• Journal of Ginseng Research
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• v.12 no.2
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• pp.135-144
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• 1988

When ginseng saponin fractions were treated with secretion regulatory agents, it increased cAMP level at the case of thyrotropin (but the amounts were small). Total saponin increased cAMP level at DEcAMP and isoproterenol, and decreased the level at carbachol and propranolol, but at NaF it had little effect. When diol saponin or triol saponin were treated with secretion regulatory agents, biol saponin decreased cAMP level but triol saponin increased it except for isoproterenol. Also, in propra%olol, which inhibits the increase of CAMP level, diol and triol saponin showed crossing effect, too. From the above results, ginseng saponin fractions are believed that it has the, effects of promotion or inhibition on cAMP production in the thyroid , both diol saponin and triol saponin have crossing effect on thyroid hormone secretion regulatory agents. The normalizatin action of ginseng saponin fractions is notable at the case of NaF and carbachol.

• YAKHAK HOEJI
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• v.26 no.4
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• pp.239-251
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• 1982

The rate of deterioration of contractile force of isolated hearts from control and panax ginseng treated rats was determined and response of contractile force of the hearts from ginseng treated rats to several autonomic and other drugs was investigated. Rats weighing 150-250g were administrered orally with ginseng ethanol extract (100mg/kg) and total ginseng saponin (50mg/kg/day) for a week. Ginsenoside Rb$_{1}$ (5mg/kg/day) and ginsenoside Re (5mg/kg/day) were administered respectively for a week. The isolated hearts from rats were perfused with Krebs-Henseleit solution by using Langendorff perfusion apparatus. The control group was only able to maintain approximately 75.5% of their initial strength after 60 min of perfusion, whereas ginseng ethanol extract, total ginseng saponin treated hearts were able to sustain nearly their initial strength even after 60 min. Ginsenoside Rol treated hearts also sustained 93% of their initial strength, but there was no significant difference in the deterioration percentage of the contractile force of ginsenoside Re treated hearts. Experiments were conducted to study the response to perfusion of ginseng treated animal heart with epinephrine, isoproterenol, propranolol, and phenobarbital. The isolated hearts were perfused with Krebs-Henseleit solution containing epinephrine (10$^{-6}$ M), isoproterenol ($10^{-7}$M), propranolol ($10^{-6}$M) and phenobarbital (7{\times}10^{-3}M$) respectively. The maximum inotropic effect of epinephrine and isoproterenol was observed after 2~3 minutes of drug perfusion. Effect of epinephrine on ginseng ethanol extract and total ginseng saponin treated hearts was reduced compared with control. On the other hand, this phenomenon was not observed in ginsenoside Re treated rats but on ginsenoside $Rb_{1}$ treated rats. The positive inotropic effect of isoproterenol was reduced in the hearts from ginseng treated rats compared with control heart, Propranolol or phenobaribital decreased the contractile force in the control rats. The depressant effect of propranolol and phenobarbitat on ginseng treated rat hearts was less than those of control rat hearts. The result suggest that ginseng ethanol extract , ind total ginseng saponin and ginsenoside $Rb_{1}$ may protect the deterioration of contractile force of the heart and may attenuate the response to several drugs on hearts.

• Biomaterials and Biomechanics in Bioengineering
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• v.2 no.4
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• pp.225-235
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• 2015

Treatments for asthma are largely pharmaceutical, with some therapies also utilising alternative breathing techniques. The objective of both medical and alternative methods is to relax contracted airway smooth muscle (ASM). In normal subjects, tidal breathing- and deep inspiration-oscillations are believed to have a bronchodilatory effect. Similarly, application of length oscillations to isolated, contracted ASM also elicits muscle relaxation. As a means of investigating more-effective alternative treatment methods for contracted airways, we analyse the combined effects of bronchodilators and length oscillations on isolated, contracted ASM. The contractile state of the muscle tissue prior to treatment is of primary interest. Thereafter, the effect of applying a combination of small superimposed length oscillations with tidal breathing-like oscillations to ASM is studied alone and in combination with a common bronchodilator, isoproterenol (ISO). This work suggests that relaxation of isolated, contracted ASM following application of combined oscillations and ISO is larger than treatments of either combined oscillations or ISO alone. Further, the observed oscillation-associated relaxation is found to be amplitude- rather than frequency-dependent. This study gives additional insight into the role of oscillations and bronchodilators on contracted airways.

• The Korean Journal of Pharmacology
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• v.6 no.1
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• pp.37-44
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• 1970

The author studied the actions of autonomic drugs on the uterine muscle isolated from Ditrema temmincki Bleeker, and the results obtained were summerized as follows. 1) The motility of the fish uterus was stimulated by epinephrine, norepinephrine and phenylephrine, but inhibited by isoproterenol. 2) The inhibitory effects of isoproterenol on the fish uterus was not affected by phenoxybenzamine, but blocked by propranolol. 3) The excitatory effects of phenylephrine on the fish uterus were blocked by phenoxybenzamine, but stimulated by propranolol. 4) The excitatory effects of epinephrine and norepinephrine were reversed by phenoxybenzamine and stimulated by propranolol. 5) The motility of the fish uterus pretreated with phenoxybenzamine and propranolol was not affected by isoproterenol, phenylephrine, epinephrine and norepinephrine. 6) It seemed that the uterine muscle of the fish had both alpha excitatory and beta inhibitory receptors. 7) The motility of the uterus of the fish was stimulated by acetylcholine. The stimulating action of acetylcholine was antagonized by atropine. 8) The motility of fish uterus was not affected by nicotine and DMPP. The actions of these drugs were not affected by pretreatment with hexamethonium and atropine. 9) It is, therefore, concluded that there are not present ganglia cells furnished with cholinergic fiber in the uterine wall of the fish.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.1
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• pp.55-62
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• 1998

${\alpha},\;{\beta}-Adrenergics$, and calcium channels were known to be related to inducing cardiac hypertrophy. Recently, it was reported that the cardiac renin-angiotensin system (RAS) was an important factor in ventricular hypertrophy. The present study was aimed to investigate the effects of ${\alpha},\;{\beta}-adrenergic$, and calcium channel blockers that might be involved in the regulation of cardiac RAS. The reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of renin gene in the perfused rat heart. Changes in angiotensin converting enzyme (ACE) activity and cyclic AMP (cAMP) content which were thought to play a role in inducing cardiac hypertrophy were measured in the perfused rat heart. The expression of renin gene was not only increased by isoproterenol with metoprolol-pretreatment but also increased by vasopressin treatment in the presence of calcium channel blocker, nifedipine or verapamil. Either prazosin alone or norepinephrine with prazosin-pretreatment significantly increased the ACE activity. However, isoproterenol with metoprolol-pretreatment significantly decreased the ACE activity. On the other hand, the ACE activity was not changed by vasopressin, nifedipine, or verapamil treatments. The content of cAMP was significantly increased by either isoproterenol or vasopressin treatment. According to these results, renin gene expression was associated with ${\beta}2$ - adrenoceptor and calcium channel. ACE activity was associated with ${\alpha}-\;and{\beta}2$ - adrenoceptor. In conclusion, ${\beta}2$ - adrenoceptor was important in cardiac renin gene expression and ACE activity and ${\alpha},\;{\beta}$ -adrenergic, and calcium channel blockers might be involved in the regulation of cardiac RAS in a complicated way.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.3
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• pp.235-241
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• 2000

We examined the expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNAs upon isoproterenol (Iso)-induced cardiac hypertrophy in rats. Then, we tried to investigate the effects of sympatholytics to see if they can modulate the expression of ANP and BNP. In this study, RT-PCR technique was used to characterize the expression of ANP and BNP in right atrium (RA) and left ventricle (LV) of the hypertrophied rat heart. Histologic findings indicated that stimulation of ${\beta}-adrenoceptors$ with Iso for 5 days was sufficient to induce cardiac hypertrophy in rats. A continuous stimulation with Iso for 7 days resulted in an increase of the ANP and BNP expression in the LV and BNP expression in the RA. The increased expressions of ANP and BNP in the LV were slightly inhibited, and the increased expressions of BNP in the RA were markedly inhibited by a continuous treatment with propranolol, metoprolol, and clonidine for 7 days. Overall, our data present a differential expression of the natriuretic peptides in Iso-induced cardiac hypertrophy, and that the mechanisms involved in this differential ANP and BNP gene expression could be mediated via sympathetic nervous system.

• The Korean Journal of Pharmacology
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• v.5 no.2
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• pp.115-119
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• 1969

The authors studied the adrenotropic receptors of isolated urinary bladder from Sebastes inermis, using adrenergic activators such as epinephrine, nor-epinephrine, isoproterenol and phenylephrine and adrenergic blocking agents such as phenoxybenzamine, pronethalol and propranolol. The studies have revealed the following results. 1) The spontaneous motility of isolated bladder from Sebastes inermis was inhibited by epinephrine nor-epinephrine, isoproterenol and phenylephrine. 2) The inhibitory effect of phenylephrine on the Sebastes inermis bladder was blocked by phenoxybensamine. 3) The inhibitory effect of isoproterenol was blocked by pronethalol and propranolol. 4) The effect of epinephrine and nor-epinephrine on the Sebastes inermis bladder was usually not blocked by either kind of blocking agent alone, but was blocked by a combination of ${\alpha}\;and\;{\beta}$ blockades. 5) It is, therefore, concluded that the Sebastes inermis bladder has alpha and that both receptors, and that both receptors subserve retaxation or inhibition.

• The Korean Journal of Pharmacology
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• v.5 no.2
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• pp.105-114
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• 1969

The author studied the action of autonomic drugs on the urinary bladder isolated from Ditrema temmincki Bleaker and the results obtained were summarized as follows: 1) The motility of the urinary bladder of the fish was stimulated by acetylcholine and physostigmine. The stimulating action of these drugs was antagonized by atropine. 2) The motility of the fish bladder was stimulated by epinephrine, nor-epinephrine and phenylephrine, but inhibited by isoproterenol. 3) The inhibitory effects of isoproterenol on the fish bladder was not affected by phenoxybenzamine, but blocked by propranolol. 4) The excitatory effects of phenylephrine on the fish bladder were blocked by phenoxybenzamine, but augmented by propranolol. 5) The excitatory effects of epinephrine and nor-epinephrine were reversed by phenoxybenzamine and augmented by propranolol. 6) The motility of the fish bladder pretreated with phenoxybenzamine and propranolol was not affected by isoproterenol, phenylephrine, epinephrine and nor-epinephrine. 7) It seemed that the bladder muscle of the fish had both alpha excitatory and beta inhibitory receptors. 8) The motility of the fish bladder was stimulated by nicotine and DMPP. The excitatory effects of these drugs were abolished by pretreatment with hexamethonium or atropine. 9) It is, therefore, concluded that there are ganglion cells furnished with cholinergic fiber in the bladder wall of the fish.

• The Korean Journal of Pharmacology
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• v.16 no.1 s.26
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• pp.9-14
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• 1980

To evaluate the adrenergic receptors for glycogenolytic responses to catecholamine, the blood glucose level, liver glycogen content and muscle glycogen level in rats were studied with treatment of epinephrine, norepinephrine and isoproterenol. In addition, to study the possibility of interconversion of adrenergic receptors, the effects of catecholamines in feeding animal were compared with those in fasting animal. The results are summarized as follow; 1) Epinephrine and norepinephine showed dose dependent increase of blood glucose level but the effect of isproterenol was not significant. 2) The prandial states of animal did not influence on effects of catecholamines on blood glucose level. 3) Liver glycogen contents were lowered by epinephrine or by norepinephrins but effect of isoproterenol was not significant. 4) Glycogen content of skeletal muscle was significantly lowered by isoproterenol and. epinephrine shifted the dose-response curve to right, but the effect of norepinephrine was not significant. 5) The effects of epinephrine and norepinephrine on blood glucose were significantly blocked by ergotamine but not by propranolol. These results indicate that the glycogenolytic response to adrenergic agents in rat is mediated by an alpha-receptor in liver and by a beta-receptor in skeletal muscle.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.353-362
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• 1990

Fluoride (F-), a known stimulator of G-protein, induced strong contraction in rabbit trachealis muscle. $AlCl_3\;(5{\sim}20\;{\mu}M)$, which is required for G-protein stimulation by $F^-$, potentiated the contractile response to $F^-$. $Ca^{2+}-removal$ and verapamil, a calcium channel blocker, inhibited the fluoroaluminate-induced contraction. Fluoroaluminate increased $^{45}Ca$ influx in the absence and presence of verapamil. In heparin-loaded muscle high $K^+-induced$ contraction was not affected, but acetylcholine and fluoroaluminate-induced contractions were inhibited. The fluoroaluminate-induced contraction was partially relaxed by isoproterenol, a stimulator of adenylate cyclase. Pertussis toxin partially inhibited fluoroaluminate-induced contraction and potentiated isoproterenol-induced relaxation in the presence of fluoroaluminate, but had no effect on acetylcholine-induced contraction and the isoproterenol-induced relaxation in the presence of acetylcholine. These results suggest that fluoroaluminate has the ability to stimulate at least two putative G-proteins in rabbit trachealis muscle; One causes $Ca^{2+}$ influx through the potential-operated $Ca^{2+}$ channel and the other induces intracellular $Ca^{2+}$ release by the increase of inositol-1, 4, 5-triphosphate.