• YAKHAK HOEJI
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• v.28 no.5
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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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• v.24 no.2
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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.

• The Korean Journal of Zoology
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• v.34 no.1
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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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• v.10 no.2
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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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• v.17 no.2
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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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• v.10 no.2
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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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• v.9 no.5
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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.

• The Korean Journal of Pharmacology
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• v.29 no.2
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• pp.253-261
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• 1993

Possible changes in the role of insulin-sensitive cyclic nucleotide phosphodiesterase(PDE) in mediating the antilipolytic action of insulin were investigated in adipocytes from streptozotocin-induced diabetic rats. Isolated adipocytes prepared from epididymal adipose tissue were incubated, with or without insulin, at $37^{\circ}C$ for 15 min following pretreatment with various drugs or toxins, and three (plasma membranes, microsomal membranes, and cytosol) fractions prepared by differential centrifugation were then assayed for cAMP phosphodiesterase activity. The PDE activities only in the crude microsomal (P2) fractions were activated by insulin both in diabetic and control rats. The basal PDE activities in P2 fractions of adipocytes from diabetic rats were higher than those from control rats, although the maximal effects observed at 2 nM of insulin, $100\;{\mu}M$ of isoproterenol or the combination of both were not significantly different from each other. The insulin-stimulated PDE activities in P2 fractions of adipocytes from diabetic rats were not changed by PIA, a $A_{1}$ adenosine receptor agonist, whereas they were decreased to the basal PDE activities in those from control rats. In addition, the adipocytes from diabetic rats showed an increased sensitivity to pertussis toxin compared to those from controls. There were no differences between diabetic and control rats in the sensitivity of adipocytes to cholera toxin. These data indicate that the impaired signalling through inhibitory receptors such as adenosine receptors in adipocytes from streptozotocin-induced diabetes relates to the loss or the decreased function of $G_i$ proteins, and leads to the increased activity of the insulin-dependent PDE at the basal states.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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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 $VDCC_L$.