) on angiotensin II-induced vasoconstriction, growth of vascular smooth muscle cells, stimulation of protein kinase C, extracellular signal-regulated kinases (ERK), and angiotensin subtype 1 receptor (AT1) and subtype 2 receptor (AT2) mRNA expression were investigated. The hemodynamic effects of angiotensin-(1-7) were measured in Wistar rats. Vasoconstriction was measured using aortic rings. DNA synthesis or protein synthesis was measured in cultured vascular smooth muscle cells using [3H] thymidine or [3H] leucine incorporation, respectively. Angiotensin II stimulated protein kinase C and ERK1/2 were measured by Western blot analysis using phosphospecific protein kinase C and ERK1/2 antibodies. AT1 and AT2 receptor mRNA expression was measured using reverse-transcription polymerase chain reaction. Infusion of angiotensin II significantly increased whereas infusion of angiotensin-(1-7) had no effects on mean arterial blood pressure in Wistar rats. Angiotensin-(1-7) dose-dependently showed partial antagonism on angiotensin II-induced contraction of aortic rings. Angiotensin-(1-7) showed partial antagonism on angiotensin II-induced DNA synthesis and protein synthesis. Angiotensin-(1-7) showed partial antagonism on angiotensin II-induced activation of protein kinase C and ERK1/2. The administration of angiotensin-(1-7) showed partial antagonism on angiotensin II-induced downregulation of AT1 receptor mRNA expression, whereas AT2 receptor mRNA expression was unchanged. Angiotensin-(1-7) showed partial antagonism on angiotensin II-induced intracellular signal transduction and may play a crucial role in the adaptation process of AT1 receptors to sustained stimulation of angiotensin II.

Angiotensin I↗

PubMed2002

[Gene expression of Ang II receptors in myocardium in congestive heart failure].

OBJECTIVE: To explore the relation among myocardial AT(1)-/AT(2)- receptor expression, myocardial remodeling and cardiac function in patients with congestive heart failure. METHODS: Pathologic and morphologic studies on myocardial tissue of 31 patients with CHF due to valvular heart disease and 5 control subjects were carried out with optical and electronic microscopy. Message RNA expression of and AT(1)-/AT(2)-receptors in myocardial tissue were analyzed using the reverse transcriptase-polymerase chain reaction. RESULTS: Pathological changes of myocardial tissue in CHF due to valvular heart disease showed typical myocardial remodeling. AT(1)-receptor mRNA expression was slightly increased in the patients with mild CHF than in the control subjects, but decreased in the moderate and severe CHF patients. No difference was observed in AT(2)-receptor mRNA expression among all the groups. CONCLUSIONS: The expression of AT(1)-receptor was up-regulated in mild CHF. Cardiomyocyte hypertrophy may be mediated by AT(1)-receptor. The expression of AT(1)-receptor was down-regulated in moderate and severe CHF. The do minant receptor subtype was transformed to AT(2). The significance of these alterations may be a local protective mechanism of myocardium. Cardiomyocyte apoptosis may be induced via AT(2)-receptor, leading to deterioration of cardiac function.

Adult↗