Study on six-minute walk test and cardiac output response against exercise in patients with chronic heart failure / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the significance of cardiac output (CO) response against exercise determined by IGR method and LVEF, 6 MWT distance in patients with chronic heart failure (CHF).</p><p><b>METHOD</b>To adopt 6 MWT, and before and after the test measuring the CO by the IGR method, furthermore, measure LVEF to 36 patients (heart failure group) with CHF, compare with the health groups (control group).</p><p><b>RESULTS</b>The 6MWT distance of heart failure group (333.00 +/- 49.64) m decrease compared with the control group (582.56 +/- 67.97) m (P < 0.01), moreover, the distance of NYHA class III (314.82 +/- 36.27) m is significantly shorter than II (361.57 +/- 55.42) m (P < 0.05). The LVEF of heart failure group (47.0 +/- 0.4)% reduce compared with the control group (66.9 +/- 5.2)% (P < 0.01), and the data of NYHA class III (43.3 +/- 10.3)% is significantly lower than II (52.8 +/- 7.6)% (P < 0.01). The increase in CO response against exercise of heart failure group (5.97 +/- 1.89) L/min decrease compared with control group (8.88 +/- 0.52) L/min (P < 0.01), furthermore, the value of NYHA class III (5.31 +/- 1.52) L/min, compared with II (7.01 +/- 1.98)L/min, is obviously lower (P < 0.01). The 6MWT distance correlates positively with the increase in CO response against exercise (r = 0.63, P < 0.01), but the correlation is not found between the increase CO response against exercise and the LVEF (r = 0.11, P > 0.05).</p><p><b>CONCLUSION</b>Our results show that CO response against exercise measured by IGR method, with the advantages of being noninvasive, safe, convenient and accurate, combining with the 6MWT can evaluate cardiac reserve in patient with CHF.</p>

G protein kinase 4gammaA142V overexpression induced hypertension by downregulating D1 receptors in transgenic mice / 中华心血管病杂志

<p><b>OBJECTIVE</b>Abnormalities in dopamine production and receptor function have been described in human essential hypertension and rodent models of genetic hypertension. We investigated the role of G protein kinase (GRK) 4gamma in essential hypertension in GRK4gamma mutant A142V transgenic mice.</p><p><b>METHODS</b>Blood pressure, renal sodium excretion, D(1) receptor protein expression and phosphorylation were measured in GRK4gammaA142V transgenic mice and control mice. Moreover, the effects of GRK4 inhibition by antisense oligonucleotides on D(1) receptor expressions were determined in HK-2 cells.</p><p><b>RESULTS</b>As compared with their control mice, GRK4gammaA142V transgenic mice had higher blood pressure, lower D(1) receptor expression (0.6 +/- 0.2 vs. 1.5 +/- 0.2, P < 0.05), higher D(1) receptor phosphorylation [(65 +/- 7) DU vs. (35 +/- 7) DU, P < 0.05] in renal cortical membranes and the diuretic and natriuretic effects after stimulation of renal D(1) receptor were impaired in GRK4gammaA142V transgenic mice. Inhibition of GRK4 expression (0.60 +/- 0.10 vs. 1.30 +/- 0.09, P < 0.05) by GRK4 antisense oligonucleotides upregulated D(1) receptor expression (1.5 +/- 0.2 vs. 0.8 +/- 0.1, P < 0.05) in HK-2 cells.</p><p><b>CONCLUSIONS</b>Our results show that GRK4gammaA142V overexpression induced hypertension is mediated by dowregulated renal D(1) receptor expressions in GRK4gammaA142V transgenic mice.</p>

Effects of insulin on the distribution of actins in vascular smooth muscle cells in the process of proliferation via mitogen-activated protein kinase in vitro / 生理学报

Proliferation of vascular smooth muscle cells (VSMCs) is often accompanied by changes in intracellular actin distribution. The changes are controlled by the signal transduction pathways of protein kinase C/mitogenic activated protein kinase (PKC-MAPK), but the mechanism is unclear. In order to study the effect of insulin on the intracellular signal transduction (PKC-MAPK) probably involved in the modulation of proliferation and redistribution of actins in the VSMCs, the DNA synthesis, MAPK activities and its gene expression, and the redistribution of intracellular actins were investigated in the isolated VSMCs of SHR pretreated with PKC inhibitor and/or insulin, respectively. We found that insulin treatment resulted in proliferation of the VSMCs and an increase in [(3)H] TdR incorporation. Meanwhile, the activities and expression of MAPK increased significantly compared to the control group. These effects of insulin were blocked by PKC inhibitor. In addition, insulin caused a redistribution of the intracellular actins in VSMCs, which was also inhibited by PKC inhibitor. It is, therefore, suggested that these effects of insulin on VSMCs proliferation and distribution of the intracellular actins may be mediated by the MAPK signal transduction pathway.