• The Journal of Internal Korean Medicine
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• v.38 no.2
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• pp.110-117
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• 2017

Objective: This study was undertaken to examine the effect of Cortex Phellodendri on prostatic urethral pressure and mean arterial blood pressure of rabbits. Methods: To measure prostatic urethral pressure and mean arterial blood pressure, a Mikro-Tip catheter transducer was inserted and positioned in the prostatic urethra and left carotid artery. After a stabilizing period, phenylephrine ($1{\mu}/kg$) was intravenously administered two or three times to increase the urethral pressure and mean arterial blood pressure. Cortex Phellodendri (2.5 mg/kg and 5 mg/kg doses of Cortex Phellodendri extracted from 80% Ethanol) was administered intravenously, followed by phenylephrine, with no time interval between the doses. The urethral pressure and mean arterial blood pressure were then measured to determine whether they had stabilized. Results and Conclusion: Cortex Phellodendri appeared to inhibit phenylephrine-induced increases in prostatic urethral pressure and mean arterial blood pressure.

• 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.

• BMB Reports
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• v.41 no.3
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• pp.223-229
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• 2008

Reactive oxygen species (ROS) are implicated in vascular homeostasis. This study investigated whether ${O_2}^{\cdot^-}$, the foundation molecule of all ROS, regulates vasomotor function. Hence, vascular reactivity was measured using rat thoracic aortas exposed to an ${O_2}^{\cdot^-}$ generator (pyrogallol) which dose-dependently regulated both $\alpha$-adrenergic agonist-mediated contractility to phenylephrine and endothelium-dependent relaxations to acetylcholine. Pyrogallol improved and attenuated responses to acetylcholine at its lower (10 nM - 1 ${\mu}M$) and higher (10 - 100 ${\mu}M$) concentrations, respectively while producing the inverse effects with phenylephrine. The endothelial inactivation by L-NAME abolished acetylcholine-induced vasodilatations but increased phenylephrine and KCl-induced vasoconstrictions regardless of the pyrogallol dose used. Relaxant responses to sodium nitroprusside, a nitric oxide donor, were not affected by pyrogallol. Other ROS i.e. peroxynitrite and $H_2O_2$ that may be produced during experiments did not alter vascular functions. These findings suggest that the nature of ${O_2}^{\cdot^-}$-evoked vascular function is determined by its local concentration and the presence of a functional endothelium.

• The Korean Journal of Pharmacology
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• v.8 no.1
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• pp.41-47
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• 1972

The author studied the adrenotropic receptors of isolated vas deferens from Ditrema temmincki Bleeker, using adrenergic activators such as epinephrine, norepinephrine, isoproterenol and phenylephrine, and adrenergic blocking agents such as phenoxybenzamine and propranolol. The results are as follows: 1. The vas deferens was stimulated by epinephrine, norepinephrine and phenylephrine, but not affected by isoproterenol. 2. The excitatory effect of phenylephrine on the vas deferens was completely blocked by phenoxybenzamine, but more stimulated by propranolol. 3. The excitatory effects of epinephrine and norepinephrine were markedly reduced by phenoxybenzamine, but stimulated by propranolol. 4. The vas deferens pretreated with phenoxybenzamine and propranolol was not affected by epinephrine and norepinephrine. 5. The vas deferens was not affected by isoproterenol and also not affected by the pretreatment with either kind of blocking agent plus isoproterenol. 6. It seemed that the vas deferens had both alpha-excitatory receptor and beta-receptor, but it was difficult to detect the character of beta-receptor whether it was inhibitory or excitatory.

• 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.

• YAKHAK HOEJI
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• v.37 no.2
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• pp.163-171
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• 1993

In order to study the functions of vascular endothelial nitric oxide(NO) generating system, we examined the effects of monomethylarginine(MMA) and dimethylarginine(DMA)(asym., sym.), arginine analogues, on modulation of vascular tone. Also, the concentrations of endogenous arginie and MMA were measured by HPLC in rat aortic tissues. The results were as follows. 1. The maximum relaxation induced by Ach (1.5$\times$10$^{-6}$M) was 80% of the contractility of rings of rat aorta induced by phenylephrine and L-Arg causes endothelium-dependent relaxation of the aorta precontracted with phenylephrine and these relaxation were concentration-dependent. 2. Endothelium-dependent contractility of rings of rat aorta induced by MMA (100 $\mu{M}$), DMA (asym., 100 $\mu{M}$) and DMA (sym., 100 $\mu{M}$) were 25.5%, 27.5% and 16.5% of that induced by phenylephrine respectively. 3. The relaxation of rat aortic ring induced by L-Arg was inhibited by MMA, DMA(asym.) and DMA(sym.). The degrees of inhibition induced by MMA, DMA(asym.) and DMA(sym.) were 45.7%, 37.1% and 18.3%, respectively. 4. The endogenous arginine and monomethylarginine contents in rat aorta were 83 pmoles/mg wet tissue, and 34.9 pmoles/mg wet tissue. After stimulation with Ach, the concentrations of L-Arg and MMA were significantly decreased. These results suggest that there are the strong relationships between the endogenous L-Arg and methylated arginines and NO-generating system.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.1
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• pp.87-92
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• 2001

Carbon monoxide (CO) binds to soluble guanylate cyclase to lead its activation and elicits smooth muscle relaxation. The vascular tissues have a high capacity to produce CO, since heme oxygenase-2 (HO-2) is constitutively expressed in endothelial and smooth muscle cells, and HO-1 can be greatly up-regulated by oxidative stress. Moreover, the substrate of HO, heme, is readily available for catalysis in vascular tissue. Although the activation of heme oxygenase pathway under various stress conditions may provide a defence mechanism in compromised tissues, the specific role of HO-1-derived CO in the control of aortic contractility still remains to be elucidated. The present study was done to determine the effect of HO-1 induction on the aortic contractility. Thus, the effects of incubation of aortic tissue with S-nitroso-N-acetylpenicillamine (SNAP) for 1 hr on the aortic contractile response to phenylephrine were studied. The preincubation with SNAP resulted in depression of the vasoconstrictor response to phenylephrine. This effect was restored by HO inhibitor or methylene blue but not by NOS inhibitor. The attenuation of vascular reactivity by preincubation with SNAP was also revealed in endothelium-free rings. $AlF4^--evoked$ contraction in control did not differ from that in SNP-treated group. These results suggest that increased production of CO was responsible for the reduction of the contractile response to phenylephrine in aortic ring preincubated with SNAP and this effect of SNAP was independent on endothelium.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.4
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• pp.339-348
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• 2020

We aimed to characterize the participation of rapid non-genomic and delayed non-genomic/genomic or genomic mechanisms in vasoactive effects to triiodothyronine (T3), emphasizing functional analysis of the involvement of these mechanisms in the genesis of nitric oxide (NO) of endothelial or muscular origin. Influences of in vitro and in vivo T3 treatments on contractile and relaxant responsiveness of isolated rat aortas were studied. In vivo T3-treatment was 500 ㎍·kg^-1·d^-1, subcutaneous injection, for 1 (T3_1d) and 3 (T3_3d) days. In experiments with endothelium-intact aortic rings contracted with phenylephrine, increasing concentrations of T3 did not alter contractility. Likewise, in vitro T3 did not modify relaxant responses induced by acetylcholine or sodium nitroprusside (SNP) nor contractile responses elicited by phenylephrine or angiotensin II in endothelium-intact aortas. Concentration-response curves (CRCs) to acetylcholine and SNP in endothelium-intact aortic rings from T3_1d and T3_3d rats were unmodified. T3_3d, but not T3_1d, treatment diminished CRCs to phenylephrine in endothelium-intact aortic rings. CRCs to phenylephrine remained significantly depressed in both endothelium-denuded and endothelium-intact, nitric oxide synthase inhibitor-treated, aortas of T3_3d rats. In endothelium-denuded aortas of T3_3d rats, CRCs to angiotensin II, and high K⁺ contractures, were decreased. Thus, in vitro T3 neither modified phenylephrine-induced active tonus nor CRCs to relaxant and contractile agonists in endothelium-intact aortas, discarding rapid non-genomic actions of this hormone in smooth muscle and endothelial cells. Otherwise, T3_3d-treatment inhibited aortic smooth muscle capacity to contract, but not to relax, in an endothelium- and NO-independent manner. This effect may be mediated by delayed non-genomic/genomic or genomic mechanisms.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.69-74
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• 2016

The present study was undertaken to investigate the influence of cardamonin on vascular smooth muscle contractility and to determine the mechanism(s) involved. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Cardamonin significantly relaxed fluoride-, phenylephrine-, and phorbol ester-induced vascular contractions, suggesting that it has an anti-hypertensive effect on agonist-induced vascular contraction regardless of endothelial nitric oxide synthesis. Furthermore, cardamonin significantly inhibited the fluoride-induced increase in pMYPT1 level and phenylephrine-induced increase in pERK1/2 level, suggesting inhibition of Rho-kinase and MEK activity and subsequent phosphorylation of MYPT1 and ERK1/2. This study provides evidence that the relaxing effect of cardamonin on agonist-induced vascular contraction regardless of endothelial function involves inhibition of Rho-kinase and MEK activity.