• Journal of Pharmaceutical Investigation
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• v.15 no.1
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• pp.22-31
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• 1985

The influence of some sympathetic blocking agents on pressor actions of norepinephrine and angiotensin was investigated in rabbits. 1. Phentolamine, sympathetic ${\alpha}-blocking$ agent, blocked the pressor action of norepinephrine, but did not affect the pressor action of angiotensin 2. Chlorisondamine, autonomic ganglionic blocking agent, potentiated the both actions of norepinephrine and angiotensin. 3. Guanethidine, bethanidine and debrisoquine, sympathetic neuronal blocking agents, potentiated the action of norepinephrine, while diminished that of angiotensin. 4. Reserpine, norepinephrine depleting agent, increased the pressor response of norepinephrine, but did not influence the pressor action of angiotensin.

• The Korean Journal of Pharmacology
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• v.3 no.1
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• pp.15-18
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• 1967

Sympathetic ganglionic stimulants (DMPP, Wy-615, TMA and McN-A-343) produced pressor response in chickens anesthetized with phenobarbital sodium. In adrenalectomized chickens the pressor activity of DMPP, Wy -615 and TMA was less than in normal chickens but that of McN-A-343 was unchanged. Hexamethonium (20 mg/kg) and chlorisondamine (5 mg/kg), ganglionic blocking agents, reduced the pressor response to DMPP and Wy-615 but did not abolish the response. The pressor effect of McN-A-343 was not potentiated by the ganglionic flocking agents, but abolished by atropine.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.4
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• pp.225-233
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• 2002

Kanagawa hemolysin (KH), an exotoxin produced from Kanagawa phenomenon-positive Vibrio parahemolyticus, has been shown to possess various biological activities including hemolysis, enterotoxicity, cytotoxicity, and cardiotoxicity. The aim of this study was to investigate the effect of KH on the cardiovascular system and its mechanism, employing in vivo and in vitro experiments of the rat. Intracerebroventricular (icv) administration of 100 mHU KH produced a marked and continuous pressor effect (icv KH-pressor effect), and the icv pressor effect was not repeatable. However, intravenous (iv) injection of the same dose of KH induced a prominent depressor effect (iv KH-depressor effect). The icv KH-pressor effect was inhibited by acid-denaturation, while the iv KH-depressor effect was not. Simultaneous icv administration of the three agents (ouabain, diltiazem, or bumetanide: $10{\mu}g/kg$ each) significantly reduced the pressor effect. The icv KH-pressor effect was inhibited by treatment with iv phentolamine or chlorisondamine, but was not affected by iv candesartan. The iv KH-depressor effect was repeatable and was attenuated by treatment with iv NAME or methylene blue. In vitro experiments using isolated thoracic aorta, $10^{-6}$ M phenylephrine (PE) and 50 mM KCl produced a sustained contraction. In rings contracted with either agents, KH showed relaxant responses in a concentration- dependent fashion and the relaxation (KH-vasorelaxation) was not dependent on the existence of the endothelium. The KH-vasorelaxation in the endothelium-intact rings contracted by PE was abolished by methylene blue treatment. In summary, the present findings suggest that in the icv KH-pressor effect the cation leak-inducing action of KH is implicated, which leads to the increased central sympathetic tone, that the iv KH-depressor effect results from the vasorelaxation via NO-guanylate cyclase system, and that the KH-vasorelaxation is independent of the endothelium and the guanylate cyclase system is involved in it. In conclusion, the mechanism of KH producing the icv pressor effect may not be identical to that of KH producing the iv depressor effect.

• The Korean Journal of Pharmacology
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• v.3 no.1
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• pp.5-13
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• 1967

It has been reported by some investigators that pressor response of rabbits to sympathetic ganglionic stimulants was weak. In this paper it was attempted to investigate this problem more thorouglhy in urethane anesthetized rabbits. 1) In rabbits the approximate doses to elicit increase of about 20 mmHg of blood pressure were $100\;{\mu}g/kg$ with DMPP, $50\;{\mu}g/kg$ with Wy-615, $500\;{\mu}g/kg$ with TMA and with nicotine. The pressor activity of these substances was markedly augmented by treating animals with syrosingopine. 2) In adrenal-ligated rabbits pressor activity of the substances was markedly reduced. Treating the adrenal-ligated animals with syrosingopine augmented significantly the pressor activity of these substances except DMPP. Direct injection of DMPP and TMA into the adrenal produced mole pressor response than intravenous injection did. These date suggest that DMPP has greater effect on the adrenal medulla than the other substances. 3) In vagotomized and atropinized rabbits the pressor activity of these compounds was more marked than in normal rabbits. 4) The above facts indicate that the pressor activity of the ganglionic stimulants in rabbits was definitely low than in cats and dogs. The low responsiveness of the rabbits to these agents was discussed in the light of catecholamine releasing mechanisms, and extraganglionic actions of these substances.

• Journal of Food Hygiene and Safety
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• v.28 no.3
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• pp.195-201
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• 2013

In atherosclerosis, blood vessels become sensitive to vessel-constricting agents leading to reduced control in the event of abrupt blood pressure changes. Mulberry trees (Morus alba L., MA) have been claimed to contain various bioactive principles that could possibly prevent atherosclerosis development caused by high cholesterol consumption. In order to examine whether MA feeding can prevent the sensitization of blood vessels, MA leaves were fed to rats for 8 weeks and pressor responses to vasoconstricting agents were assessed. Animals were pithed before blood pressure assessments to eliminate reflex compensation in vessel responses. Feeding diets containing high levels of cholesterol led to potentiated pressor responses to sympathetic nerve stimulation, or to injection of norepinephrine, phenylephrine, angiotensin II and vasopressin in pithed rats. These potentiated pressor responses were prevented in rats fed MA leaf-containing diets at 2 or 10% levels. It was also examined in anesthetized non-pithed rats whether similar cholestrol-related sensitization and MA prevention could be observed. However, high cholesterol-induced sensitization in pressor responses were not observed, suggesting that destruction of central cardiovascular control by pithing must have revealed the sensitization responses. It was concluded that MA leaves seem to be active in preventing abnormal blood vessel reactivity caused by hypercholesterolemia.

• The Korean Journal of Pharmacology
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• v.27 no.1
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• pp.21-31
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• 1991

When administered intracerebroventricularly (icv), cholinergic nicotinic agents, nicotine and DMPP, as well as cholinergic muscarinic agents, muscarine and bethanechol, produced pressor responses in urethane-anesthetized vagotomized rabbits. The response patterns to nicotine and to DMPP were similar, while the bethanechol response resembled the muscarine pattern. The pressor response to nicotine and DMPP was markedly inhibited by icv mecamylamine but not by icv pirenzepine, whereas the response to muscarine and bethanechol was inhibited by icv pirenzepine but not by icv mecamylamine, suggesting that both nicotinic and muscarinic receptors in the brain are involved in the action. Intravenous pretreatments of animals with regitine, reserpine, enalapril, saralasin, both regitine and enalapril, both regitine and saralasin, SK&F-100273 did not prevent the pressor response to nicotine and muscarine. Iv pretreatments with both regitine and SK&F-100273 inhibited the nicotine response without affecting the muscarine response, whereas pretreatments with three agents, regitine, enalapril and SK&F-100273, inhibited the muscarine response. The nicotine-induced elevated blood pressure as well as the muscarine-induced were lowered by regitine but not by enalapril or by SK&F-100273. Enalapril was without effect on the nicotine hypertension in rabbits treated with regitine or both regitine and SK&F-100273, whereas SK&F-100273 lowered the nicotine hypertension in regitine-treated animals. Enalapril did not enhance the lowering effect of SK&F-100273 in regitine-treated ones, nor did it cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and SK&F-100273. Likewise, SK&F-100273 did not cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and enalapril. These data suggest that the nicotine-induced hypertensive state is related to at least two systems in the periphery-sympathetic and vasopressin, whereas in the muscarine-induced hypertensive state three systems in the periphery are involved, i.e., the sympathetic, vasopressin and angiotensin system. The hypotensive effect of regitine on basal arterial blood pressure levels of rabbits was not influenced by pretreatment with either of enalapril or SK&F-100273, but significantly potentiated by treating with both enalapril and SK&F-100273, suggesting participation of the sympathetic and the renin-angiotensin system as well as the vasopressin system in maintenance of arterial blood pressure.

• The Korean Journal of Pharmacology
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• v.6 no.1
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• pp.27-35
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• 1970

1) In whole anesthetized rabbits and spinal rabbits, the potentiating effect of syrosingopine and reserpine on pressor action of norepinephrine (NE) was compared. 2) The doses of syrosingopine and reserpine were 8, 40, $200\;{\mu}g$ and 1 mg per kg of body weight. The pressor responses to NE(0.1, 0.5, 0.25, 1.2, 6.0, 30.0, $150.0\;{\mu}g/kg$) were examine at 4, 10 and 24 hours after administration of the drugs. 3) In whole rabbits, potentiation by syrosingopine of pressor effect of NE was observed after administration of above the dose of $40\;{\mu}g/kg$, potentiation by reserpine was above $8\;{\mu}g/kg$. The maximal potentiation was achieved 10 hours after administration of $200\;{\mu}g/kg$ of each agent. 4) In spinal rabbits, syrosingopine $(200\;{\mu}g/kg)$ produced slight potentiation of pressor effect of NE. The same dose of reserpine produced more pronounced potentiation. 5) In the whole rabbits carbachol inhibited the potentiation observed 4 hours after administration of $40\;{\mu}g/kg$ of reserpine and syrosingopine. 6) In spinal rabbits, the potentiation observed 10 hours after $200\;{\mu}g/kg$ of reserpine and syrosingopine was inhibited by administration of carbachol. 7) The onset of potentiation of the pressor effect of NE was within 15 min after administration of syrosingopine and reserpine (1 mg/kg, each). 8) The above data suggest that the development of NE supersensitivity by syrosingopine and reserpine in rabbits has more intimate relationship with the decrease of central catecholamine contents than with that of peripheral ones. The depression of central sympathetic tone produced by these agents seems to play an important role in development of supersensitivity.

• Journal of Yeungnam Medical Science
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• v.11 no.2
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• pp.388-397
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• 1994

Bartter's syndrome is a rare tubular disorder characterized by hypokalemic, hypochloremic metabolic alkalosis, hyperreninemic, hyperaldosteronism, hyporesponsiveness to pressor agents and juxtaglomerular apparatus hyperplasia. We report a case of Bartter's syndrome of a 5 month-old male infant with subdural hematoma who was confirmed by characteristic clinical, laboratory findings and kidney biopsy. In addition to a case report, brief review of related lituratures was done.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.153-164
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• 1988

The potential role of endogenous opioid peptides (EOPS) in cardiovascular regulation has only recently been entertained. EOPS have been localized in brain, spinal cord, autonomic ganglia, particularly the adrenal gland, and many other peripheral tissues. There are at least five major types of opioid receptors; namely ${\mu},\;{\delta},\;k,\;{\sigma},\;and\;{\varepsilon}$ and Experimental evidence indicates that cardiovascular actions of the peptide are mediated primarily by ${\mu},\;{\delta}$ and k receptors, and that these receptor types may be allosterically coupled. In anesthetized rabbits met-enkephalin decreased blood pressure and heart rate, which closely paralleled a reduction in sympathetic discharge. Naloxone, but not naloxone methobromide, antagonized these effects, which suggests a central site of action of met-enkephalin. A number of autonomic agents, particularly adrenergic ${\alpha}$-and, ${\beta}-agonists$ and antagonists modify the cardiovascular actions of met-enkephalin. Experiments in reserpine-treated and adrenalectomized rats provide no evidence of sympathetic nervous system involvement in the pressor responses to intravenous injection of opioid peptides, but rather suggest a direct peripheral action. Finally, activation of a beta-endorphinergic pathway projecting from the arcuate nucleus to the nucleus tractos solitarii in rats can cause naloxone reversible hypotension and bradycardia. There is evidence to implicate this pathway in antihypertensive drug action and in the modulation of baroreflex activity.

• Toxicological Research
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• v.12 no.2
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• pp.195-201
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• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.