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Biomedical subjects

Q D Han

Publications and source records attributed to Q D Han.

At least 55 records · Page 3Linked to original sources
PubMed1995

Thrombin-induced neuropeptide Y secretion from rat platelets.

AIM: To study the thrombin-induced secretion of platelet neuropeptide Y (NPY) in rats. METHODS: The platelet aggregation induced by ADP or thrombin was recorded by an aggregometer. NPY in platelet and plasma was measured by radioimmunoassay. The intracellular free Ca2+ ([Ca2+]i) was measured by Fura-2 fluorescent assay. RESULTS: Thrombin 0.75 or 2.5 kU L-1 increased [Ca2+]i from 119 +/- 8 nmol L-1 to 530 +/- 60 or 1340 +/- 100 nmol L-1, respectively together with the secretion of platelet NPY. Edetic acid 2 mmol L-1 almost abolished the thrombin-induced increases of [Ca2+]i and reduced the NPY secretion by 56% and 30%, respectively. Neither [Ca2+]i increase nor platelet NPY secretion induced by thrombin was affected by verapamil. The thrombin-induced NPY secretion was inhibited by 55%-70% by indometacin or creatine phosphate plus creatine phosphokinase. CONCLUSION: Thrombin-induced platelet NPY secretion was related to an Ca2+ influx through non-voltage dependent Ca2+ channels and positive feedbacks of arachidonate metabolites or/and released ADP.

Adenosine Diphosphate↗
PubMed1995

[Mechanisms of mobilization of intracellular stored calcium].

The release of intracellular stored Ca2+ is mainly regulated by an inositol 1,4,5-triphosphate (IP3) receptor system and a ryanodine receptor system. The former induces Ca2+ release directly when the receptors are bound to IP3. The later may function through the Ca2+ induced Ca2+ release mechanism when the ryanodine receptors are activated. Cyclic ADP ribose, a metabolite of NAD+ which is regulated by complicated mechanisms, is one of the most important factors causing activation of ryanodine receptors. The two systems may interact with each other to regulate Ca2+ release from intracellular calcium pool.

Adenosine Diphosphate Ribose↗
PubMed1995

Alterations of subtypes of cardiac adrenoceptors in old rat.

AIM: To determine alterations of subtypes of myocardial adrenoceptors in senescence. METHODS: Heart membrane preparations were made from 3- and 25-month old Wistar rats. Alpha 1- and beta-adrenoceptors were measured by radioligand, 125I-BE2254 and 125I-pindolol, binding assays, respectively. RESULTS: In the old rat heart, alpha 1- and beta-adrenoceptor densities were declined from the young rats of 119 +/- 4 and 45.9 +/- 1.9 pmol L-1 to 70 +/- 6 and 36.4 +/- 1.6 pmol L-1 (P < 0.01), with a greater change in alpha 1-AR and in beta-AR. The ratio of alpha 1A/alpha 1B subtypes was decreased from the young rats of 39/61 to the old rats of 26/74 (P < 0.05). CONCLUSION: The cardiac adrenoceptors are decreased with different extents in the different subtypes in old rats.

Aging↗
PubMed1995

Differences of desensitization and hypersensitization between alpha 1A- and alpha 1B-adrenoceptors in rat isolated blood vessels.

AIM: To study the differences of the agonist-induced desensitization and the reserpinization-induced hypersensitization between alpha 1A- and alpha 1B-adrenoceptors (AR) mediated vasoconstriction. METHODS: The thoracic aortae, mesenteric, and renal arteries of rats were isolated. The cumulative-concentration response-curve (CCRC) of vasoconstriction for NE was recorded. NE activated only alpha 1-AR since the perfusing Krebs solution contained propranolol 1 mumol . L-1 and yohimbine 0.1 mumol . L-1 to block beta- and alpha 2-AR. CCRC for NE was made, preparations were pretreated with CEC 50 mumol . L-1 for then washed, and CCRC for NE was repeated. After i.p. reserpine 4 mg . g-1 i.p., the rats were killed, the thoracic aortae and renal arteries were taken, CCRC for NE was compared with the corresponding blood vessels in control rats. RESULTS: Pretreatment with CEC caused reductions of the NE-induced maximal constriction by 82.5 +/- 3.0% (P < 0.01) and 54.2 +/- 9.5% (P < 0.01) in thoracic aortae and mesenteric arteries, respectively, but no effect in renal arteries. Preincubation with NE caused the alpha 1-AR mediated-vasoconstriction diminished 14.4 +/- 5.9, 1.8 +/- 0.8 and 7.3 +/- 1.8 times in aortae, renal arteries, and mesenteric arteries, respectively. In reserpinized rats, the contraction in renal arteries induced by NE increased by 56%, but showed no change in aortae. CONCLUSION: Alpha 1B-AR mediated vasoconstriction is easier to be desensitized, while alpha 1A-AR mediated vasoconstriction is easier to be hypersensitized in rats.

Adrenergic alpha-Agonists↗
PubMed1995

[Effects of some physical and chemical factors on CGRP release from mesenteric arterial bed].

We have shown that calcitonin gene-related peptide (CGRP) is released into the circulation during endotoxin or hemorrhagic shock. In the present study, it was observed that low pH, elevated levels of lactic acid, hypertonic NaCl and hypertonic sucrose caused CGRP release from isolated mesenteric arterial bed (MAB) of rat. All the responses were blocked when MAB was pretreated with capsaicin. Ruthenium red, an inhibitor of Ca(2+)-induced Ca2+ release from intracellular Ca2+ pools, significantly inhibited the release of CGRP. In Ca2+ free medium, low pH, lactic acid and hypertonic solutions became no longer capable of inducing the release of CGRP. The above results suggest that the observed release of CGRP in MAB was mediated by capsaicin-sensitive sensory nerve endings, as a result of Ca(2+)-induced Ca2+ release from the intracellular Ca2+ store which is sensitive to ruthenium red.

Animals↗
PubMed1994

[Evaluation of plasma neuropeptide Y levels in patients with congestive heart failure].

Plasma neuropeptide Y (NPY) was measured by radioimmunoassay in 43 patients with congestive heart failure (CHF) and 20 healthy control subjects. The results showed that plasma NPY levels were elevated in patients with CHF compared with control subjects (366 +/- 28 ng/L VS. 89 +/- 22 ng/L, P < 0.001). There was a close relationship between the severity of CHF and plasma NPY levels. The severer the CHF, the higher the NPY level. In addition, 20 of the 43 patients with symptoms improved after treatment for heart failure were followed. The results indicated a significant decrease of plasma NPY levels (333 +/- 42 ng/L VS. 157 +/- 25 ng/L, P < 0.01) in these patients. Furthermore, multiple logistic regression analysis demonstrated that the presence and severity of CHF were related to plasma NPY levels significantly and independently. Because of its potent vasoconstrictive and negative cardiac inotropic effects, NPY might be involved in the pathophysiology of CHF. Plasma NPY levels might be taken as a prognostic indicator in patients with CHF, but further investigation is needed.

Adult↗
PubMed1994

[Effect of alpha 1-adrenoceptor subtypes on beta-adrenoceptor mediated positive inotropic response in rat left atria].

The distribution of the alpha 1-adrenoceptor (alpha 1-AR) subtypes and the effects of activation of alpha 1-AR subtypes on the beta-adrenoceptor (beta-AR) mediated positive inotropic response were investigated. The radioligand binding assays indicated that the Bmax and Kd values were 11.7 +/- 18 fmol/mg.protein and 86.0 +/- 9.6 pmol/L respectively. Pretreatment of the preparations with 20 mumol/L chloroethylclonidine (CEC) which inactivated alpha 1B subtype, decreased the Bmax to 45.7 +/- 5.2 fmol/mg.protein (P < 0.01). The inhibition curves of 5-methyl-urapidil were best fitted to two site model and indicated that alpha 1A subtype took 28.5% of total 125IBE specific binding sites. In the functional experiments, norepinephrine (NE) induced a positive inotropic response in a concentration dependent manner by activation of both beta- and alpha 1-AR. The concentration-response curves (CRC) for NE were shifted rightward after the pretreatment of the preparations with 20 mumol/L CEC, but leftward in the presence of 1 nmol/L WB4101. In the presence of 10 mumol/L phentolamine which inactivated both alpha 1-AR subtypes, the CRC for NE were shifted leftward. When alpha 1-AR was activated by phenylephrine the CRC for isoproterenol (selective beta-AR agonist) were shifted rightward. The results suggested that the alpha 1B subtype enhanced while the alpha 1A subtype inhibited the beta-AR mediated positive inotropic response. When both alpha 1A and alpha 1B subtypes were activated simultaneously the alpha 1A subtype showed a dominate role.

Animals↗
PubMed1994

[Neuropeptide Y reduces desensitization of alpha 1-adrenoceptors in rat blood vessels].

Vasoconstrictive responses to norepinephrine (NE) in isolated rat aorta and renal artery were respectively taken to represent the biological responses mediated by alpha 1B and alpha 1A subtype adrenoceptor (AR). After blood vessels were incubated with 10 mumol/L NE for 2 h, alpha 1-AR mediated vasocontraction was desensitized significantly, alpha 1B-AR being more marked than alpha 1A-AR. In the presence of 0.5 mumol/L neuropeptide Y (NPY), desensitization of alpha 1B-AR was attenuated significantly. In rat aorta the NE-mediated contraction comprised both phasic and tonic elements. After the incubation with NE, the phasic contraction period was prolonged but magnitude decreased, while no change was found for the tonic contraction. In the presence of NPY, the changes of phasic contraction caused by NE preincubation disappeared. It is suggested that retardation and reduction of intracellular Ca2+ release were involved in the mechanism for desensitization of alpha 1B-AR.

Animals↗
PubMed1993

A new alpha 1-adrenergic receptor subtype with low affinity for 5-methyl-urapidil but insensitive to chlorethylclonidine.

In the present study, we found that a novel alpha 1-adrenergic receptor subtype existed in rat heart by radioligand binding assay. This new alpha 1-adrenergic receptor subtype was different from alpha 1A-, alpha 1B-, alpha 1C-, and alpha 1D-subtypes reported recently. It had high affinity for WB4101, as the same of alpha 1A-subtype, but low affinity for 5-methyl-urapidil, and was insensitive to chlorethylclonidine.

Adrenergic alpha-Antagonists↗
PubMed1993

[Platelet neuropeptide Y and its vasoconstriction effect in rat].

Specific radioimmunoassay showed that in rat neuropeptide Y (NPY) immuno-reactivities (IR) in platelets and platelet rich plasma (PRP) were respectively 90 +/- 16 ng/10(7) platelets and 93 +/- 19 ng/ml. Both values were much greater than those in the plasma (1.2 +/- 0.1 ng/ml, P < 0.001) and platelet poor plasma (PPP) (1.7 +/- 0.3 ng/ml, P < 0.001). The NPY-IR in rat platelets eluted at the same position as authentic NPY on reverse phase HPLC. The NPY-IR in the platelets prepared from the PRP aggregated maximally by collagen reduced to 34 +/- 5 ng/10(7) platelets, while the NPY-IR in the PPP prepared from the same PRP increased to 26 +/- 4 ng/ml. PPP 1.6 ml prepared from the aggregated PRP induced contraction of isolated rat caudal arteries with the maximal tension of 380 +/- 80 mg; while the maximal contraction induced by 1.6 ml of the same PPP pretreated with NPY anti-serum was only 190 +/- 40 mg (P < 0.001). Authentic NPY 1 nmol/L did not cause any contraction. The results indicate that rat platelets contain a high concentration of NPY, which can be released during irreversible platelet aggregation. The NPY released can potentiate vasoconstriction responses induced by co-released substances during platelet aggregation.

Animals↗
PubMed1993

[Effects of anoxia and reoxygenization on the vascular contraction induced by two subtypes of alpha 1-adrenergic receptor].

The changes of the contraction induced by activation of alpha 1-adrenergic receptors during anoxia and reoxygenization were observed in isolated rat renal arteries (containing mainly alpha 1A), aortae (containing mainly alpha 1B) and pulmonary arteries (containing both alpha 1A and alpha 1B). In the renal arteries, pD2 values were increased and the maximal contractile responses were decreased during anoxia, which could be recovered 60 min after reoxygenation. In the aorta, pD2 values were decreased and the maximal responses were unchanged during anoxia, but did not return to normal 60 min after reoxygenization. The pulmonary arteries showed both the changes of renal arteries and of aorta. The results suggest that the changes during anoxia and reoxygenization are different in the different subtypes of alpha-adrenergic receptor.

Animals↗
PubMed1992

[Changes of subtypes of alpha 1-adrenoceptor in blood vessels of spontaneously hypertensive rats].

The two subtypes of alpha 1-adrenoceptors in blood vessels were compared between stroke prone spontaneously hypertensive rats (SHRSP) and WKY rats in vitro and in vivo. Pretreatment with 50 mumol/L chlorethylclonidine (CEC) for 30 min decreased the maximal contractions induced by norepinephrine (NE) to 31.4 +/- 8.3% and 35.2 +/- 2.9% (aortae); 68.4 +/- 8.2% and 80.1 +/- 7.2% (renal arteries); 68.4 +/- 6.3% and 5.4 +/- 7.0% (mesenteric arteries) of the controls in the SHRSP and the WKY rats, respectively. All the differences between the SHRSP and WKY rats were not statistically significant. In contrast, the blocking effects of nifedipine were much stronger in the SHRSP rats than those in the WKY rats. In the presence of 10 mumol/L nifedipine the maximal contractions induced by NE were decreased to 3.1 +/- 1.5% and 56.5 +/- 4.8% (P < 0.01, aortae); 9.0 +/- 4.1% and 23.6 +/- 3.5% (P < 0.05, renal arteries); 5.9 +/- 2.5% and 28.0 +/- 0.8% (P < 0.01, mesenteric arteries) of the controls in the SHRSP and the WKY rats, respectively. The experiment in vivo also showed that the effects of nifedipine on decreasing basal blood pressure and on antagonizing phenylephrine were increased in the SHRSP rats, as compared to the WKY rats. Analyses of two components of the contractions induced by 10 mumol/L NE in aortae demonstrated that both phasic and tonic contractions were mainly caused by activations of the alpha 1B subtype. There were no significant differences of blocking effects of nifedipine on the phasic contractions between the SHRSP and WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Alpha adrenoceptor subtypes in smooth muscles of rat pulmonary artery].

The contributions of subtypes of alpha-adrenoceptor to contraction induced by agonists were studied in smooth muscles of isolated rat pulmonary arteries. The results showed that the antagonizing effects of prazosin on the contraction induced by norepinephrine (NE) or phenylephrine (Phe) were more potent than those of yohimbine. The effect of prazosin against Phe was more potent than against NE, and yohimbine was just the reverse. Preincubation of preparations with chlorethylclonidine (CEC) 50 mumol.L-1, after which only alpha 1A adrenoceptors were left, reduced the vascular contraction induced by NE to 36% of the control (P < 0.01). While in the presence of nifedipine 10 mumol.L-1, during which only the responses of alpha 1B adrenoceptors were left, the contraction was weakened to 70% (P < 0.05). The pKA values of alpha 1A subtype (3.37 +/- 0.34) were smaller than those of alpha 1B (6.64 +/- 0.40, P < 0.01). But the values of KA/EC50 were much higher in alpha 1A than those in alpha 1B. The results suggest that in smooth muscle of rat pulmonary artery both alpha 1 and alpha 2 adrenoceptors exist, but alpha 1 is superior functionally. Both subtypes of alpha 1 adrenoceptor are involved in the contraction induced by NE. Compared with alpha 1B subtype, alpha 1A subtype has a lower affinity but a more reserve and a higher efficacy for NE.

Animals↗
PubMed1991

[Changes of alpha 1-adrenoceptor and its subtypes in blood vessels of old rats].

Differences in the vascular alpha 1-adrenoceptor reserve and alpha 1a to alpha 1b subtype ratio between old (18 months) and young (3 months) rats were investigated by both in vitro and in vivo experiments. For the in vitro experiments, ring preparations of blood vessels with endothelium removed were prepared and were perfused with Kreb's solution. Antagonists for alpha 2- and beta-adrenoceptors were put in perfusate in order that norepinephrine (NE) could only activate alpha 1-receptor. The results showed that, in comparison with young rats, the maximal contractions induced by NE in aorta, renal arteries and mesenteric arteries isolated from old rats were not changed but the concentration-response curves were shifted to the right. Functional dissociation constant KA for NE was not changed but the ratio of KA to EC50 was decreased. In the aortae and mesenteric arteries from old rats, the blocking effect of chlorethylclonidine (CEC, selective alpha 1b-subtype antagonist) on NE-induced contraction was decreased significantly, while the effect of nifedipine (selectively blocks the response of alpha 1a-subtype) was increased. The in vivo experiments showed that the effect of nifedipine in lowering blood pressure was stronger in the old rats than in the young rats, while following administration of nifedipine, the effect of phenylephrine in raising blood pressure was weaker. These results indicate that, in comparison with the young rats, the alpha 1-adrenoceptor reserve is decreased and the ratio of alpha 1a-subtype to alpha 1b subtype is increased in blood vessels of old rats.

Aging↗
PubMed1991

[Antiinflammatory drugs inhibit the elevation of plasma CGRP concentration in endotoxin shock in rats].

In the present study, we observed the effects of indomethacin, ibuprofen, naloxone and morphine on plasma CGRP concentration 3 h after endotoxin shock in conscious rats. The results showed that indomethacin, ibuprofen and naloxone significantly inhibited the elevation of plasma CGRP concentration as well as reduced the lesion in the intestine during endotoxin shock. However, morphine had no significant effect. The data are consistent with our hypothesis that prostaglandin, as one of the inflammatory mediators which increase in shock may be an important endogenous factor for triggering the CGRP release during endotoxin shock.

Animals↗