• 약학회지
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• 제28권5호
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• pp.249-256
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• 1984

The effects of $Ca^{2+}-antagonist$, cinnarizine, on the antihypertensive effects of propranolol and metoprolol were investigated in normal cat (i. v.) and SHR (p. o.). Cinnarizine increased the antihypertensive effect of propranolol, but not of metoprolol. It inhibited the heart rate decreasing effects of propranolol and metoprolol slightly. It decreased the norepinephrine-induced blood pressure increasing effect and isoproterenol-induced blood pressure decreasing effect when coadministered with metoprolol orally for 4 weeks in SHRs.

• Journal of Oral Medicine and Pain
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• 제24권2호
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• pp.163-169
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• 1999

We investigated the culture condition and effects of various growth factors on the culture of salivary gland acinar cells. Male, Sprague-Dawley rats (about 6 weeks old) were sacrificed and their submandibular, sublingual, and parotid glands were used as specimens. High oxygen level more than 90% and coating of Matrigel on culture dish were important factors to help increase the survival time of acinar cells, Proper concentration of enzymes such as collagenase and hyaluronidase during isolation steps was also important. Addition of various growth factors such as dexamethasone, insulin, transferrin, selenous acid, reduced glutathione, epidermal growth factor, isoproterenol, and putrescine in culture medium helped to increase lifetime of cultured salivary acinar cells.

• 한국동물학회지
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• 제34권1호
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• pp.8-19
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• 1991

Atrial natriuretic peptide(ANP)의 유리기전에 대한 특성을 알아보고자, 흰쥐의 적출심장 관류모형을 사용하여 연구한 바 다음과 같은 결과를 얻었다. 1. 심방을 확장시켰을 때 ANP의 유리는 촉진되었다. 그러나 과용량을 부하하면 확장기간보다 회복기간에 ANP의 유리가 현저하게 증가하였다. 2. Epinephrine과 phenylephrine을 주입하면 ANP의 유리 량이 증가했으나, isoproterenol을 주입하면 심박수와 우심방 내압이 현저하게 증가했는데도 ANP의 유리량은 오히려 감소하였다 3. 미주신경을 자극하면 심박수의 현저한 감소에도 불구하고 ANP의 유리량은 증가하였다. 이상과 같은 결과에서 볼 때 결론적으로, 심방의 용량부하에 의해 심방근의 신장수용체가 자극을 받아 ANP의 유리가 촉진되는 것은 분명하고, 심방근이 확장할 때 보다는 확장 후 다시 원래의 길이로 환원될 때 ANP가 유리될 것으로 사료된다. 그리고 ANP의 유리에 대한 adrenergic조절은 o-receptor가 관련되어 있으며 심박수와 심방내압이 ANP의 유리를 변화시키는 데는 반드시 필수적인 인자가 아닌 것으로 여겨진다. 또한 특히 미주신경의 자극으로도 ANP의 유리가 조절될 수 있다는 것이 본 연구를 통해 새로이 발견되었다.

• Journal of Ginseng Research
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• 제10권2호
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• pp.151-158
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• 1986

On the cAMP content in isolated gastric glands from rabbit stomach, the effect of ginseng components (total saponin, diol saponin, triol saponin) with pepsinogen secretion regulatory agents (cholecystokinin, isoproterenol, carbachol, propranolol, atropine, DECAMP, DBcGMP) were studied in vitro. According to the results, ginseng components may have the effect of stimulation or inhibition on cAMP production, and both dial saponin and triol saponin may be reciprocal effect to pepsinogen secretion regulatory agents. It seemed that the ginseng components may have the normalization action to pepsinogen regulatory agents on cAMP content in isolated rabbit gastric glands.

• Annals of Clinical Neurophysiology
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• 제17권2호
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• pp.80-81
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• 2015

Syncopes are the most common non-epileptic attacks mimicking epileptic seizures. Among them, cardiogenic syncope is potentially life threatening. A 49 year old man was refered for the recurrent episodes of loss of consciousness with tonic posture and upward eyes deviation. The electrocardiogram showed polymorphologic ventricular tachycardia during attacks, which normalized after that. He was treated with isoproterenol and symptoms subsided. Here, we report a case of ventricular tachycardia manifested as epileptic seizures.

• Biomolecules & Therapeutics
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• 제10권2호
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• pp.71-77
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• 2002

Heme oxygenase-1 (HO-1) is the inducible from of the rate-limiting enzyme of heme degradation; it regulates the cellular contents of heme. HO-1 is up-regulated by various stimuli including oxidative stress so that it is thought to participate in general cellular defense mechanisms against oxidative stress in mammalian cells. To investigate the role of the cAMP-dependent protein kinase A (PKA) signaling pathway on nitrogen oxidative stress-induced HO-1 gene expression, RAW 264.7 cell cultures were treated with sodium nitroprusside (SNP). SNP increased the expression of HO-1 mRNA and protein, time- and concentration-dependently. Treatment with H89, PKA inhibitor, but not LY83583, guanylate cyclase inhibitor, significantly diminished the HO-1 expression by SNP, indicating that cAMP plays a crucial role in the induction of HO-1. Incubation with cAMP-elevating agents, such as forskolin or isoproterenol resulted in up-regulation of the expression of HO-1. Forskolin-induced expression of HO-1 was inhibited by H89. Furthermore, propranolol, $\beta$-adrenoceptor blocker, inhibited the isoproterenol-induced HO-1 expression, supporting the importance of cAMP in the induction of HO-1 expression. Higenamine-S, but not higenamineR, enhanced the HO-1 expression induced by SNP. Furthermore, cellular toxicity induced by hydrogen peroxide was attenuated by the presence of SNP, which was further increased by the presence of ZnPPIX, HO-1 inhibitor. Collectively, these results strongly suggest that up-regulation of HO-1 expression in RAW 264.7 cells involves PKA signal pathway.

• The Korean Journal of Physiology and Pharmacology
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• 제9권5호
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• pp.299-304
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• 2005

Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO)-evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery, during ISO-induced cardiac hypertrophy compared to heart itself. The results show that the mRNA level of c-fos (not c-jun and c-myc) in heart and these genes in cerebral artery were considerably increased during cardiac hypertrophy. These results that the PKA activity and activations of Ras/Raf/ERK cascade as well as c-fos expression in rabbit heart during cardiac hypertrophy were consistent with previous reports. Interestingly, however, we also showed a novel finding that the decreased PKA activity might have differential effects on Ras and Raf expression in cerebral artery during cardiac hypertrophy. In conclusion, there are differences in molecular mechanisms between heart and cerebral artery during cardiac hypertrophy when stimulated with β2 adrenoreceptor (AR), suggesting a possible mechanism underlying cerebrovascular dysfunction during cardiac hypertrophy.

• 대한약리학회지
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• 제29권2호
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• pp.253-261
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• 1993

Streptozotocin으로 당뇨병을 유발시킨 흰쥐를 모델로 하여 당뇨병으로 인한 인슐린의 antilipolytic action을 매개하는 insulin-sensitive cyclic nucleotide phosphodiesterase의 역할의 변화 가능성을 연구하였다. 흰쥐의 epididymal adipose tissue로부터 분리한 지방세포를 여러 약물과 toxin으로 전처치한 다음, insulin을 처치 또는 처치하지 않고 $37^{\circ}C$에서 15분 동안 incubation하였다. 그리고 나서 differential centrifugation으로 3 fractions로 분리한 다음 cAMP phosphodiesterase activity를 assay하였다. Insulin에 의한 PDE activities의 증가는 당뇨병군과 대조군 모두 crude microsomal (P2) fraction에서만 볼 수 있었다. P2 fraction을 2 nM insulin, $100\;{\mu}M$ isoproterenol, 또는 두 약물을 함께 처치하여 나타난 maximal effect는 두 군 모두에서 유의한 차이가 없었다. 그러나 basal PDE activities는 당뇨병균이 대조군에 비해 증가한 것으로 나타났다. 당뇨병군의 P2 fraction의 insulin-sensitive PDE activities는 $A_{1}$ adenosine receptor agonist 인 PIA에 의해서 영향을 받지 않은 반면, 대조군의 경우 PIA에 의해 basal PDE activities와 같게 감소하였다. 그리고 지방세포의 pertussis toxin에 대한 sensitivity는 당뇨병군이 대조군보다 더욱 민감하였다. 그러나 cholera toxin에 대한 sensitivity는 당뇨병군과 대조군 사이에 큰 차이를 볼 수 없었다. 이러한 결과로 보아 streptozotocin으로 당뇨병을 유발시킨 흰쥐의 지방세포에서, adenosine receptor와 같은 inhibitory receptor를 경유한 signalling의 감소는 $G_{i}$ proteins의 소실 또는 기능의 감소와 관련이 있으며, 또한 basal state에서 insulin-dependent PDE의 활성을 증가시키는 것으로 사료된다.

• 대한약리학회지
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• 제24권2호
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• pp.189-195
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• 1988

인체 정관 평활근에서 각종 자율신경전달체 수용체의 유무를 조사하고 benzodiazepine계의 진정-항불안제인 diazepam이 평활근 운동성에 미치는 작용을 관찰하기 위하여, 32내지 45세의 건강한 지원자로부터 정관절편을 얻었다. 정관 절제술은 국소마취하에 시행되었고, 정관절편의 수축력 측정은 등장성장력측정기에 의하였다. 적출장기실험조 내에서 정관절편의 자율수축은 관찰되지 않았으나, norepinephrine에 대한 반응성은 $33^{\circ}C$에서 가장 예민하였던 바, 이 norepinephrine에 의한 농도의존적 수축력증가작용은 알파-아드레날린성 차단제인 phentolamine에 의해 억제되었다. 또 인체 정관절편은 본 실험의 조건하에서 isoproterenol 의하여 수축하였고, 이 수축작용은 베타-아드레날린성 차단제인 propranolol 의하여 완전히 제거되었다. 동시에 인체 정관절편은 acetylcholine에의해서도 비교적 강하게 수축하였고, 이 수축작용은 콜린성 무스카린성 차단제인 atropine에 의하여 완전히 억제되었다. Diazepam은 norepinephrine에 의한 수축을농도 의존적으로 억 제 하였다. 이상의 결과를 종합하면, 인체 정관 평활근은 체온보다 낮은 $33^{\circ}C$에서 그 활동성이 가장 강하고, 자율신경에 대하여서는 아드레날린성 및 콜린성 수용체가 공존하고 있으며, diazepam은 그 수축력을 약화시킨다고 사료된다.

• The Korean Journal of Physiology and Pharmacology
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• 제13권6호
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• pp.503-510
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• 2009

To elucidate the mechanism of cyclic nucleotides, such as adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP), in the regulation of human gastric motility, we examined the effects of forskolin (FSK), isoproterenol (ISO) and sodium nitroprusside (SNP) on the spontaneous, high $K^+$ and acetylcholine (ACh)-induced contractions of corporal circular smooth muscle in human stomach. Gastric circular smooth muscle showed regular spontaneous contraction, and FSK, ISO and SNP inhibited its phasic contraction and basal tone in a concentration-dependent manner. High $K^+$ (50 mM) produced sustained tonic contraction, and ACh $(10\;{\mu}M)$ produced initial transient contraction followed by later sustained tonic contraction with superimposed phasic contractions. FSK, ISO and SNP inhibited high $K^+$-induced tonic contraction and also ACh-induced phasic and tonic contraction in a reversible manner. Nifedipine $(1\;{\mu}M)$, inhibitor of voltage-dependent L-type calcium current $(VDCC_L)$, almost abolished ACh-induced phasic contractions. These findings suggest that FSK, ISO and SNP, which are known cyclic nucleotide stimulators, inhibit smooth muscle contraction in human stomach partly via inhibition of $VDCC_L$.