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Chao-Shu Tang

Publications and source records attributed to Chao-Shu Tang.

71 records · Page 4Linked to original sources

Role of I1-imidazoline receptors within the caudal ventrolateral medulla in cardiovascular responses to clonidine in rats.

Although it is recognized that imidazoline receptors play an important role in the central regulation of cardiovascular activities, little is known about their role in the caudal ventrolateral medulla. In male Sprague-Dawley rats anesthetized with urethane, we used antagonists of I1-imidazoline receptor or alpha2-adrenoceptor to assess the function of these receptors in the caudal ventrolateral medulla in controlling the cardiovascular effects of clonidine. Unilateral microinjection of clonidine (6 nmol/50 nl) into the caudal ventrolateral medulla significantly (P<0.01) increased blood pressure and the discharge of the rostral ventrolateral medulla presympathetic neurons, while heart rate remained unchanged. Microinjection of yohimbine (a selective alpha2-adrenoceptor antagonist, 500 pmol/50 nl) into the caudal ventrolateral medulla did not modify blood pressure, heart rate, or the discharge of the rostral ventrolateral medulla presympathetic neurons, and failed to attenuate the local caudal ventrolateral medulla clonidine-induced blood pressure elevation. However, unilateral microinjection of idazoxan (a mixed antagonist of imidazoline receptor and alpha2-adrenoceptor, 2 nmol/50 nl) into the caudal ventrolateral medulla significantly (P<0.01) decreased mean arterial pressure, heart rate, and the discharge of the rostral ventrolateral medulla presympathetic neurons, and completely abolished the pressor effect of clonidine. In addition, bilateral microinjection of idazoxan (4 nmol in 100 nl for each side) into the caudal ventrolateral medulla effectively (P<0.01) blocked the depressor effects of clonidine administered intravenously (5 and 50 microg/kg). These results confirm that I1-imidazoline receptors within the caudal ventrolateral medulla are involved in maintaining the tonic cardiovascular activities and in the pressor effect of clonidine in the caudal ventrolateral medulla. In addition, it seems that the caudal ventrolateral medulla plays an important role in the antihypertensive effects of systemically administered clonidine in rats.

Action Potentials↗

Effect of ghrelin on septic shock in rats.

AIM: To study the role of ghrelin in the late stage of septic shock in rats. METHODS: The rat model of septic shock was made by caecal ligation and perforation. At the time of operation ghrelin 10 nmol/kg was infused through femoral vein followed by a sc injection at 8 h after operation. Hemodynamic parameters including heart rate (HR), mean arterial blood pressure (MABP), LVdp/dtmax, and left ventricular end-diastolic pressure (LVEDP) in survival rats were measured at 18 h after surgery. Plasma glucose and lactate concentrations, plasma ghrelin level and myocardial ATP content were assayed. The mortality rate in rats with septic shock was also observed. RESULTS: Compared to that of septic shock group, MABP of rats in ghrelin-treated group increased by 33 % (P <0.01). The values of +LVdp/dtmax and -LVdp/dtmax increased by 27 % and 33 %, respectively (P <0.01), but LVEDP decreased by 33 % (P < 0.01). The plasma glucose concentration and myocardial ATP content increased by 53 % and 22 %, respectively, but plasma lactate concentration decreased by 40 % in ghrelin-treated rats (P < 0.01). The plasma ghrelin level in rats with septic shock was 51 % higher than that of rats in sham group, and was negatively correlated with MABP and blood glucose concentration (r=-0.721 and -0.811, respectively, P <0.01). The mortality rates were 47 % (9/19) in rats with septic shock and 25 % (3/12) in rats of ghrelin-treated group, respectively. CONCLUSION: Treatment with ghrelin could correct partly the abnormalities of hemodynamics and metabolic disturbance in septic shock of rats.

Adenosine Triphosphate↗

Non-NMDA receptors within caudal ventrolateral medulla are involved in transmission of baroreflex of rats.

AIM: To investigate the role of non N-methyl-D-aspartate acid (non-NMDA) receptors within the caudal ventrolateral medulla (CVLM) in mediating the baroreflex. METHODS: In urethane-anesthetized, paralyzed, and artificially ventilated rats, the effects of 6-cyano-7-nitroquinoxaline-2,3-dinoe (CNQX, a selective non-NMDA receptors antagonist) locally injected into the CVLM on the depressor responses evoked by aortic nerve stimulation and the barosensitivity of the rostral ventrolateral medulla (RVLM) barosensitive neurons were observed. RESULTS: Bilateral microinjection of CNQX (200 pmol in 100 nL for each side) into the CVLM significantly (P<0.01) increased the blood pressure (BP) and heart rate, and markedly (P<0.01) attenuated the depressor response to the aortic nerve stimulation. CNQX (200 pmol in 100 nL) unilaterally injected into the CVLM significantly (P<0.01) increased the firing rate of the ipsilateral RVLM barosensitive neurons and reduced the inhibitory responses of neurons evoked by stimulation of aortic nerve and elevation of BP, and partially inhibited the neuronal cardiac cycle-related rhythm. CONCLUSION: The CVLM played an important role in maintaining the tonic excitatory cardiovascular activities and transmitting the baroreceptor information via activation of non-NMDA receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Dysfunction of myocardial and vascular taurine transport in spontaneously hypertensive rats.

The alterations of taurine transport and the expression of taurine transporter (TAUT) mRNA in myocardium and aortic wall were investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. It was demonstrated that plasma taurine concentration and taurine release from myocardium and aortic wall in SHR were higher than those in WKY rats, whereas taurine content, taurine uptake and TAUT mRNA in myocardium and aortic wall of SHR were lower than those of WKY rats. In SHR, the maximal velocity (V(max)) of taurine transportation in myocardium and aortic wall was lower by 24% (P<0.05) and 35% (P<0.05) than that in WKY, their michaelis constants (Km) values were higher by 16% (P<0.05) and 39% (P<0.05), respectively. The results suggest that there is dysfunction of taurine transport in myocardium and aortic wall in SHR, which may be partly resulted from the decrease of TAUT activity and affinity, and down-regulation of TAUT gene expression.

Animals↗

[Effect of urotensin II on the nitric oxide production in neonatal rat cardiomyocytes].

The aim of this study was to investigate the effect of urotensin II (U II) on the nitric oxide (NO) production in cultured neonatal rat cardiomyocytes. The endothelial nitric oxide synthase (eNOS) mRNA expression was assessed by semi-quantitative reverse transcription-polymerase chain reaction. The activity of nitric oxide synthase (NOS) and NO content in cardiomyocytes were measured. The current results showed that U inhibited eNOS mRNA expression, the NOS activity and the NO production of cardiomyocytes. U II (0.1 micromol/L) inhibited the NOS activity and the NO production in cardiomyocytes in a time-dependent manner. These results suggest that the cardiovascular effect of U II might be partially associated with NO production in cultured neonatal rat cardiomyocytes.

Animals↗

[Changes in adrenomedullin and receptor activity-modifying protein 2 mRNA in myocardium and vessels during L-NNA-induced hypertension in rats].

To explore the changes in adrenomedullin (ADM) and receptor activity-modifying protein 2 (RAMP2) mRNA in myocardium and vessels in hypertension, a hypertensive rat model was prepared by administering L-NNA. Contents of ADM in plasma, myocardium and vessels were measured by radioimmunoassay (RIA). The levels of pro-ADM mRNA of myocardium and vessels were determined by competitive quantitative RT-PCR. The results showed that L-NNA induced hypertension and cardiomegaly. The ratio of heart to body weight increased by 35.5% (P<0.01). In hypertensive rats the ir-ADM in plasma, myocardium and vessels was increased by 80%, 72% and 57% (P<0.01), respectively compared with the control. The amounts of ADM mRNA in myocardium and vessels were increased by 50% and 109.2% (P<0.05), respectively, and the amounts of RAMP2 mRNA was increased by 132% and 87% (P<0.01), respectively, compared with control. The levels of ADM in myocardium and vessels were positively correlated with RAMP2 mRNA, the correlation coefficients were 0.741 and 0.885 (P<0.01), respectively. The results obtained indicate that in hypertensive rats, ADM is elevated in plasma, myocardium and ves-myocardium and vessel, and ADM and RAMP2 mRNA are up-regulated in myocardium and vessel. The ADM/RAMP2 system may play an important role in the pathogenesis of hypertension.

Adrenomedullin↗

Cardiovascular effects of urotensin II in different brain areas.

It has been shown that intracerebroventricular injection of urotensin II (UII)-induced hypotensive and bradycardiac responses. Here, we tested the cardiovascular roles of UII in different brain areas by microinjection of UII into the A1 and A2 areas (noradrenergic cells found in the lower part of the medulla that have been designated either A1 or A2 areas), the paraventricular and the arcuate nucleus. In urethane-anaesthetized rats, we observed that: (1) microinjection of UII into the A1 area induced dose-related depressor and bradycardiac responses; (2) mean arterial blood pressure (mABP) and heart rate (HR) did not change significantly after microinjection of UII into the A2 area; and (3) significant increases in mABP and HR were induced after microinjection of 10 pmol UII into either the paraventricular or arcuate nucleus. The above results suggest that UII, in different brain areas, plays different roles in cardiovascular regulation and the A1 area is a very important action site for UII in cardiovascular regulation.

Animals↗

Probucol inhibits oxidized-low density lipoprotein-induced adhesion of monocytes to endothelial cells in vitro.

AIM: To investigate the mechanism by which probucol (PBC) affected adhesion of monocytes to human umbilical vein endothelial cells (HUVEC). METHODS: Effects of PBC on expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), P-selectin, a nd E-selectin in human umbilical vein endothelial cells were examined. Moreover, the inhibitory effect of PBC were compared with that of monoclonal antibodies (mAbs) to ICAM-1, VCAM-1, P-selectin, and E-select in on adhesion induced by oxidized-low density lipoprotein(Ox-LDL). RESULTS: PBC at 10 to 80 micromol/L inhibited Ox-LD L-induced adhesion index from 16.7 % to 7.0 % (P < 0.01) and Ox-LDL-induced expression of ICAM-1 (75 %) and P-selectin (72 %). mAbs to ICAM -1 or P-selectin, when used alone, could only slightly reduce the adhesion of monocyte to HUVEC. When both monoclonal antibodies were used in combination, the adhesion was markedly inhibited from 16.7 % to 11.3 % (P < 0.01), but the effect was still weaker than that of PBC (average 9.3 %). CONCLUSION: PBC exerts its inhibitory effect on the adhesion of monocyte to HUVEC by inhibiting the expression of ICAM-1 and P-selectin.

Anticholesteremic Agents↗

Changes of plasma adrenomedullin and proadrenomedullin N-terminal 20 peptide concentrations in patients with heart failure.

OBJECTIVE: To study the changes in plasma adrenomedullin (ADM) and proadrenomedullin N-terminal 20 peptide (PAMP) concentrations and their clinical significance in the pathological process of congestive heart failure (CHF). METHODS: Plasma ADM and PAMP concentrations in 45 patients with CHF (according to the functional classification of New York Heart Association, NYHA) and 20 control subjects were measured by specific radioimmunoassay. RESULTS: Plasma ADM concentrations were 51.464+/-.52 pg/ml and 70.39+/-3.22 pg/ml respectively in patients of NYHA class II and class III, which were significantly higher than those in control subjects (24.12+/-1.59 pg/ml, P<0.05 for both comparisons), while significant differences in plasma PAMP concentrations were not identified in the 2 groups of patients (6.24+/-1.71 pg/ml and 7.38+/-1.28 pg/ml, respectively) in comparison with the control level(8.56+/-2.44 pg/ml, P>0.05 for both comparisons). Patients of NYHA class IV, when compared with the 2 groups of patients mentioned above, had significantly decreased plasma ADM and PAMP concentrations (36.33+/-2.17 pg/ml and 2.79+/-0.89 pg/ml respectively, P<0.05 in both cases), but had higher plasma ADM and lower PAMP concentrations when compared with the control subjects, (P<0.05 respectively). CONCLUSION: The changes of plasma ADM and PAMP concentrations at different stages of CHF indicate intramolecular regulation disturbances of vasodilator peptides of proadrenomedullin, and ADM may play a more important role in the development of CHF.

Adrenomedullin↗

Dysfunction of myocardial taurine transport and effect of taurine supplement in rats with isoproterenol-induced myocardial injury.

AIM: To study the alterations of myocardial taurine transport function, taurine transporter (TAUT), and cysteine sulfinate decarboxylase (CSD) mRNA as well as effect of exogenous taurine in rats with isoproterenol (ISO)-induced cardiomegaly. METHODS: [3H]-Taurine uptake and release on myocardium were determined. Binding sites of [3H]-taurine for myocardial sarcolemma were measured. TAUT and CSD mRNA levels were assayed using competitive quantitative reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: ISO group as compared with control group, myocardial taurine uptake markedly reduced, taurine release obviously increased; Bmax value of [3H]-taurine binding on cardiac sarcolemma reduced by 42% (P<0.05); TAUT and CSD mRNA levels decreased by 40% and 38% (P<0.05), respectively. ISO+taurine group as compared with ISO-treated group, the amounts of taurine uptake and TAUT mRNA returned to normal; taurine release reduced; Bmax increased by 92% (P<0.01), and CSD mRNA content augmented by 23% (P<0.05). There were no statistical differences of Kd values among the four groups (P>0.05). CONCLUSION: The data indicate that the failure to generate sufficient TAUT on myocardial sarcolemma may be the fundamental abnormality in ISO-induced cardiac injury. The mechanism by which administration of taurine considerably improves ISO-induced cardiac damage is probably to increase the expression of TAUT gene and recover taurine transport function.

Animals↗

Group II Phospholipase A(2) Activity and Its Molecular Regulation in Rat Heart during Sepsis.

Changes of activity and content of myocardial group II phospholipase A(2) and its mRNA transcription and stability during rat sepsis were investigated. Results showed that, compared with control group,myocardial group II phospholipase A(2) activity in early and late sepsis decreased by 25.0%(P<0.05) and increased by 47.6%(P<0.01),respectively group II phospholipase A(2) protein concentration reduced by 27.0% and augmented by 48.0%(P<0.01),respectively. Myocardial group II phospholipase A(2) mRNA transcription rate and content showed similar two-phases changes. The mRNA transcription rate during early and late sepsis decreased by 45.0% and increased by 70.0%(P<0.01),respectively. The mRNA content decreased by 34.1% in early sepsis and increased by 157.0% in late sepsis(P<0.01), respectively. The half-life of group II phospholipase A(2) mRNA remained unchanged notably during early and late stage of sepsis. These data suggest that myocardial group II phospholipase A(2) activity decreased in early stage of sepsis and increased in its late stage, and these changes were regulated transcriptionally.

Journal Article↗

A Study of the Myocardial Nuclear Calcium Transport of Rabbit in vitro.

The characteristics of nuclear calcium regulation were investigated in isolated rabbit myocardial nuclei. It was found that calcium concentration in myocardial nuclei was 2.6 fold more than that in myocardial homogenate (P<0.O1), and the nuclear calcium content was only l/6 of the total cellular calcium. Ca-ATPase of myocardial nuclei was [Ca(2+] and [ATP] dependent. [Ca2+] dependent K(a) and V(max) at 2.O mmol/L [ATP] were 226 nmol/L and 3 460 nmol/(h.mg) protein respectively. [ATP] dependent K(m) value and V(max) at 400 nmol/L [Ca2+] were 376.5 &mgr;mol/L and 2 445 nmol/(h.mg) protein respectively. A positive correlation between nuclear 45)Ca2+ transport and Ca-ATPase activity was observed (r=O.945, P<0.01). The above result suggests that myocardial nuclei are able to transport calcium actively. The pathophysiological role of myocardial nuclear calcium transport should be further determined.

Journal Article↗

Changes of Myocardial Muscarinic Receptor during Septic Shock of the Rat.

The present study reports the structural and functional changes of myocardial muscarinic receptor during early and late septic shock, Septic shock was induced by caecum ligation and puncture (CLP). The results showed that the number of M receptor on sarcolemma (SL) increased and that on the light vesicle (LV) decreased during early septic shock. The (3)H-QNB binding of M receptor on SL increased by 33.37%. By contrast during late septic shock, the number of M receptor on LV increased and that on SL decreased. The (3)H-QNB binding of LV M receptor was increased by 29.26%. At the same time phosphorylation of the M receptor was decreased during early septic shock and increased during late septic shock. These results suggest that the changes of M receptors may be related to the myocardial dysfunction during septic shock.

Journal Article↗