摘要:

Veratridine caused a positive inotropic action in the electrically driven left atria of rats. Quinacrine (a phospholipase A2 inhibitor), indomethacin (a cyclooxygenase inhibitor) and aspirin (a cyclooxygenase inhibitor), but not nordihydroguaiaretic acid (a lipoxygenase inhibitor), inhibited the response to veratridine. Verapamil and nifedipine also inhibited the response to veratridine. The positive inotropic effect of arachidonic acid was abolished by aspirin and indomethacin. However, the positive inotropic effect of PGF2α was not affected by indomethacin, quinacrine or aspirin. PGE2, but not STA2 and PGI2, also caused the positive inotropic effect. However, the negative inotropic effect was observed in the presence of PGE1 and PGD2. Veratridine shifted the concentration-response curve of Ca2+ to the left in a Ca2+-free medium. Indomethacin only inhibited the veratridine-induced potentiation of Ca2+ responses. Veratridine increased the level of PGF2α in the left atria and this action was completely inhibited by indomethacin, aspirin and quinacrine. Veratridine also increased the level of PGE2. These results imply that the positive inotropic action of veratridine is partly due to stimulation of the release of arachidonic acid leading to the increase in prostaglandins in rat atri

ISSN:0031-7012    

DOI:10.1159/000138774

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The purpose of this study was to investigate the effect of the synthetic Met-enkephalin, D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin (FK 33-824), on blood pressure, heart rate, respiratory rate and survival, after its injection into the 4th cerebral ventricle of Wistar rats. The animals were either anesthetized with pentobarbital and breathing spontaneously or unanesthetized. The unanesthetized rats were previously instrumented with cannulas in the 4th cerebral ventrical and a systemic artery. In anesthetized rats, intracerebroventricular administration of FK 33-824 produced a transient increase in blood pressure followed by sustained hypotension, bradycardia and respiratory depression in a dose-dependent manner. Fatalities were observed over a 150-min observation period and were a function of dose. Pretreatment with atropine sulfate (1 mg/kg i.v.) produced an accentuated response with greater hypotension, bradycardia and shorter survival. In another group of anesthetized rats, in which hypoventilation was prevented by mechanical ventilation, blood pressure and heart rate were not as reduced as in spontaneously breathing rats. Hypotension, bradycardia and hypoventilation were less marked in unanesthetized rats, compared to anesthetized rats. Thus, FK 33-824 in the 4th cerebral ventricle of the rat produces marked changes in blood pressure in anesthetized as well as unanesthetized animals, but these changes were less in the unanesthetized or mechanically ventilated animal and greater after atropine, suggesting that these effects are mediated by respiratory depression and are antagonized by the cholinergic nervous system.

ISSN:0031-7012    

DOI:10.1159/000138775

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The aim of the present investigation was to examine the ability of adrenaline to modulate presynaptically the stimulation-evoked release of noradrenaline from postganglionic sympathetic nerves in the rabbit ear artery. Strips of rabbit central ear artery were incubated with 3H-noradrenaline. Subsequently, they were washed repeatedly with physiological salt solution containing cocaine and corticosterone. The strips were subjected to repeated electrical-field stimulation (S1–S8, 150 pulses, 0.5 ms, 225 mA, 3 Hz) and the resultant 3H overflow was determined. Adrenaline (10–8 to 10–6 mol/l) and clonidine (10–9 to 10–6 mol/l) reduced the stimulation-evoked 3H overflow. Rauwolscine (10–7 to 10–5 mol/l) and phentolamine (3 × 10–7 to 3 × 10–5 mol/l) enhanced markedly the stimulation-evoked 3H overflow. Rauwolscine (10–6 mol/l) abolished the inhibitory effect of low concentrations of adrenaline (10–8 to 10–7 mol/l) and clonidine (10–9 to 10–7 mol/l) and attenuated the inhibitory effect of the highest concentration (10–6 mol/l) of clonidine, but not that of adrenaline. In some experiments, the stimulation current was reduced to 175 mA in order to obtain similar reference release (S3) values despite the presence of rauwolscine. Even then, only the highest concentration (10–6 mol/l) of adrenaline decreased the stimulation-evoked 3H overflow. Facilitation was not seen. It is concluded that adrenaline activates inhibitory presynaptic α2-adrenoceptors. Furthermore, adrenaline does not reveal the presence of presynaptic facilitatory β-adr

ISSN:0031-7012    

DOI:10.1159/000138776

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The vasomotor effects of histamine and its interaction with serotonin were studied in isolated human placental chorionic veins. Histamine induced concentration-dependent contractions with an EC50 of 8.7 ± 1.2 × 10–6 mol/l. The H1 antagonist, pyrilamine (10–9 to 10–7 mol/l), inhibited histamine-induced contractions, with a pA2 of 8.33 ± 0.32 at a slope of 0.635. Cimetidine (H2 antagonist) had no effect on histamine-induced contractions. Serotonin (10–9 to 10–8 mol/l) significantly potentiated the contractile effect of histamine. The possible implications of the interaction between both amines in the regulation of placental blood flow

ISSN:0031-7012    

DOI:10.1159/000138777

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effects of parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) on renal arteriolar tone and proximal tubule adenylate cyclase were examined. In both afferent and efferent arterioles, PTH produced concentration-dependent relaxation of norepinephrine-induced tone with EC50 values of 8.7 and 9.9 nmol/l, respectively. PTHrP also produced relaxations that were indistinguishable from PTH. In proximal convoluted tubules PTH and PTHrP stimulated adenylate cyclase to the same extent and with similar potencies. The PTH antagonist, bPTH(7–34), totally blocked PTH-induced arteriolar relaxation but had no effect on proximal tubule adenylate cyclase. The results demonstrate that PTH and PTHrP are potent relaxants of glomerular arterioles and that PTH receptors present on the renal microvasculature may differ from those present on proximal tubule

ISSN:0031-7012    

DOI:10.1159/000138778

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effects of κ-opiate agonists on gastrointestinal motility was assessed in Swiss Webster, C57BL/6, BALB/c and DBA/2 strains of mice. The κ-agonists, PD 117302, U-69593 and U-50488H (3 mgkg–1), were injected subcutaneously and the distance travelled by a charcoal meal in the gastrointestinal tract was measured. All κ-agonists induced significant inhibition of charcoal meal transit; however, there were significant strain differences in the antitransit effect. It is concluded that κ-receptors are involved in the inhibition of gastrointestinal transit and that the negative data reported in the literature may be due to a genotype-dependent effect of κ-ag

ISSN:0031-7012    

DOI:10.1159/000138779

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Radioreceptor-binding assay and autoradiography were used to study the pharmacological profile and the anatomical localization of GABA-A-receptor sites in sections of rat duodenum, jejunum and ileum. (3H)-Muscimol, used as a ligand, was bound by sections of the intestinal portions investigated in a manner consistent with the labeling of GABA-A-receptor sites. The dissociation constant (Kd) was about 12.5 nmol/l in the three different intestinal portions. The maximum density of binding sites (Bmax) was highest in the duodenum (118.9 ± 7.4 fmol/mg tissue followed, in descending order, by the jejunum (105.8 ± 6.3 fmol/mg tissue) and the ileum (67.8 ± 5.9 fmol/mg tissue). Light microscope autoradiography revealed a dense accumulation of specific silver grains within intestinal smooth muscle. In the duodenum (3H)-muscimol-binding sites were rather homogeneously distributed both in circular and longitudinal smooth muscle. In the jejunum the density of silver grains was similar to that seen in the duodenum in the circular musculature and lower in the longitudinal musculature. The ileum displayed the lowest accumulation of (3H)-muscimol-binding sites, with no significant differences in the density of silver grains between the two muscular layers. The possible significance of the GABA-A-receptor sites observed in the intestinal musculature is discuss

ISSN:0031-7012    

DOI:10.1159/000138780

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

This study was designed to evaluate the antimotion sickness activity of ginger root (Zingiber officinale) and to characterize the effects of ginger on gastric function. Twenty-eight human volunteers participated in the project. Subjects made timed head movements in a rotating chair until they reached an endpoint of motion sickness short of vomiting (malaise III or M-III). Each subject was tested with either ginger or scopolamine and a placebo. A substance was judged to possess antimotion sickness activity if it allowed a greater number of head movements compared to placebo control. Gastric emptying of a liquid was measured by nuclear medicine techniques in normal and motion sick subjects. Gastric electrical activity was monitored by cutaneous (surface) electrodes positioned over the abdominal area. Powder ginger (whole root, 500 or 1,000 mg) or fresh ginger root (1,000 mg) provided no protection against motion sickness. In contrast, subjects performed an average of 147.5 more head movements (p < 0.01) after scopolamine (0.6 mg p.o.) than after placebo. The rate of gastric emptying was significantly (p < 0.05) slowed when tested immediately after M-III but was inhibited less when tested 15 min after M-III. Powdered ginger (500 mg) had no effect on gastric emptying in normal or motion-sick subjects. Gastric motility was also changed during motion sickness. The frequency of the electrogastrogram (EGG) was increased after M-III (tachygastria) and the normal increase in EGG amplitude after liquid ingestion was reduced in motion sick subjects. Although powdered ginger (500 mg) partially inhibited tachygastria in motion sickness, it did not enhance the EGG amplitude in motion sick subjects. We conclude that ginger does not possess antimotion sickness activity, nor does it significantly alter gastric function during motion sickness.

ISSN:0031-7012    

DOI:10.1159/000138781

出版商:S. Karger AG    

年代:1991

数据来源: Karger