• 대한수의학회지
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• 제28권1호
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• pp.29-36
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• 1988

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor rsponses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into a ear vein, and then same procedures were performed 1~2 min after treatment with intravenous verapamil. The results are summarized as follows: 1. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylphrine($30{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 3. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$), phenylephrine($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. 4. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$) and phenylephrine($10{\mu}g/kg$) were inhibited by pretreatment with intravenous verapairlil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 5. Pressor responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine($30{\mu}g/kg$) and clonidine($100{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in pithed rats. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that verapamil significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors and the inhibition is greater in alpha-2 adrenoceptor-induced response than in alpha-1 adrenoceptor-induced one, and calcium channel takes part in the process of the pressor response mediated by alpha-1 adrenoceptors as well as alpha-2 adrenoceptors.

• 대한수의학회지
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• 제28권1호
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• pp.23-28
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• 1988

To examine the selectivity of diltiazem, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor responses, effect of diltiazem on alpha-adrenocepter agonist-induced pressor responses were investigated in urethane-anesthetized rabbits and spinal rabbits. The results are summarized as follows: 1. Intravenous diltiazem(10, 30, 100, 300, $1000{\mu}g/kg$) produced dose-dependent depressor response in rabbits. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylephrine ($30{\mu}g/kg$) were inhibited by pretreatment with intravenous diltiazem in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by diltiazem. 3. Presser responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine ($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous diltiazem in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by diltiazem. The inhibition of clonidine-induced pressor response by diltiazem was slightly prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that diltiazem significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors.

• The Korean Journal of Physiology
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• 제25권2호
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• pp.201-209
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• 1991

The rostral ventrolateral medulla (RVLM) has been established recently as a sympathoexcitatory area. The present study was conducted to investigate whether the somatosympathetic pressor and/or depressor responses are mediated through RVLM in cats anesthetized with ${\alpha}-chloralose$. An occipital craniectomy was performed and ventrolateral medulla were stimulated either electrically or chemically to evoke changes in arterial blood pressure. And then the effect of lesions in the ventrolateral medulla on the changes in blood pressure elicited by the peripheral nerve stimulation was observed. Followings are the results obtained: 1) Pressor areas were found in the ventrolateral medulla, lateral reticular nucleus and rostral dorsal area. 2) Depressor areas were found mainly in the ventrolateral medulla rostral to the pressor areas. 3) Some areas showed biphasic responses: a depressor response to lower frequency and a pressor response to higher frequency stimulation. 4) After electrical lesion in pressor area in RVLM, the somatosympathetic pressor response was abolished or depressed markedly. The somatosympathetic depressor response, however, remained after the lesion. 5) Electrical lesion in the depressor area abolished somatosympathetic depressor response. From the above results it is concluded that somatosympathetic pressor response is mediated through RVLM, while somatosympathetic depressor response is not mediated through RVLM.

• 대한약리학회지
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• 제3권1호
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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.

• 대한약리학회지
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• 제15권1_2호
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• pp.7-12
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• 1979

1. 두개내압상승(頭蓋內壓上昇)에 혈압상승(血壓上昇)이 중추(中樞)의 교감신경기능(交感神經機能)과의 관계(關係)가 있음을 확인(確認)하기 위하여, clonidine, phenoxybenzamine 및 phentolamine을 사용(使用)하여 이들 약물(藥物)이 두 개내압상승(頭蓋內壓上昇)에 따른 협압상승(血壓上昇)에 미치는 영향(影響)을 조사(調査)하였다. 2. 정맥내(靜脈內) clonidine은 측뇌실내(側腦室內) 주입시(注入時)와 같이 두개내압상승(頭蓋內壓上昇)에 따른 혈압상승(血壓上昇)을 억제(抑制)하였다. 3. Phenoxybenzamine 및 phentolamine의 정맥내주입후(靜脈內注後)에 두 개내압상승(頭蓋內壓上昇)에 따른 혈압상승(血壓上昇)은 현저히 약화(弱化)되었다. 4. 측뇌실내주입(側腦室內注入) phenoxybenzamine은 두개내압상승(頭蓋內壓上昇)에 따른 혈압상승(血壓上昇)에 영향(影響)을 미치지 않았다. 5. 측뇌실내(側腦室內)에 phenoxybenzamine을 주입후(注入後)에는 clonidine의 측뇌실내주입(側腦室內注入)이 두개내압상승(頭蓋內壓上昇)에 따른 혈압상승(血壓上昇)을 억제(抑制)치 못하였다. 6. 두개내압상승(頭蓋內壓上昇)에 따른 혈압상승(血壓上昇)에는 중추(中樞) 및 말초(末梢)의 교감신경기능(交感神經機能)이 관여(關與)함을 확인(確認)하였다.

• The Korean Journal of Physiology
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• 제23권1호
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• pp.129-138
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• 1989

척수 전근내 구심신경의 특성을 알아보기 위하여 고양이에서 L7 척수 전근을 전기자극하여 유발되는 동맥혈압의 변동을 관찰하였다. morphine을 정맥내 혹은 직접 척수에 투여하여 그 효과를 관찰하였으며 척수에 부분적인 손상을 가하여 척수 전근의 구심정보가 척수의 어느 부위를 통하여 중추로 올라가 승압반응을 유발하는지를 결정하여 다음과 같은 결과를 얻었다. 1. 척수전근을 C-강도, 높은 빈도로 자극하면 현저한 승압반응을 유발하였으며 낮은 빈도로 자극할 때에는 피부 혹은 근육감각신경을 자극할 때 보이는 감압반응이 유발되지 않았다. 2. 경수부위를 절단하였을 경우 승압반응이 소실되어 승압반응이 전적으로 척수 상부구조를 통하여 일어남을 알 수 있었다. 3. 승압 반응의 척수내 상행경로는 척수의 dorsolateral funiculus에 양측성으로 존재하였다. 4. 정맥내로 주사한 morphine은 척수 전근내 구심섬유가 자극되어 유발되는 승압반응을 강화시켰으나 척수에 직접 투여한 morphine은 승압반응을 억제하였다. 이상의 결과로부터 척수 전근내에 존재하는 구심성 섬유들은 기능적으로 근육 감각신경 중에 승압반응을 유발하는 C-섬유와 유사한 성질을 갖는다고 사료된다.

• The Korean Journal of Physiology
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• 제26권1호
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• pp.69-74
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• 1992

Central cardiovascular effects of bradykinin were examined in anesthetized normotensive (NTR) and 2-kidney, 1 clip Goldblatt hypertensive rats (GHR). Bradykinin ($0.5{\sim}10nmol$) was administered into the right lateral cerebral ventricle, while blood pressure and heart rate (HR) were continuously monitored. In both NTR and GHR, intracerebroventricular bradykinin produced a dose dependent increase in mean arterial pressure (MAP) without significant changes in HR. GHR were more sensitive in the pressor response than NTR. The pressor response to bradykinin was attenuated by treatment with hexamethonium (2.5mg/kg/min, IV) or phentolamine (2mg/kg, IV) in both NTR and GHR. Reserpine treatment (2mg/kg/day, intramuscularly,2 days) did not affect the central pressor effect of bradykinin in NTR but it attenuated the pressor effect in GHR. Pretreatment with indomethacin (10mg/kg, intraperitoneally) or saralasin ($20{\mu}g$/kg/min, IV) was without effects on the pressor response to bradykinin. These results indicate that the central pressor effect of bradykinin is, at least in part, due to excitation of the autonomic nervous activity. Mechanisms other than the enhanced sympathetic nervous activity ran. not be ruled out, However. It is also suggested that the sensitivity to bradykinin is increased in the GHR.

• 대한약리학회지
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• 제3권1호
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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.

• The Korean Journal of Physiology
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• 제22권2호
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• pp.231-243
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• 1988

This study was performed to investigate the mechanism of changes in arterial blood pressure, as a typical example of somatosympathetic reflex, induced by activation of muscular afferent nerves. Cats were anesthetized with ${\alpha}-chloraloae$ (60 mg/kg, i.p.). Afferent fibers in muscle nerve were activated by various method muscle contraction, electrical stimulation of muscle nerves, intraarterial injection of some algesic substances and noxious mechanical stimulation etc-and the evoked changes in arterial blood pressure were monitored. The effects of intravenous or direct spinal administration of morphine on the changes in arterial blood pressure induced by activation of the muscle afferent fibers were observed and also the effects of spinal lesions made in the $L1{\sim}L3$ spinal cord on them were studied to identify the ascending spinal pathways of the somatosympathetic reflexes. Followings are the results obtained. 1) The stimulation of medial gastrocnemius nerve under non-paralyzed condition with C-strength, low frequency (lower than 20 Hz) stimuli elicited a depressor response and a pressor response was elicited with C-strength, high frequency stimuli, of which the maximal response was observed at 100 Hz stimulation. 2) When the animal was paralyzed, depressor response to stimulation of the medial gastrocnemius nerve was observed with C-strength, $0.5{\sim}5Hz$ stimuli although the amplitude of the depressor response was decreased. The maximal pressor response was observed during stimulation with C-strength, $20{\sim}100Hz$ stimuli. 3) Intraarterial injection of some algesic substances induced marked pressor responses while noxious mechanical stimulation of the medial gastrocnemius muscle was not enough to elicit any significant changes (larger than 10 mmHg) in arterial blood pressure. 4) Systemically administered morphine (2 mg/kg) lowered the arterial blood pressure immediately and persistently and it was reversed by administration of naloxone. Direct spinally administered morphine did not elicit any changes. 5) The pressor response elicited by the activation of muscle afferent nerves was strengthened by systemic morphine administration while the depressor response tended to decrease. 6) Morphine administered on the spinal cord directly, decreased pressor response but did not change depressor response. From the above results it is concluded that there are separate groups of afferent nerves in the medial gastrocnemius nerve, which elicit pressor and depressor responses and the spinal ascending pathways of them are also separated from each other.

• The Korean Journal of Physiology
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• 제28권2호
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• pp.191-196
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• 1994

Captopril, an inhibitor of angiotensin converting enzyme, is also known to inhibit the degradation of bradykinin. We examined the effects of intracerebroventricular (ICV) captopril on the central pressor response to bradykinin in normotensive, 2-kidney, 1 clip Goldblatt (GHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Captopril (1 mg) and bradykinin (5 nmol) were administered into the right lateral cerebral ventricle, and blood pressure and heart rate were continuously monitored throughout the experiment. ICV captopril alone did not affect the blood pressure within 10 minutes but it significantly augmented the central pressor response to bradykinin in GHR. On the contrary, captopril was without effect on the pressor response to bradykinin in normotensive and DOCA-salt rats. These findings indicate that endogenous kinins are not critical in regulating arterial pressure in normotensive and DOCA hypertensive rats. However, in GHR, an enhanced activity of the brain kallikrein-kinin system in maintaining the high blood pressure is suggested.