Journal of autonomic pharmacology最新文献

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Propranolol stereoselectively inhibits alpha-adrenoceptor-mediated vasoconstriction in mesenteric arterial beds of rats. 心得安立体选择性抑制肾上腺素受体介导的大鼠肠系膜动脉床血管收缩。
Journal of autonomic pharmacology Pub Date : 1996-06-01
R E Stauber, A Heinemann
{"title":"Propranolol stereoselectively inhibits alpha-adrenoceptor-mediated vasoconstriction in mesenteric arterial beds of rats.","authors":"R E Stauber,&nbsp;A Heinemann","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>1. The optical isomers of propranolol were compared for their effects on pressor responses to adrenergic and non-adrenergic vasoconstrictors in mesenteric arterial beds of rats. 2. R(+)-propranolol (10(-7)-10(-5) M) had no effect on vessel preparations stimulated with noradrenaline, methoxamine, or arginine-vasopressin. 3. S(-)-propranolol 10(-7) M did not alter pressor responses to noradrenaline. However, S(-)-propranolol 10(-6) and 10(-5) M inhibited vasoconstriction induced by noradrenaline. This effect was similar in the presence of indomethacin 3 x 10(-6) M. 4. S(-)-propranolol 10(-5) M also inhibited vasoconstriction induced by methoxamine, shifting the dose-response curves to the right, but did not affect pressor responses to arginine-vasopressin. 5. Schild analysis for equilibrium vasoconstrictor responses to methoxamine indicated stereoselective competitive alpha-adrenoceptor antagonism by propranolol. 6. These data suggest selective inhibition of alpha-adrenoceptor-mediated vasoconstriction by S(-)-propranolol at higher concentrations by competitive alpha-adrenoceptor antagonism.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"16 3","pages":"125-9"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19850568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effect of tamsulosin, a novel alpha 1-adrenoceptor antagonist, on urethral pressure profile in anaesthetized dogs. 新型α - 1肾上腺素受体拮抗剂坦索罗辛对麻醉犬尿道压力谱的影响。
Journal of autonomic pharmacology Pub Date : 1996-06-01
K Sudoh, H Tanaka, O Inagaki, M Asano, T Takenaka
{"title":"Effect of tamsulosin, a novel alpha 1-adrenoceptor antagonist, on urethral pressure profile in anaesthetized dogs.","authors":"K Sudoh,&nbsp;H Tanaka,&nbsp;O Inagaki,&nbsp;M Asano,&nbsp;T Takenaka","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>1. The effect of tamsulosin (YM617, (R) (-)-S-[2-[[2-(o-ethoxyphenoxy)ethyl]amino] propyl]-2-methoxybenzenesulfonamide HCl), a potent and selective alpha 1-adrenoceptor antagonist, was examined on urethral pressure profile (UPP) and mean arterial blood pressure (MBP) in pentobarbital anaesthetized male dogs. 2. Selective alpha 1-adrenoceptor antagonists tamsulosin (1-100 micrograms kg-1 i.v.), prazosin (1-100 micrograms kg-1 i.v.) and bunazosin (1-100 micrograms kg-1 i.v.) produced a dose dependent reduction in prostatic pressure in the UPP. Doses required to reduce prostatic pressure in UPP by 30% were 3.6 +/- 0.8 (n = 8), 6.9 +/- 1.5 (n = 8) and 4.6 +/- 0.9 (n = 8) micrograms kg-1 i.v., respectively. At the highest dose, tamsulosin exerted less hypotensive effect than prazosin and bunazosin. 3. The calcium antagonist nicardipine (0.1-10 micrograms kg-1 i.v.) and angiotensin converting enzyme inhibitor captopril (10-1,000 micrograms kg-1 i.v.) reduced MBP in a dose dependent manner, but exerted no effect on prostatic pressure in the UPP. The diuretic trichloromethiazide (1-100 micrograms kg-1 i.v.) exerted no effect on UPP or MBP. Treatment with nicardipine (3 micrograms kg-1 i.v.), captopril (100 micrograms kg-1 i.v.) or trichlormethiazide (100 micrograms kg-1 i.v.) did not affect relaxant effect of tamsulosin on prostatic pressure in UPP, or potentiate its hypotensive effect. 4. These results suggest that the alpha 1-adrenoceptor regulates urethral pressure as well as blood pressure in anaesthetized dogs, and that alpha 1-adrenoceptor antagonists may be useful in the treatment of micturition disorders associated with benign prostatic hyperplasia. In addition, as tamsulosin decreased urethral pressure with less hypotension, and as its effect was not influenced by treatment with hypotensive drugs, it may be a useful drug for the treatment of micturition disorders with few cardiovascular side effects.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"16 3","pages":"147-54"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19850570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibition of calcium influx and tonic response to K+ of intestinal smooth muscle by hydralazine. 肼嗪抑制肠平滑肌钙内流及对K+的强直反应。
Journal of autonomic pharmacology Pub Date : 1996-06-01
T Nasu, S Yanagimoto
{"title":"Inhibition of calcium influx and tonic response to K+ of intestinal smooth muscle by hydralazine.","authors":"T Nasu,&nbsp;S Yanagimoto","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>1. Evidence concerning the mechanism of the inhibition of contraction caused by hydralazine has been sought in ileal longitudinal muscle and taenia coli of guinea-pig. Hydralazine (10(-3)-3 x 10(-3) M) markedly inhibited K+ (60 mM) induced tonic response with smaller effects on the phasic response in the ileal muscle. However, 10(-2) M hydralazine completely abolished both responses. 2. Hydralazine increased the threshold for Ca2+ induced contraction in Ca2+ free, K+ depolarized taenia coli and reduced the maximal response size. A low concentration (3 x 10(-10) M) of nifedipine, an L-type Ca2+ channel blocker, further caused a parallel shift to the right in the presence of hydralazine in the concentration-response curves obtained with Ca2+ 3. Hydralazine caused a significant decrease in Ca2+ uptake measured by the lanthanum method during the K+ induced tonic response in ileal muscle; however, it did not affect the Ca2+ efflux. 4. In ileal muscle fibres treated with Triton-X-100, in which the Ca2+ release sites are destroyed, 10(-3) M hydralazine had no effect on the contractions induced by 10(-5) M Ca2+; however, hydralazine at a higher concentration (10(-2) M) had a slight inhibitory effect on the contraction. 5. The present finding indicates that the inhibitory action on contractions produced by hydralazine may result mainly from the interference of calcium permeability at the cell membrane in ileal muscle. There is the possibility that hydralazine of higher concentrations may have a minor action on the contractile system.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"16 3","pages":"169-76"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19850573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effect of the Ca(2+)-channel agonist Bay K 8644 on the contractile responses in human placental veins. Ca(2+)通道激动剂Bay k8644对人胎盘静脉收缩反应的影响
Journal of autonomic pharmacology Pub Date : 1996-06-01
M T Barrús, J Reviriego, J Marín
{"title":"Effect of the Ca(2+)-channel agonist Bay K 8644 on the contractile responses in human placental veins.","authors":"M T Barrús,&nbsp;J Reviriego,&nbsp;J Marín","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>1. The aim of the present study was to analyse, in segments of human placental veins, the effect of the Ca2+ channel agonist Bay K 8644 (0.1 microM) and Ca2+ channel antagonists nifedipine (0.1 microM) and diltiazem (1 microM) on vascular contractility and 45Ca2+ uptake. 2. The Ca2+ channel agonist Bay K 8644 (0.1 microM) caused small concentration dependent contractions that were increased by a moderate membrane depolarization with 7.5 mM K+. This increase was reversed by nifedipine and diltiazem. Ca2+ addition to segments previously depolarized with 75 mM K+ and exposed to a Ca(2+)-free medium caused contractile responses that were increased by 0.1 microM Bay K 8644; such an increase was blocked by 0.1 microM nifedipine and 1 microM diltiazem. 3. K+ and 5-HT induced concentration dependent contractile responses which were increased by Bay K 8644 (0.1 microM). Both 0.1 microM nifedipine and 1 microM diltiazem inhibited the increasing effect of Bay K 8644. Bay K 8644 (30 nM and 0.1 microM) caused an enhancement in 45Ca2+ accumulation over the basal value, that was increased by membrane depolarization with K+ (7.5, 15 and 30 nM) and inhibited by nifedipine (0.1 microM). K+ (15 and 30, but not 7.5 mM) and 5-HT (1 microM) induced 45Ca2+ uptake over the basal level that was increased by Bay K 8644 (0.1 microM). Such an increase was antagonized by nifedipine (0.1 microM). 4. These data indicate that: (1) a small depolarization with K+ is needed for Bay K 8644 to be able to produce consistent contractile responses, suggesting that voltage gated Ca2+ channels (VGCCs) are not activated in a basal situation in placental veins; (2) the increase of 5-HT contraction by Bay K 8644 may be produced by either the capability of this amine to depolarize the membrane of smooth muscle cells and subsequent facilitation of Ca2+ influx through VGCCs or direct activation by Bay K 8644 of receptor (5-HT) operated Ca2+ channels (ROCs), and (3) the increasing effect of Bay K 8644 appears to be due to a Ca2+ entry activation through VGCCs.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"16 3","pages":"161-7"},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19850572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
8th Meeting on Adrenergic Mechanisms. Porto, Portugal, 20-22 September 1993. Proceedings and abstracts. 肾上腺素能机制第8次会议。1993年9月20日至22日,葡萄牙波尔图。会议记录和摘要。
Journal of autonomic pharmacology Pub Date : 1994-02-01
{"title":"8th Meeting on Adrenergic Mechanisms. Porto, Portugal, 20-22 September 1993. Proceedings and abstracts.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"14 1","pages":"1-28"},"PeriodicalIF":0.0,"publicationDate":"1994-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18908073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of some antipsychotic drugs on cardiovascular catecholamine receptors in the rat. 一些抗精神病药物对大鼠心血管儿茶酚胺受体的影响。
Journal of autonomic pharmacology Pub Date : 1989-12-01 DOI: 10.1111/j.1474-8673.1989.tb00480.x
M L Cuffí, E Vila, A Badia
{"title":"Effects of some antipsychotic drugs on cardiovascular catecholamine receptors in the rat.","authors":"M L Cuffí,&nbsp;E Vila,&nbsp;A Badia","doi":"10.1111/j.1474-8673.1989.tb00480.x","DOIUrl":"https://doi.org/10.1111/j.1474-8673.1989.tb00480.x","url":null,"abstract":"<p><p>1. Experiments were performed to determine the activity of four antipsychotic drugs on several catecholamine receptors that control the sympathetic cardiovascular responses in rats. 2. Chlorpromazine, thioridazine (0.03 and 0.1 mg kg-1) and haloperidol (0.3 and 1 mg kg-1) inhibited methoxamine-induced diastolic blood pressure increases in the pithed rat, whereas sulpiride (1 and 3 mg kg-1) was without effect. 3. Only sulpiride (3 mg kg-1) antagonized the pressor responses induced by xylazine. 4. Xylazine inhibited the heart rate increase induced by electrical stimulation of the spinal cord (C7-Th1) in the pithed rat. This effect was partially prevented by sulpiride (1 and 3 mg kg-1) and chlorpromazine (0.3 mg kg-1). A higher dose of chlorpromazine (1 mg kg-1) abolished the inhibitory effect of xylazine. 5. Apomorphine infusion inhibited the pressor responses induced by electrical stimulation (Th5-L4) in pithed rats. This effect was reversed by sulpiride (0.01, 0.03 and 0.1 mg kg-1) and partially antagonized by haloperidol (0.1 mg kg-1). 6. The depressor response to fenoldopam in anaesthetized rats was only inhibited by the higher dose of chlorpromazine and thioridazine (3 mg kg-1). 7. Our results suggest that, in the peripheral nervous system of the rat, haloperidol and sulpiride act as antagonists of DA2 receptors while chlorpromazine and thioridazine antagonized DA1 receptors. Furthermore, thioridazine and haloperidol show alpha 1-adrenoreceptor antagonist properties, whereas sulpiride antagonizes alpha 2-adrenoreceptors. Chlorpromazine shows mixed alpha 1/alpha 2-adrenoreceptor antagonism.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"9 6","pages":"397-409"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13718597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Isoprenaline and the pancreas in dogs. 异丙肾上腺素和狗的胰腺。
Journal of autonomic pharmacology Pub Date : 1989-12-01 DOI: 10.1111/j.1474-8673.1989.tb00478.x
L Bennett, A Pap, S Naruse, D F Magee
{"title":"Isoprenaline and the pancreas in dogs.","authors":"L Bennett,&nbsp;A Pap,&nbsp;S Naruse,&nbsp;D F Magee","doi":"10.1111/j.1474-8673.1989.tb00478.x","DOIUrl":"https://doi.org/10.1111/j.1474-8673.1989.tb00478.x","url":null,"abstract":"<p><p>1. In conscious dogs basal pancreatic secretion per 100 min was significantly reduced by 0.75 microgram kg-1h-1 of isoprenaline. The expected spontaneous peaking was seen only after stopping the drug. 2. Following propranolol, the 100-min pancreatic secretion was less than control but greater than secretion after isoprenaline. The interpeak interval was increased, and the perigee levels (interpeak) were higher than in the controls. Peak protein secretion was unaltered but volume was reduced. 3. Guanethidine did not abolish periodicity but it prolonged the interpeak interval. Protein peaks and 100-min totals were lower than control and volume perigees higher. 4. It is concluded that beta-adrenoreceptor stimulation inhibits pancreatic secretion. Adrenergic antagonists exert similar inhibitory effects indicating a complex role for the sympathetic nervous system in the control of pancreatic secretion.</p>","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"9 6","pages":"379-85"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13762401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of some antipsychotic drugs on cardiovascular catecholamine receptors in the rat. 一些抗精神病药物对大鼠心血管儿茶酚胺受体的影响。
Journal of autonomic pharmacology Pub Date : 1989-12-01 DOI: 10.1111/J.1474-8673.1989.TB00499.X
M. Cuffí, E. Vila, A. Badía
{"title":"Effects of some antipsychotic drugs on cardiovascular catecholamine receptors in the rat.","authors":"M. Cuffí, E. Vila, A. Badía","doi":"10.1111/J.1474-8673.1989.TB00499.X","DOIUrl":"https://doi.org/10.1111/J.1474-8673.1989.TB00499.X","url":null,"abstract":"1. Experiments were performed to determine the activity of four antipsychotic drugs on several catecholamine receptors that control the sympathetic cardiovascular responses in rats. 2. Chlorpromazine, thioridazine (0.03 and 0.1 mg kg-1) and haloperidol (0.3 and 1 mg kg-1) inhibited methoxamine-induced diastolic blood pressure increases in the pithed rat, whereas sulpiride (1 and 3 mg kg-1) was without effect. 3. Only sulpiride (3 mg kg-1) antagonized the pressor responses induced by xylazine. 4. Xylazine inhibited the heart rate increase induced by electrical stimulation of the spinal cord (C7-Th1) in the pithed rat. This effect was partially prevented by sulpiride (1 and 3 mg kg-1) and chlorpromazine (0.3 mg kg-1). A higher dose of chlorpromazine (1 mg kg-1) abolished the inhibitory effect of xylazine. 5. Apomorphine infusion inhibited the pressor responses induced by electrical stimulation (Th5-L4) in pithed rats. This effect was reversed by sulpiride (0.01, 0.03 and 0.1 mg kg-1) and partially antagonized by haloperidol (0.1 mg kg-1). 6. The depressor response to fenoldopam in anaesthetized rats was only inhibited by the higher dose of chlorpromazine and thioridazine (3 mg kg-1). 7. Our results suggest that, in the peripheral nervous system of the rat, haloperidol and sulpiride act as antagonists of DA2 receptors while chlorpromazine and thioridazine antagonized DA1 receptors. Furthermore, thioridazine and haloperidol show alpha 1-adrenoreceptor antagonist properties, whereas sulpiride antagonizes alpha 2-adrenoreceptors. Chlorpromazine shows mixed alpha 1/alpha 2-adrenoreceptor antagonism.","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"46 1","pages":"397-409"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82585870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Isoprenaline and the pancreas in dogs. 异丙肾上腺素和狗的胰腺。
Journal of autonomic pharmacology Pub Date : 1989-12-01 DOI: 10.1111/J.1474-8673.1989.TB00497.X
L. Bennett, A. Pap, S. Naruse, D. F. Magee
{"title":"Isoprenaline and the pancreas in dogs.","authors":"L. Bennett, A. Pap, S. Naruse, D. F. Magee","doi":"10.1111/J.1474-8673.1989.TB00497.X","DOIUrl":"https://doi.org/10.1111/J.1474-8673.1989.TB00497.X","url":null,"abstract":"1. In conscious dogs basal pancreatic secretion per 100 min was significantly reduced by 0.75 microgram kg-1h-1 of isoprenaline. The expected spontaneous peaking was seen only after stopping the drug. 2. Following propranolol, the 100-min pancreatic secretion was less than control but greater than secretion after isoprenaline. The interpeak interval was increased, and the perigee levels (interpeak) were higher than in the controls. Peak protein secretion was unaltered but volume was reduced. 3. Guanethidine did not abolish periodicity but it prolonged the interpeak interval. Protein peaks and 100-min totals were lower than control and volume perigees higher. 4. It is concluded that beta-adrenoreceptor stimulation inhibits pancreatic secretion. Adrenergic antagonists exert similar inhibitory effects indicating a complex role for the sympathetic nervous system in the control of pancreatic secretion.","PeriodicalId":15103,"journal":{"name":"Journal of autonomic pharmacology","volume":"38 1","pages":"379-85"},"PeriodicalIF":0.0,"publicationDate":"1989-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79510563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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