Dibenamine inhibited [$^{3}$H]quinuclidinyl benzilate ([$^{3}$H]QNB) binding in both concentration and incubation time-dependent manners. The $IC_{50}$/ value of dibenamine for the inhibition of the specific binding of 100 pM [$^{3}$'H]QNB following incubation of cerebral microsomes with dibenamine at 37.deg. C for 15 min was 20.mu.M. Dibenamine irreversibly decreased the binding site concentration for [$^{3}$H]QNB binding without affecting the affinity of [$^{3}$H]QNB for the muscarinic receptor. Analysis of the pirenzepine inhibition curve of [$^{3}$H]QNB binding to cerebral microsomes indicated the presence of two receptor subtypes with high(M$_{1}$ receptor, Ki=5nM) and low (M$_{2}$ receptor, Ki=160nM) affinity for pirenzepine. However, dibenamine(20.mu.M) treatment under the condition employed in these experiments caused steepening of the pirenzepine competition curve. The Ki value for pirenzepine in dibenamine treated-microsomes was approximately 120nM. suggesting a selective decrease in the number of M$_{1}$ receptor. Although dibenamine also inhibited [$^{3}$H]QNB binding to ventricular microsomes with $IC_{50}$/ value of 120.mu.M, the sensitivity for dibenamine in the ventricle was much lower than that in the cerebrum. These results indicate that dibenamine at low concentrations welectively inactivates the muscarinic M$_{1}$ receptor.
Adrenergic receptors are now classified into alpha type and beta type These adrenergic receptors are distributed in various tissue in different patterns. Therefore, the adrenergic response of a certain tissue may be different from those of the other tissues, and such differences may exist among various species of animals. In this paper, the authors attempt to reevaluate the effect of epinephrine on the isolated atria, aortic strips, and vas deferenses of rabbits preincubated with alpha receptor blockades (ergotamine and dibenamine) and beta receptor blockades (propranolol and dichloroisoproterenol) in Locke-Ringer bathing medium. The results obtained were summarized as follows; 1) The dose dependent responses of isolated atria to epinephrine were significantly inhibited by propranolol and dichloroisoproterenol, and slightly inhibited by dibenamine, but not affected by ergotamine. 2) The dose dependent responses of excised aortic strips to epinephrine were significantly inhibited by ergotamine and dibenamine, but the responses were slightly potentiated by propranolol, and significantly by dichloroisoproterenol. 3) The dose dependent responses of isolated vas deferenses to epinephrine were significantly inhibited by ergotamine and dibenamine, but slightly potentiated by propranolol and dichloroisoproterenol.
The effects of an irreversible or a reversible $\alpha_1$-adrenoceptor antagonist (dibenamine or prazosin) on $\alpha_1$-adrenoceptor-mediated vasoconstrictions were studied in the endothelium-denuded rat aorta. In these experiments, the mobilization of intracelluier calcium and translocation of extracellular calcium were also studied. To exclude the modulation of endothelium releasing EDRF and EDCF, the endothelium was removed in all rat aortas. Contraction induced by phenylephrine (a full $\alpha_1$-adrenoceptor agonist) was separated into a fast phasic component of the response due to the release of intracellular calcium and a slow tonic one due to the influx of extracellular calcium. Pretreatments with increasing doses of reversible $\alpha_1$-adrenoceptor antagonist prazosin, as well as irreversible $\alpha_1$-adrenoceptor antagonist dibenamine, inhibited the phasic component of phenylephrine-induced contraction more effectively than the tonic one. Pretreatment of dibenamine (0.2 $\mu{M}$) or prazosin (10 nM) to the rat aorta abolished phasic response but remained tonic one about 41% and 51%, respectively. These results suggest that as the efficiency of phenylephrine was progressively reduced by pretreatments with increasing doses of an irreversible or a reversible $\alpha_1$-adrenoceptor antagonist (dibenamine or prazosin), the contraction induced by phenylephrine became progressively more dependent on the influx of extracellular calcium.
A portion of duodenum laid pancreatic duct opening were perfused continuously with physiological saline under urethane anesthesia in rats. The pancreatic amylase secretory response to caerulein was studied with autonomic blockers, such as phenoxybenzamine, dibenamine, phentolamine, hexamethonium, propranolol, atropine, and cyproheptadine. The pancreatic amylase output to caerulein, 7.5ng/kg i.v., was markedly increased and the value was approximately three times greater than control. The caerulein-stimulated pancreatic amylase secretion was significantly decreased by i.v. phenoxybenzamine and propranolol treatment, but not by phentolamine or dibenamine. Secretory response of pancreatic amylase to caerulein was not affected by i.v. atropine, hexamethonium or cyproheptadine. These result lead to the conclusion that phenoxybenzamine may inherently inhibit the secretory response of pancreatic amylase to caerulein, and this effect was not related with ${\alpha}-adrenergic$ receptor blocking action.
Pharmacological investigation was performed in chickens which were pretreated with reserpine. Transmural stimulations were given to the isolated jejunum of chickens and studied the responses and the effects of dibenamine, propranolol, atropine and tetrodotoxin on them. The results obtained were summerized as follows: 1. Three different patterns of response were obtained from the isolated jejunum of non-treated chickens after giving them transmural stimulation. The first pattern was contraction followed by relaxation, the second pattern was contraction only and the third pattern was relaxation only. 2. The transmural stimulation of the jejunum preparations evoked relaxation while the periarterial stimulation evoked contraction in the reserpinized chick. 3. The relaxation response to the transmural stimulation was not affected by the pretreatment with dibenamine, propranolol and atropine. 4. The relaxation response to the transmural stimulation was abolished by tetrodotoxin. The results obtained in these studies indicate that the relaxation response to the transmural stimulation is due to non-adrenergic inhibitory fibers.
A comparison was made of the effects of selective ${\alpha_1}-adrenoceptor$ agonist phenylephrine and selective ${\alpha_2}-adrenoceptor$ agonist clonidine on endothelium-containing and endothelium-denuded rings of the rat aorta. In the case of phenylephrine, removal of endothelium increased sensitivity 2.5 fold at $EC_{50}$ level and maximum contractive response 1.4 fold. In the case of clonidine, which gave only 15% of maximum contractive response given to phenylephrine on endothelium-containing rings, removal of the endothelium increased sensitivity 5.6 fold at $EC_{50}$ level and maximum contractive response 5 fold, which was about 55% of that given by phenylephrine. In endothelium-denuded ring, phenylephrine-induced contraction tended to be more increased in tonic contraction than in phasic contraction as compared to that in endothelium-containing ring, while clonidine-induced contraction was monophasic and was increased only in tonic contraction. In the calcium-free solution or in the presence, of verapamil, contraction stimulated by clonidine was almost abolished while that stimulated by phenylephrine produced only phasic contraction. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium derived relaxing factor (EDRF), because hemoglobin, a specific blocking agent of EDRF, abolished this depression. It is unlikely that the endothelium-dependent relaxation was due to stimulation of release of EDRF, because clonidine did not produce endothelium-dependent relaxation in 5-hydroxytryptamine-precontracted ring even when its contractile action was blocked by the ${\alpha_1}-adrenoceptor$ antagonist, prazosin. When the efficacy of phenylephrine was reduced to about the initial efficacy of clonidine by pretreatment with dibenamine, the contraction-response curves for phenylephrine became very similar to the corresponding curves obtained for clonidine before receptor inactivation. In the dibenamine-treated rings, contraction of phenylephrine was abolished in calcium-free solution or in the presence of verapamil like that obtained for clonidine before receptor inactivation. These results suggest that EDRF spontaneously released from endothelium depress contraction more profoundly in a case of an agonist with low efficacy and the phenylephrine-induced contraction was totally dependent on extracellular calcium as was that obtained for clonidine when the efficacy of phenylephrine was reduced to that of clonidine by irreversible inactivation of ${\alpha_1}-adrenoceptor$ with dibenamine.
The present study was undertaken to investigate depressor action of tannic acid and the mechanism underlies it in the rabbit. The changes in arterial blood pressure were studied after intravenous administration of tannic acid in normal rabbits and the animals pretreated with atropine, propranolol, dibenamine, and hexamethonium. The results obtained were as follows; 1) Following administration of 1.5 mg/kg, 3.0 mg/kg, and 5.0 mg/kg of tannic acid into rabbits the maximum depressor responses observed were $12.0{\pm}0.9\;mmHg$, $23.4{\pm}1.0\;mmHg$, and $34.0{\pm}1.8\;mmHg$ respectively and generally depressor responses increased in proportion to dosage of tannic acid. 2) Since there were no changes in depressor responses to tannic acid in animals pretreated. separately with atropine, propranolol, dibenamine, and hexamethonium, the depressor responses appeared to be resulting from direct vasodilator action of tannic acid on the vascular smooth muscle. Comparing tannic acid and acorn extract in their mechanisms of depressor responses, it is strongly indicated that in acorn there might exist another depressor substance. 3) After administration of large doses of tannic acid, in addition to respiratory changes, the mean arterial blood pressure decreased markedly and was never recovered throughout the experiment. comma Therefore it is also suggested that the lethal action of tannic acid resides in a drastic decline of arterial blood pressure and in respiratory changes as well.
The effects of phenoxybenzamine and other related drugs were studied for their interaction with caerulein on gallbladder contraction in anesthetized animals and isolated gallbladder strips. Cholecystostomy and cystic duct ligation were made on anesthetized dog, cat and pig. Pressure changes of gallbladder were measured by a physiological pressure transducer connected to polygraph recorder. Isolated rabbit gallbladder strips were placed in a muscle chamber containing Locke-Ringer solution maintained at $38^{\circ}C$. The contractile responses were measured by a force-displacement transducer connected to polygraph recorder. Caerulein ($30{\sim}200$ ng/kg i.v.) produced marked contraction of gallbladder in situ and the cholecystokinetic potencies appear in decreasing order; dog, cat and pig. The response of caerulein was abolished by the large doses of phenoxybenzamine (15 mg/kg i.v.) but not affected with dibenamine, phentolamine or tolazoline. Cholecystokinetic effect of methacholine or barium chloride was also partially inhibited by phenoxybenzamine and the effect of caerulein was weakly inhibited intravenous injection of cyclophosphamide or papaverine. In isolated rabbit gallbladder strips, the response of contraction to caerulein were progressively inhibited by pretreatment of phenoxybenzamine along with time exposed. These results lead to the conclusion that phenoxytenzamine may inherently inhibit the contractile response of gallbladder to caerulein, and this effect was not related with ${\alpha}-adrenergic$ receptor blocking action.
The present study was undertaken to investigate effect of water extracts of the mulberry leaves (MWE) on arterial blood pressure and respiration in cats. And also studied were depressor responses to intravenously administered MWE in the animals pretreated separately with atropine(2.5 mg/kg), propranolol(2 mg/kg), dibenamine (15 mg/kg), and hexamethonium (1.5 mg/kg) in order to find out the mechanism of depressor activity of MWE. The results obtained were as follows; 1) Following intravenous administration of 0.25 ml/kg and 0.5 ml/kg of MWE into the cat the maximum depressor responses observed were $60.2{\pm}2.3\;mmHg$ and $72.3{\pm}1.7\;mmHg$ respectively. 2) Since depressor responses to intravenously administered MWE were partially inhibited by hexamethonium and markedly by atropine, it is strongly suggested that depressor activity of MWE mainly results from its vagal effects. 3) After administration of MWE respiratory rate was invariably increased following a short period of apnea.
It has been generally understood that the intestinal tracts are under the control of the autonomic nerves; the parasympathetics are excitatory and the sympathetics inhibitory. However, it is recently reported that the actions of these autonomic nerves in the newborn animals are shown to be different from those in the adult animals in some species. In order to elucidate the role of sympathetic innervation to the intestinal tracts, the effects of periarterial nerve stimulation were studied in the periarterial sympathetics-jejunum preparations of the chick and the effects of some autonomic drugs on the isolated muscle strips were also studied. The results obtained were as follows: 1. The periarterial stimulation in the periarterial sympathetics-jejunum preparation elicited the responses of three patterns; 1) contrcation followed by relaxation 2) contraction only 3) relaxation only. The excitatory response was most effective in the stimulus frequencies of 40 cps, whereas the inhibitory response was maximal in the stimulus frequencies of 30 cycle per second. 2. The excitatory response to the periarterial stimulation was not affected by the pretreatment with phenoxybenzamine, dibenamine, propranolol and atropine, whereas the inhibitory response was completely blocked by the pretreatment with phenoxybenzamine and propranolol. 3. In the periarterial syrnpathetics-jejunum preparation treated with reserpine, the periarterial stimulation evoked only contraction, and the contraction was not affected by the pretreatment with phenoxybenzamine, propranolol and atropine. 4. The administration of norepinephrine evoked a relaxation in the isolated jejunum muscle strips and the effect was completely blocked by the pretreatment with phenoxybenzamine. 5. The administration of isoproterenol produced a relaxation in the isolated jejunum muscle strips and the effect was not affected by pretreatment with phenoxybenzamine, whereas the effect was completely blocked by the pretratment with propranolol. 6) The administration of acetylcholine produced a marked contraction in the isolated jejunum muscle strips and the effect was completely abolished by the pretreatment of atropine. These experimental evidences indicate that the inhibitory response to the periarterial stimulation is due to adrenergic fibers and the excitatory response is due to neither adrenergic nor cholinergic component.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.