• 대한핵의학회지
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• 제38권5호
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• pp.331-337
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• 2004

Cardiac neurotransmission imaging allows in vivo assessment of presynaptic reuptake, neurotransmitter storage and postsynaptic receptors. Among the various neurotransmitter, I-123 MIBG is most available and relatively well-established. Metaiodobenzylguanidine (MIBG) is an analogue of the false neurotransmitter guanethidine. It is taken up to adrenergic neurons by uptake-1 mechanism as same as norepinephrine. As tagged with I-123, it can be used to image sympathetic function in various organs including heart with planar or SPECT techniques. I-123 MIBG imaging has a unique advantage to evaluate myocardial neuronal activity in which the heart has no significant structural abnormality or even no functional derangement measured with other conventional examination. In patients with cardiomyopathy and heart failure, this imaging has most sensitive technique to predict prognosis and treatment response of betablocker or ACE inhibitor. In diabetic patients, it allow very early detection of autonomic neuropathy. In patients with dangerous arrhythmia such as ventricular tachycardia or fibrillation, MIBG imaging may be only an abnormal result among various exams. In patients with ischemic heart disease, sympathetic derangement may be used as the method of risk stratification. In heart transplanted patients, sympathetic reinnervation is well evaluated. Adriamycin-induced cardiotoxicity is detected earlier than ventricular dysfunction with sympathetic dysfunction. Neurodegenerative disorder such as Parkinson's disease or dementia with Lewy bodies has also cardiac sympathetic dysfunction. Noninvasive assessment of cardiac sympathetic nerve activity with I-123 MIBG imaging nay be improve understanding of the pathophysiology of cardiac disease and make a contribution to predict survival and therapy efficacy.

• 대한약리학회지
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• 제30권1호
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• pp.75-86
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• 1994

선천성 고혈압 흰쥐(SHR)와 정상혈압 흰쥐에서 교감신경성 신경전달에 미치는 부신수질 및 renin-angiotensin계의 역할을 알아보기 위해, 부신수질을 제거하거나 angiotensin 변환 효소 억제제를 장기간 처치한 뒤 중추신경계가 파괴된 상태에서 절전신경을 자극했을 때 나타나는 승압반응과 대동맥의 catecholamine농도 및 angiotensin 변환 효소 활성도의 변화를 비교 검토하였다. 부신수질을 제거하더라도 중추신경계를 파괴하기 전후의 혈압에는 영향을 주지 못했으며, 절전 신경 자극에 의한 승압반응은, 자극 주파수에 의존적으로 증가하였으며 prazosin 전처치로서 거의 완전히 억제되었다. 정상혈압 흰쥐에서와는 달리, 선천성 고혈압 흰쥐에서는 부신수질을 제거했을 때는 절전신경 자극에 의한 승압반응이 부신수질을 제거하지 않는 군(이하 대조군)에 비하여 유의하게 약화되었다. SHR에서 부신수질 제거로 부신 catecholamine 함량은 현저히 감소되었고, 혈청의 angiotensin 변환 효소 활성도는 감소되는 경향을 나타내었다. 그러나 혈장 및 대동맥 절편의 catecholamine 함량, 대동맥 절편의 angiotensin 변환 효소의 활성도는 대조군과 유의한 차이가 없었다. 그러나 WKY에서는 부신수질이 제거된 군에서 대동맥 절편의 angiotensin 변환 효소의 활성도와 catecholamine함량이 대조군에 비해 유의하게 증가되어 있었다. Enalapril처치에 의해서 선천성 고혈압 흰쥐 평균 혈압은, 부신 catecholamine 함량 및 대동맥 절편의 angiotensin 변화 효소의 활성도와 함께 현저히 저하되어 정상혈압 흰쥐와 유사하였다. 그리고 선천성 고혈압 흰쥐에서 부신수질의 제거로 절전신경 자극에 의한 승압반응이 대조군에 비하여 약화되는 현상은 enalapril을 처치하였을 때는 관찰되지 않았다. 이상의 결과로 미루어보아 교감신경성 신경전달을 항진시키는 부신수질의 작용은 renin-angiotensin계의 활성화에 의존적이었으며, 부신수질의 제거로 정상혈압 흰쥐에서는 renin-angiotensin계가 보상적인 조절이 일어났으나, 선천성 고혈압 흰쥐에서는 보상적인 조절이 일어나지 않았다.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.128-128
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• 2003

Bradykinin modulates the sympathetic system in various ways. It can stimulate sympathetic neurotransmission directly through presynaptic receptors (Llona et al., 1991) and indirectly via its hypotensive or nociceptive effects which activate central and ganglionic mechanisms (Kuo and Keeton, 1991; Dray et al., 1988). However, it has been found that bradykinin can also liberate prostaglandins in peripheral tissues, thereby attenuating the release of catecholamines(Starke et al., 1977). (omitted)

• Biomolecules & Therapeutics
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• 제19권3호
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• pp.315-319
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• 2011

Galanin (Gal) is a 29-amino-acid neuropeptide which is expressed in superior cervical ganglion (SCG) neurons and plays a trophic role in the adult animal and acts as an inhibitory modulator of cholinergic and noradrenergic neurotransmission. Whether activation or inhibition of alpha-adrenoreceptors infl uences Gal mRNA expression in SCG neurons remains unknown. Here, we have evaluated the possible regulation of Gal mRNA expression with acute (4 h) and chronic (4 days) stimulation of alpha 1- and alpha 2-adrenoreceptor agonists or antagonists in primary cultured SCG neurons. The results showed that the amount of Gal mRNA expression in cultured SCG neurons increased signifi cantly after chronic stimulation with alpha 2-adrenoreceptor antagonist yohimbine compared with control SCG neurons at the same time point, whereas the amount of Gal mRNA expression decreased signifi cantly after chronic stimulation with alpha 2-adrenoreceptor agonist clonidine as compared with that in control group. All these effects were not dose-dependent on the administration of alpha 2-adrenoreceptor agonist clonidine or alpha 2-adrenoreceptor antagonist yohimbine. Alpha 1-adrenoreceptor agonist phenylephrine or antagonist prazosin chronic stimulation did not have effects on Gal mRNA expression. Acute exposure of these agents did not have effects on Gal mRNA expression. The present study showed that Gal may be regulated by activation or inhibition of alpha 2-adrenoreceptors, but not alpha 1-adrenoreceptors in sympathetic neurons.

• 한국식품영양과학회지
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• 제28권3호
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• pp.607-612
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• 1999

Cigarette smoking is the potential risk factor for lung cancer and chronic pulmonary disease, as well as inflammatory bowel disease and reproductive malfunction. Nicotine and tar have been im plicated as a major factor in the pathogenesis of the diseases. Nicotine increases heart rate and blood pressure due to stimulation sympathetic neurotransmission and tar also accounts for the severe damage of peridontal diseases and osteoporosis in postmenopausal women. Portulaca oleracea, which contains significant amount of K+, noradrenaline and dopamine as well as various nutrients, has been used for many medicinal purposes and one of which is the detoxification of insect or snake toxins. The purpose of this study was to investigate the action of Portulaca oleracea extracts on the reduction of harmful materials of tabacco. The reduction percentages were measured in the presence and absence of each solvent extract of Portulaca oleracea using reversed C18 column of HPLC. Nicotine reduction effects were obtained from aqueous, methanol and chloroform extracts of Portulaca oleracea as 89%, 55% and 51%, respectively. The results suggest that the polar extracts of Portulaca oleracea affects the reduction of nicotine which is responsible for many diseases.

• Journal of Microbiology and Biotechnology
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• 제27권6호
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• pp.1163-1170
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• 2017

Clostridium difficile releases two exotoxins, toxin A and toxin B, which disrupt the epithelial cell barrier in the gut to increase mucosal permeability and trigger inflammation with severe diarrhea. Many studies have suggested that enteric nerves are also directly involved in the progression of this toxin-mediated inflammation and diarrhea. C. difficile toxin A is known to enhance neurotransmitter secretion, increase gut motility, and suppress sympathetic neurotransmission in the guinea pig colitis model. Although previous studies have examined the pathophysiological role of enteric nerves in gut inflammation, the direct effect of toxins on neuronal cells and the molecular mechanisms underlying toxin-induced neuronal stress remained to be unveiled. Here, we examined the toxicity of C. difficile toxin A against neuronal cells (SH-SY5Y). We found that toxin A treatment time- and dose-dependently decreased cell viability and triggered apoptosis accompanied by caspase-3 activation in this cell line. These effects were found to depend on the up-regulation of reactive oxygen species (ROS) and the subsequent activation of p38 MAPK and induction of $p21^{Cip1/Waf1}$. Moreover, the N-acetyl-$\text\tiny L$-cysteine (NAC)-induced down-regulation of ROS could recover the viability loss and apoptosis of toxin A-treated neuronal cells. These results collectively suggest that C. difficile toxin A is toxic for neuronal cells, and that this is associated with rapid ROS generation and subsequent p38 MAPK activation and $p21^{Cip1/Waf1}$ up-regulation. Moreover, our data suggest that NAC could inhibit the toxicity of C. difficile toxin A toward enteric neurons.

• Restorative Dentistry and Endodontics
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• 제27권5호
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• pp.543-551
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• 2002

Nitric oxide (NO) is a small molecule (mol. wt. 30 Da) and oxidative free radical. It is uncharged and can therefore diffuse freely within and between cells across membrane. Such characteristics make it a biologically important messenger in physiologic processes such as neurotransmission and the control of vascular tone. NO is also highly toxic and is known to acts as a mediator of cytotoxicity during host defense. NO is synthesized by nitric oxide synthase (NOS) through L-arginine/nitric oxide pathway which is a dioxygenation process. NO synthesis involves several participants, three co-substrates, five electrons, five co-factors and two prosthetic groups. Under normal condition, low levels of NO are synthesized by type I and III NOS for a short period of time and mediates many physiologic processes. Under condition of oxidant stress, high levels of NO are synthesized by type II NOS and inhibits a variety of metabolic processes and can also cause direct damage to DNA. Such interaction result in cytostasis, energy depletion and ultimately cell death. NO has the potential to interact with a variety of intercellular targets producing diverse array of metabolic effects. It is known that NO is involved in hemodynamic regulation, neurogenic inflammation, re-innervation, management of dentin hypersensitivity on teeth. Under basal condition of pulpal blood flow, NO provides constant vasodilator tone acting against sympathetic vasoconstriction. Substance P, a well known vasodilator, was reported to be mediated partly by NO, while calcitonin-gene related peptide has provided no evidence of its relation with NO. This review describes the roles of NO in dental pulp in addition to the known general roles of it.

• 대한약리학회지
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• 제28권1호
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• pp.49-60
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• 1992

선천성 고혈압 흰쥐(SHR)에서 endothelin-1(ET)과 neuropeptide Y(NPY) 투여에 의한 심혈관계 반응에 미치는 enallapril 장기처치의 영향을 검토하였다. 생후 6주의 SHR에 enalapril(3 mg/kg/day)을 6주간 투여하였을 때 고혈압 발현이 현저히 억제되었다(이하 enalapril 처치군). Enalapril 처치군에서 ET 및 NPY에 의한 승압반응이 현저히 억제되었지만, ET 측뇌실투여에 의한 혈압상승 및 NPY측뇌실 투여로 야기되는 혈압하강효과에는 영향이 없었다. 뇌척수제거 흰쥐에서 전기적 자극으로 야기되는 빈맥효과는 enalapril처치나 ET투여로 억제되었는데, ET의 작은 ${\alpha}_2$-수용체 길항제인 yohimbine 전처치로 봉쇄되었다. SHR의 적출 대동맥에서 전기자극 빈도수에 따르는 수축반응이 ET 전처치로 항진되었으나 NPY 전처치로는 차이가 없었다. 전기자극 빈도수에 따른 수축반응은 enalapril투여한 군의 것이 투여하지 않은 군의 것에 비하여 약화되었다. ET투여에 의한 혈중 norepinephrine의 증가작용이 enalapril처치로 감소되었으며, 이러한 감소작용이 뇌척수제거 흰쥐에서 현저하였다. 위의 결과로 미루어 고혈압흰쥐에 enalapril을 장기처치함으로써 고혈압 발현을 효과적으로 억제할 수 있으며, 이는 ET 및 NPY에 의한 승압반응 및 교감신경말단의 신경전달과정의 억제가 관여될 수도 있을 것 같다.