• Korean Journal of Ichthyology
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• v.12 no.1
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• pp.38-45
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• 2000

Depending on the fish species the vascular tone is distinctively regulated by numerous vasoactive substances. In most fish species the regulatory role of autonomic neurotransmitters and other vasoactive substances are not well defined. This research was designed to delineate the regulatory role of various endogenous autonomic neurotransmitters known to be important in mammalian vascular systems on isolated Israeli carp ventral aorta. Acetylcholine(ACh) contracted the aorta regardless of the pre-existing level of vascular tone, and the contraction was almost completely abolished by a cholinergic-muscarinic antagonist atropine. Endogenous, multiple receptor ($\alpha$ and $\beta$)-acting adrenergic agonist epinephrine (Epi) relaxed the vessel in the presence and absence of the pre-existing tones. Another endogenous multiple receptoracting agonist norepinephrine (NE) weakly contracted the aorta in non-preconstrcted state, but the response was reversed to relaxation when preconstricted. Isoproterenol, ${\alpha}\;{\beta}$ adrenergic receptor agonist, was a potent vasodilator whereas an ${\alpha}_1$ agonist phenyephrine was a contractor. The ${\alpha}_2$ adrenergic receptor agonist clonidine has not any significant effect in altering the vascular tone. The vasorelaxing action of Epi, NE and isoproterenol was significantly attenuated by $\beta$ receptor antagonist propranolol. These results imply that ACh may primarily play a contractor role via muscarinic receptor activation while adrenergic agonists, Epi and NE, are relaxants through activation of $\beta$ adrenergic receptors in vivo.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.189-195
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• 1988

This study aimed to investigate the autonomic innervations of human vas deferens and the effect of diazepam, a benzodiazepine sedative antianxiety drug, on the smooth muscle contractility of vas deferens. The specimens were obtained from healthy volunteers undergoing elective vasectomy with local anesthesia. The muscle preparation did not show any spontaneous contraction, but showed a good contraction induced by norepinephrine exerting the strongest response at $33^{\circ}C$. Phentolamine inhibited the norepinephrine-induced contraction concentration-dependently. Isoproterenol, a beta-adrenergic agonist evoked a considerable extent of contraction, and this contractile activity was antagonized by propranolol, a beta-adrenergic blocking agent. Acetylcholine induced a dashing contraction of the human vas deferens, and atropine, a muscarinic receptor blocking agent abolished the acetylcholine-induced contraction. Diazepam inhibited the norepinephrine-induced contraction in a concentration dependent manner. These results suggest that the smooth muscle of human vas deferens has cholinergic muscarinic and beta adrenergic receptors as well as the predominant alpha adrepergic receptor. Diazepam inhibits the motility, especially norepinephrine-induced contraction of human vas deferens.

• 대한임상약리학회:학술대회논문집
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• 2006.11a
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• pp.91-91
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• 2006

• Clinical and Experimental Pediatrics
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• v.50 no.6
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• pp.556-564
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• 2007

Purpose : We hypothesized that the persisting bronchial hyperresponsiveness (BHR) of adolescents with asthma remission may be controlled mainly by genetic factors, and the BHR of symptomatic asthma by airway inflammation. ${\beta}_2$-adrenoceptor gene is considered to be a candidate gene in the development of BHR. Thus, ${\beta}_2$-adrenoceptor gene polymorphism may be associated with the BHR of adolescents with asthma remission, but not with the BHR of symptomatic asthma. To evaluate this hypothesis, ${\beta}_2$-adrenoceptor gene polymorphism at 2 sites (Arg16-Gly, Gln27-Glu) were examined. Methods : Two hundred two adolescents with BHR ($PC_{20}<18\;mg/mL$) and long term remission (neither asthma-related symptoms nor medication during the previous 2 years) of their asthma (remission group), 182 adolescents with symptomatic asthma (symptomatic group), and 200 healthy adolescents (control group) were studied. Asthma phenotypes were determined using methacholine bronchial provocation test and skin prick test. Genotypes of ${\beta}_2$-adrenoceptor polymorphism were evaluated by PCR-based methods. Results : Gly/Gly allele and Gly16-Gln27 haplotype were more prevalent in the remission group than in the control group (P=0.01, P=0.02), although there was no difference between the symptomatic group and the control group. In the remission group, there was significant difference in geometric mean of $PC_{20}$ among the 3 groups subdivided by the number of Gly16-Gln27 haplotype, showing that the Gly16-Gln27 haplotype was positively associated with BHR. However, no association was found between Gly16-Gln27 haplotype and BHR in the symptomatic group. Conclusion : This study demonstrates that ${\beta}_2$-adrenoceptor polymorphism at amino acid 16 and 27 was associated with BHR persisting in adolescents with asthma remission.

• Journal of Yeungnam Medical Science
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• v.9 no.2
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• pp.382-395
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• 1992

GABA is an inhibitory neurotransmitter in central nervous system and produce sedative, antianxiety and muscle reaxing effects via $GABA_A$ receptor or $GABA_B$ receptor. Recently it is known that GABA is widely distributed throughout peripheral organs and may playa physiological role in certain organ. The vas deferens is innervated by species-difference. These study, therefore, was performed to investigate the mode and the mechanism of action of GABA on the norepiniphrine-, ATP- and electric stimulation-induced contraction of vas deferens of rat. Sprague-Dawley rats were sacrificed by cervical dislocation. The smooth muscle strips were isolated from the prostastic portion and were mounted in the isolated muscle bath. PSS in the bath was aerated with 95/5%-$O_2/CO_2$ at $33^{\circ}C$. Muscle tensions were measured by isometric tension transducer and were recorded by biological recording system. 1. GABA, muscimol, a $GAB_A$ agonist, and baclofen, a $GABA_B$ agonist inhibited the electric field stimulation(EFS, 0.2Hz, 1mSec, 80 V, monophasic square wave)-induced contraction with a rank order of potency of GABA greater than baclofen greater than muscimol. 2. The inhibitory effect of GABA was antagonized by delta aminovaleric acid(DAVA), a $GABA_B$ antagonist, but not by bicuculline, a $GABA_A$ mtagonist. 3. The inhibitory effect of baclofen was antagonized by DAVA, but the effect of muscimol was not antagonized by bicuculline. 4. Exogenous norepinephrine(NE) and ATP contracted muscle strip concentration dependently, but the effect of acetylcholine was negligible : and GABA did not affect the NE-and ATP-induced contractions. 5. GABA, baclofen and muscimol did not affect basal tone, and GABA did not affect the NE-and ATP-induced contractionsm 6. EFS-induced contraction was including 2 distinctable components. The first phasic component was inhibited by beta gamma-methylene ATP(mATP), a desensitizing agent of APT receptor and the second tonic component was reduced by pretreatment of reserpine(3 mg/Kg, IP). 7. GABA inhibited the EFS-induced contraction of reserpinized strips, but not the mATP-treated strips. These results suggest that in the prostatic portion of the rat vas deferens, adrenergic and purinergic neurotransmissions are exist, and GABA inhibits the release of ATP via presynaptic $GABA_B$ receptor on the excitatory neurons.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.83-92
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• 1988

Although the release of lysosomal enzymes from activated PMN leukocyte can be regulated by intracellular cyclic nucleotide levels, other responses of PMN leukocyte according to the binding of neurotransmitters to either ${\beta}$-adrenergic or muscarinic receptors are still not clarified. In addition, the function of PMN leukocyte mediated by ${\alpha}$-adrenergic receptors is uncertain. Atropine, phentolamine and propranolol inhibited calcium uptake, superoxide generation, NADPH oxidase activity and phagocytic activity in activated PMN leukocyte, whereas carbachol and isoproterenol slightly further stimulated the responses of activated cells. Either carbachol or isoproterenol stimulated superoxide generation was inhibited by their antagonists, atropine and propranolol, respectively. The response of activated PMN leukocyte was inhibited by chlorpromazine, verapamil and dantrolene but slightly stimulated by lithium. On the other hand, chlorpromazine and dibucaine did not affect NADPH oxidase activity. Atropine, phentolamine and propranolol suppressed the calcium dependent phagocytic activity. Thus, the results suggest that atropine, phentolamine and propranolol may inhibit superoxide generation in activated PMN leukocyte by the inhibition of calcium influx and by their direct action on the NADPH oxidase system which is associated with autonomic receptors.

• YAKHAK HOEJI
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• v.49 no.1
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• pp.44-50
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• 2005

The purpose of this study was to investigate the relationship between Trp64Arg polymorphism in the ${\beta}_3$-adrenergic receptor gene and complex phenotypes such as blood pressure, body compositions and bone parameters in young men about 20 years, and to collect the fundamental data in designing the exercise program. Eighty healthy young men including 41 controls and 39 athletes were recruited, Trp64Arg polymorphism in the ${\beta}_3$-adrenergic receptor gene was genotyped by PCR-RFLP method. By association study, there were no significance in genotype and allele frequencies of Trp64Arg polymorphism in the ${\beta}_3$-adrenergic receptor gene between controls and athletes, respectively (p>0.05). When the relationship between physiological parameters and Trp64Arg polymorphism in the ${\beta}_3$-adrenergic receptor gene was tested, this polymorphism was significantly associated with 3th lumber and left femoral neck Z-score values in controls (p<0.05), but these associations were not detected in athletic groups (p>0.05). It is likely that Trp64Arg polymorphism in the ${\beta}_3$-adrenergic receptor gene is a genetic marker for the bone mineral density index in young men, but environmental factors such as exercise modify the significant effect of this polymorphism. Thus, our results suggest that Trp64Arg polymorphism in the ${\beta}_3$-adrenergic receptor gene may be applicable as a predictive marker for osteoporosis in Korean young men, and regular exercise may prevent the disadventageous effect of this polymorphism for bone mineral density in male athletic group.

• Korean Journal of Veterinary Research
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• v.32 no.1
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• pp.41-49
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• 1992

Higenamine is an Aconiti tuber derived compound whose chemical structure is 1-(4'-hydroxybenzyl)-6, 7-dihydroxy-1, 2, 3, 4-tetrahydroisoquinoline containing catechol ring and tetrahydroisoquinoline nucleus in its own structure, both of which are well known to have agonistic effects on adrenergic receptors. Using guinea-pig atria(rich in ${\beta}_1$-receptor) and treachea(rich in ${\beta}_2$-receptor), we studied pharmacological actions of higenamine on these organs with special interest of its relevancy of ${\beta}$-receptor selectivity. In order to further clarify its pharmacological characteristics, the influncences of pretreatment of reserpine or cocaine were also investigated. The results were summarized as follows : 1. Higenamine had remarkable chronotropic, inotropic and bronchodilator effects in guinea-pig spontaneously beating right atria, left atria and trachea, in dose-dependent manners. 2. All of above actions were blocked competitively by propranolol, which shows nonselectivity of higenamine on ${\beta}$-receptor. $pA_2$ values of propranolol against higenamine were 7.93, 7.76 and 8.46 in guinea-pig right atria, left atria and treachea, respectively. 3. Reserpine pretreatment(5mg/kg, ip, 24h) did not show my decrease in pharmacological actions of higenamine, which suggests higenamine has direct action on ${\beta}$-receptor not via catecholamine release. 4. Cocaine pretreatment$(1{\mu}M)$ had no influence on pharmacological actions of higenamine in contrast with nor epinephrine, which suggests there is no neuronal uptake mechanism of higenamine in the studied organ preparations.

• Korean Journal of Oriental Medicine
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• v.5 no.1
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• pp.1-15
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• 1999

Chronic asthma is considered as an incurable disease in modern society. This study focused on development of an animal model for the chronic asthma to investigate new drugs from traditional herbal medicine. And we tested the animal model with a typical prescription, Chungsangboha-tang and tried to find biochemical markers such as catecholamines and cAMP in serum, and as densities of beta-receptor in lung tissues. SD rats were actively sensitized by exposure to ovalbumine (OA). Ten days after sensitization, rats were challenged with OA aerosol by nebulizer six times every three days. Mucin was increased in bronchoalveolar lavages (BALs) after antigen (OA) challenge. Serum concentration of epinephrine was decreased significantly although there were not changed much in serum concentration of cAMP and the densities of beta-receptor in lung tissues. Chungsangboha-tang (5 g/kg/day) was given orally to ovalbumin-sensitized rats (n=8) for 15 days. Mucin in bronchoalveolar lavages (BALs) was increased significantly after treatment of Chungsangboha-tang although concentrations of epinephrine and cAMP were not changed significantly. The densities of beta-receptor in lung tissues were not different from those of controls. These results suggest that the ovalbumin-sensitized rats can be a good animal model of chronic asthma and Chungsangboha-tang is a possible drug in the treatment of chronic asthma.

• The Korean Journal of Pharmacology
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• v.22 no.2
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• pp.96-104
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• 1986

Higenamine, dl-1-( 4-hydroxybenzyl)-6, 7-dihydroxy-1 ,2, 3 ,4-tetrahydroisoquinoline has been synthesized and evaluated for hemodynamic actions using rabbits under pentobarbital anesthesia. Concentration-related fall of mean blood pressure was observed, where diastolic blood presure was significantly lowered at 10 ug/kg/min or above (p<.05), while the systolic blood pressure was slightly increased or unaffected, thereby, causing increment of pulse pressure. No significant change was occured in heart rate, however, carotid artery blood flow was significantly (p<.05) increased. These actions were inhibited with pretreatment of 0.3 mg/kg of propranolol, beta-adrenoceptor antagonist, 5 minutes before infusion of higenamine indicating that higenamine compete with propranolol for the so-called beta adrenergic receptor. As comparison, the same procedure was applied to isoproterenol as well, where typical antagonism of propranolol against isoproterenol was shown. From these findings the vasodilating and diastolic blood pressure lowing effects could be explained in terms of cardiac beta stimulating action, however, dopamine receptor activation could not be excluded because no significant changes observed in chronotropism.