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H W Deng

Publications and source records attributed to H W Deng.

89 records · Page 5Linked to original sources
PubMed1996

Ischemic preconditioning mediated by calcitonin gene-related peptide in isolated rat hearts.

AIM: To study the mediating effect of calcitonin gene-related peptide (CGRP) in ischemic preconditioning in the isolated perfused rat heart. METHODS: Isolated rat hearts were subjected to 3 cycles of a 5-min ischemia and a 5-min reperfusion before a 30-min global ischemia followed by a 30-min reperfusion. RESULTS: Ischemic preconditioning caused an improvement of heart functions, reduced the incidence of ventricular arrhythmias and decreased the release of creatine kinase (CK) during reperfusion (CK activities = 0.30 +/- 0.07, 2.03 +/- 0.49, and 0.92 +/- 0.40 U.min-1/g wet wt for control, ischemia-reperfusion, and preconditioning, respectively). However, pretreatment with CGRP8-37 (0.1 mumol.L-1) abolished the improvement of cardiac contractivity, the reduction of the incidence of arrhythmias, and the inhibition of CK release by preconditioning (CK activities = 0.9 +/- 0.4 vs 2.55 +/- 0.32 U.min-1/g wet wt, P < 0.01). CONCLUSION: CGRP is an endogenous myocardial protective substance that played an important role in mediation of ischemic preconditioning.

Animals↗
PubMed1995

Effects of ginsenosides on vasodilator nerve actions in the rat perfused mesentery are mediated by nitric oxide.

This study was designed to explore the effect of ginsenosides, saponins from Panax ginseng, on the vasodilator nerve actions in the rat perfused mesentery and the mechanism of this effect. In the rat perfusion mesentery, when adrenergic nerves were blocked by guanethidine (5 x 10(-6) M) and vascular muscle tone was increased with methoxamine (5 x 10(-6)-10(-5) M), transmural field stimulation produced a frequency-dependent vasodilator response, which is due to the release of calcitonin gene-related peptide; ginsenosides significantly suppressed this vasodilator response in a concentration-dependent manner (3-30 micrograms mL-1). After pretreatment with saponin (50 micrograms mL-1, 3 min) to damage endothelial cells, this suppressing effect of ginsenosides was unaltered. However, the effect was abolished by N omega-nitro-L-arginine methyl ester (L-NAME) (10(-4) M), an inhibitor of nitric oxide synthesis and addition of L-arginine (3 x 10(-4) M) restored this suppressing effect. Methylene blue (10(-5) M), an inhibitor of guanylate cyclase, also abolished the suppressing effect of ginsenosides. However, ginsenosides did not alter the relaxation responses caused by exogenous calcitonin gene-related peptide administration. We conclude that ginsenosides can produce an inhibitory effect on the vasodilator response prejunctionally in the rat perfused mesentery and that this effect of ginsenosides may be mediated by nitric oxide released from non-adrenergic, non-cholinergic nerves.

Adrenergic Agents↗
PubMed1994

Protection of bradykinin on neonatal rat myocytes subjected to anoxia/reoxygenation injury.

This study was to investigate the effects of bradykinin (BK) on myocyte cultures. The effects of BK against lipid peroxidation and oxygen free radicals were estimated on an anoxia/reoxygenation injured model. A salicylate hydroxylation product dihydroxybenzoic acids (DHBA) was detected using HPLC with electrochemical detection, a sensitive device for assaying the hydroxyl free radical. BK (10 nmol.L-1) reduced thiobarbituric acid reactive substances (TBARS, from 1.94 +/- s 0.28 to 0.25 +/- 0.03 nmol/10(6) cells, n = 5, P < 0.01), lactate dehydrogenase (LDH) release (1.28 +/- 0.23 to 0.63 +/- 0.12 u.ml-1, n = 8, P < 0.01) and DHBA (60 +/- 5 to 44 +/- 12 nmol.L-1, n = 6, P < 0.01). These improvements were nullified by pretreatment with K86/4321 (1 mumol.L-1), a kind of BK receptor antagonist. Indometacin (Ind, 1 mumol.L-1) had a synergic action with BK to decrease the LDH release, but Ind (30 mumol.L-1) attenuated the protection of BK, while both LDH and TBARS were increased. The mechanism for protection of BK was ascribable to the activation of BK receptor, the inhibition of lipid peroxidation, and the decreased hydroxyl free radical formation.

Animals↗
PubMed1994

Protection of l-arginine against oxygen free radicals-injured rabbit aortic endothelium.

This study was to investigate the protective effect of l-arginine, a precursor of endothelium-derived relaxing factor (EDRF), against damages due to endogenous or exogenous oxygen free radicals (OFR) on the aortic endothelium. The superfusion cascade bioassay of rabbit thoracic aorta was used. Endogenous OFR were generated by diethyldithiocarbamate (DETC) to deplete the cytosolic Zn-Cu form of superoxide dismutase (SOD). Exogenous OFR were generated by electrolysis of Krebs' solution. Acetylcholine (ACh) was infused through the donor aortic segment and relaxation of detector aortic ring was used as an indicator of the release of EDRF. The content of malondialdehyde (MDA) in the donor aorta was assayed biochemically. Both DETC and electrolysis inhibited vasodilator responses to ACh and increased MDA content in the aortic segment. Inhibition of DETC was abolished by exogenous SOD. l-Arginine improved impairment of endothelium-dependent relaxation and reduced elevation of MDA content by DETC or electrolysis. These results suggest that l-arginine presents a protective effect of endothelium against damage due to endogenous or exogenous OFR, and that the protective effect of l-arginine may be correlated with reduction in lipid peroxidation.

Animals↗
PubMed1993

The regulatory effect of bradykinin on the actions of sensory nerves in the perfused rat mesentery is mediated by nitric oxide.

In the perfused rat mesentery, when adrenergic nerves were blocked with guanethidine and vascular smooth muscle tone was increased with methoxamine, transmural field stimulation caused a dilator response. Bradykinin significantly suppressed vasodilator responses to a transmural field stimulation in a concentration-dependent manner. After pretreatment with saponin to damage endothelial cells, bradykinin still suppressed vasodilator responses to transmural field stimulation. The effect of bradykinin was unaltered by indomethacin. N omega-Nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis, abolished the inhibition of vasodilator responses to transmural field stimulation elicited by bradykinin. However, in the presence of L-arginine and L-NAME the inhibitory effect of bradykinin reappeared. Furthermore, methylene blue itself caused potentiation of vasodilator responses to transmural field stimulation and reversed the effect of bradykinin. These findings suggest that bradykinin can produce an inhibitory modulation of the actions of sensory nerves in the perfused rat mesentery and that the effect of bradykinin may be mediated by nitric oxide released from non-adrenergic, non-cholinergic nerves.

Animals↗
PubMed1993

Nitric oxide modulates responses to sensory nerve activation of the perfused rat mesentery.

The modulatory actions of nitric oxide on sensory nerves were investigated on dilator responses of the perfused rat mesentery to transmural nerve stimulation. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis, caused a significant augmentation of vasodilator responses to transmural nerve stimulation, an effect which was abolished by L-arginine. L-NAME had no effect on vasodilator responses to exogenous calcitonin gene-related peptide. In preparations without endothelium L-NAME still caused potentiation of vasodilator responses to transmural nerve stimulation. Methylene blue, an inhibitor of guanylate cyclase, also significantly enhanced vasodilator responses to transmural nerve stimulation. After pretreatment with diethyldithiocarbamate to inhibit superoxide dismutase, vasodilator responses to transmural nerve stimulation were also potentiated. This response was abolished by exogenous superoxide dismutase. These findings suggest that endogenous nitric oxide modulates, in an inhibitory fashion, the actions of sensory nerves in the rat mesentery. The results also suggest that endogenous superoxide dismutase may participate in the regulation of the actions of sensory nerves via control of cellular superoxide anion level.

Animals↗
PubMed1992

Tetrandrine is not a selective calcium channel blocker in vascular smooth muscle.

The effects of tetrandrine (Tet) on the contractile properties of rat aortic ring preparations were studied to test the hypothesis that Tet is a Ca2+ antagonist acting on voltage-operated Ca2+ channels (VOC). The tests were performed on contractions induced by depolarizing concentrations of KCl and by alpha 1-adrenoceptor agonist, phenylephrine (Phe). These vascular effects of Tet were compared to those of nifedipine (Nif). We found that Tet behaved qualitatively similar to, but less potent than, Nif in that it inhibited KCl-induced contraction in a concentration-dependent fashion and its inhibitory effect was long-lasting. However, the effects on Phe-induced contraction of Tet was different from those of Nif in that the extracellular Ca(2+)-dependent contraction was inhibited by Tet, but not by Nif. Tet (60 mumol.L-1) completely inhibited the 45Ca2+ uptake induced by KCl and Phe in rat aortic muscle strips. When the aortic muscle contractile response was induced by addition of Ca2+ following depletion of intracellular stores by Phe in the presence of sarcoplasmic reticulum Ca(2+)-pump inhibitor, cyclopiazonic acid, Tet (60 mumol.L-1) was more effective than Nif 1 mumol.L-1 in inhibiting such a response to extracellularly added Ca2+. Furthermore, Tet, but not Nif, also significantly inhibited the contraction to Phe in Ca(2+)-free medium. Collectively, these results led us to conclude that Tet does not behave as a selective VOC blocker like Nif.

Alkaloids↗
PubMed1991

Cyclopiazonic acid is a sarcoplasmic reticulum Ca(2+)-pump inhibitor of rat aortic muscle.

The effects of a mycotoxin, cyclopiazonic acid (CPA), on the contractile function of rat aortic smooth muscle rings were investigated to test the hypothesis that CPA selectively inhibits the sarcoplasmic reticulum Ca(2+)-pump. This hypothesis was tested by two types of experimental approaches. First, we compared the ability of the vascular muscle rings to relax upon washout of the agonists following the contraction induced by high concentration of depolarizing KCl (60 mmol.L-1) and supramaximal concentration of phenylephrine (Phe; 10(-5) mol.L-1). In this case, we found that CPA treatment resulted in slowing the rate of relaxation to both stimuli. In the second approach, the status of Phe-sensitive intracellular Ca2+ pool was assessed by the ability of Phe to elicit sequential responses in Ca(2+)-free medium with loading of Ca2+ by reintroduction of extracellular Ca2+ in the presence and absence of CPA following the first response to Phe 10(-5) mol.L-1 and the washout of the agonist. We found that effective Ca2+ loading resulted in total restoration of the second response to Phe, while CPA treatment caused ineffective loading leading to ultimate prevention of the second response to Phe. Our finding are consistent with the hypothesis that CPA acts by inhibiting the SR Ca(2+)-pump, thus interfering an effective refilling of the agonist-sensitive intracellular Ca2+ stores.

Animals↗
PubMed1987

Protective effects of ginsenosides on anoxia/reoxygenation of cultured rat myocytes and on reperfusion injuries against lipid peroxidation.

Lactic acid dehydrogenases (LDH) release from cultured rat myocytes during anoxia and reoxygenation were significantly reduced by ginsenosides (G) and its components Rb+Ro, both in 83 micrograms/ml, but not by Rg. G in higher concentration (250 micrograms/ml) enhanced the LDH release. G and Rb+Ro both 8.3 micrograms/ml in the perfusate, also significantly reduced CPK release from isolated rat heart. Rb component 50 mg/kg protected rat myocardial infarct in vivo against lipid peroxidation signified by significant reduction of malondialdehyde (MDA) and increase of superoxide dismutase (SOD) in rat myocardium. It was concluded that G in adequate dose can protect myocyte anoxia and reoxygenation as well as reperfusion damage in isolated rat heart, and the mechanism of protection may partly attribute to its action on oxygen free radical formation and lipid peroxidation. The active components of myocardial protection are Rb+Ro, and not Rg.

Animals↗
PubMedDate not supplied

Role of calcitonin gene-related peptide in ischaemic preconditioning in diabetic rat hearts.

1. It has been suggested that calcitonin gene-related peptide (CGRP) is involved in the protection provided by ischaemic preconditioning in rat hearts and that ischaemic preconditioning is absent in diabetic rat hearts. 2. In the present study, we tested the relationship between sensory nerve function and ischaemic preconditioning in diabetic rats. 3. In 4- and 8-week diabetic rats and age-matched non- diabetic controls, 30 min global ischaemia and 40 min reperfusion caused a significant decrease in cardiac function and a marked increase in creatine kinase (CK) release. Ischaemic preconditioning, by three cycles of 5 min ischaemia and 5 min reperfusion, improved the recovery of cardiac function and decreased CK release during reperfusion in 4-week diabetic rat hearts. However, the cardioprotection afforded by ischaemic preconditioning was lost in 8-week diabetic rat hearts. Pretreatment with CGRP for 5 min also significantly improved the recovery of cardiac function and decreased CK release in rats subjected to 4 or 8 weeks of diabetes. 4. The content of CGRP in the coronary effluent during ischaemic preconditioning was significantly increased in 4-week diabetic rat hearts (P < 0.05). However, only a slight increase in the release of CGRP was shown in 8-week diabetic rat hearts (P > 0.05). 5. In summary, the present results suggest that the protection afforded by ischaemic preconditioning is attenuated in diabetic rats and that the change may be related to the reduction in CGRP release in diabetic rat hearts.

Animals↗
PubMedDate not supplied

Induction of alpha-calcitonin gene-related peptide mRNA expression in rat dorsal root ganglia by heat stress involves the heme oxygenase-1/carbon monoxide pathway.

SD rats were pretreated with whole body hyperthermia (rectal 42 degrees C) for 15 min. The level of calcitonin gene-related peptide (CGRP) in plasma, and alpha- and beta-CGRP mRNA as well as heme oxygenease-1 and heme oxygenase-2 mRNA in dorsal root ganglia were determined by radioimmunoassay and semi-quantitative reverse-transcription polymerase chain reaction, respectively. Heat stress induced only the expression of alpha-CGRP or heme oxygenease-1 but not beta-CGRP or heme oxygenase-2 mRNA, and the release of CGRP and induction of alpha-CGRP mRNA expression were abolished by pretreatment with Zinc protoporphyrin IX, the heme oxygenase inhibitor, or methylene blue, the inhibitor of soluble guanylate cyclase. These results indicate that induction of alpha-CGRP mRNA expression in rat DRG by heat stress involves the heme oxygenase-1/carbon monoxide pathway.

Animals↗
PubMedDate not supplied

Ethnic difference in osteoporosis-related phenotypes and its potential underlying genetic determination.

Osteoporosis is a serious health problem in both Caucasians and Asians. Caucasians and Asians are two distinct major ethnic groups, which may have differential genetic determination underlying complex genetic diseases such as osteoporosis. However, to date, there has been no systematic review focusing on the aspect of ethnic difference in risk to osteoporosis and its potential underlying genetic determination between Asians and Caucasians. Here, we firstly review diverse aspects of osteoporosis-related differences, including the differences of epidemiology of osteoporotic fractures, peak bone mass, bone loss, bone area, bone geometry and drug treatment response between Asians and Caucasians. Then, we provide some potential genetic evidence on the different heritability and inheritance mode of bone phenotypes, the different osteoporosis candidate genes and the differential results in related molecular studies between them, to explain the above osteoporosis-related phenotypic differences. The results suggest that the osteoporosis-related phenotypic differences between Asians and Caucasians may be partially the result of the different ethnic genetic background. The present review may increase our understanding of potential different mechanisms related to ethnicity in pathogenesis of osteoporosis for effective and potentially customized treatments in different major ethnic groups.

Adolescent↗