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Volume 103 (1994)
- Issue 6 Pages 245-
- Issue 5 Pages 193-
- Issue 4 Pages 141-
- Issue 3 Pages 83-
- Issue 2 Pages 43-
- Issue 1 Pages 1-
Volume 103, Issue 4
Displaying 1-4 of 4 articles from this issue
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Yushi ITO, Kazuhiro TASHIRO1994 Volume 103 Issue 4 Pages 141-150
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWhile the airway epithelium provides a diffusion barrier to the access of inhaled stimulants, it has recently been considered to have a more active physiological and pharmacological role in the regulation of the airway smooth muscle tone. The initial evidence for this comes from the fact that mechanical removal of the airway epithelium increases the in vitro responsiveness of airway smooth muscle to various spasmogens 3-5 times, although the nature of these regulatory mechanisms on the smooth muscle by the epithelium remains largely unresolved. One of the possible explanations is that the epithelium a generates factor(s) that inhibits the responsiveness of the underlying smooth muscle cells (epithelium-derived inhibitory or relaxing factor EpDIF/EpDRF). Furthermore, recent investigations revealed that airway epithelial cells also release a factor(s) that modulates the vascular smooth muscle tone, excitatory-neuroeffector transmission and resting membrane potential of the airway smooth muscle cells (epithelium-derived hyperpolarizing factor: EpDHF). This review will present and discuss the evidence indicating that the epithelium generates and releases a factor(s) that modulates smooth muscle tone, resting membrane potential of airway smooth muscle cells (EpDHF) and excitatory neuro-effector transmission in the airway.View full abstractDownload PDF (22538K) -
Masami NIWA1994 Volume 103 Issue 4 Pages 151-160
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe quantitative receptor autoradiographic method has been developed to determine the precise location and kinetic properties of receptors for biologically active transmitters, besed on the original technique for benzodiazepine receptors in the rat brain with a 3H-labeled ligand. The autoradiography with hyperfilm-3H of cryostat sections (10- to 20-μm thick) incubated with appropriate 3H- or 125I-labeled ligands and analysis of the autoradiogram by computerized microdensitometry makes feasible quantitative determinations and complete characterization of receptors in tissues from a single animal and in human tissues obtained at autopsy. Furthermore, the autoradiographic technique has advantages over receptor binding assays with partially purified membrane preparations because it enables precise anatomical localization and has high sensitivity. In some cases, the autoradiogram can be quantitated with a computerized radioluminographic imaging-plate system. Special care has to be taken when a 3H-labeled ligand is used, since tissue quenching of the radioisotope energy of 3H is linked to the failure to attain precise quantitation of receptors in myelin-rich areas such as brain white matter. In combination with quantitative radioimmunohistochemical and in situ hybridization techniques, the quantitative receptor autoradiographic method should enable investigators to elucidate the roles of receptors for biologically active transmitters.View full abstractDownload PDF (25149K) -
Hiroshi SAITOH, Yasuo ETOH, Makoto MURAKAMI, Tetsuhiro KUBOTA, Mizuo M ...1994 Volume 103 Issue 4 Pages 161-173
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe possibility of using KRI-1314, a new cyclohexylnorstatine derivative, as an antihypertensive drug was examined using common marmosets. KRI-1314 strongly inhibited plasma renin activity (PRA) in both humans and marmosets, with a 50% inhibitory concentration of 4.7×10-9 and 6.9×10-9 M, respectively. In anesthetized marmosets, the increase in both blood pressure and PRA induced by bolus intravenous injection of RH-renin (0.15 μg/kg) was suppressed by constant intravenous infusion of KRI-1314 (0.01 and 0.1 mg/kg/min) in a dose-dependent manner. In the sustained hypertension induced by continuous intravenous infusion of RH-renin (0.1 μg/kg/min), a dose-dependent hypotensive response was produced by bolus intravenous injection of KRI-1314 (0.03-3 mg/kg). In the sodium-depleted model, whose PRA was increased by a two-week low-sodium diet coupled with furosemide loading, both intravenous injection (0.1-3 mg/kg) and oral administration (10 and 30 mg/kg) of KRI-1314 to anesthetized and conscious animals, respectively, lowered blood pressure dose-dependently with PRA suppression. The hypotensive activity of orally administered KRI-1314 (30 mg/kg) was almost equal to that of orally administered captopril (1 mg/kg). KRI-1314 did not affect heart rate in any of the experiments. These results indicate that the potent human renin inhibitor KRI-1314 may become an orally effective drug for treating renin-dependent hypertension.View full abstractDownload PDF (27193K) -
Naoaki SUYAMA, Kazuo TODOKI, Eiichiro OKABE1994 Volume 103 Issue 4 Pages 175-186
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSTo understand the contractile response to histamine, drug-induced tension developments were measured in intact and staphylococcal α-toxin-treated permeabilized smooth muscle preparations of rabbit lingual artery. Histamine produced an endothelium-independent contraction; the observed effect was antagonized by diphenhydramine and was attenuated by nifedipine. Histamine produced only transient contraction in the Ca2+-free bathing media. In permeabilized preparations, histamine-induced contraction was abolished by ryanodine (in the presence of caffeine) or prior repeated application of caffeine; however, contraction produced by IP3 was still observed under the same experimental condition as that of the histamine study. Histamine- or caffeine-induced contraction was abolished in the permeabilized preparations by prior repeated application of IP3; caffeine or IP3 produced contraction after repeated application of histamine. Ryanodine in the presence of histamine was ineffective on caffeine-induced contraction, suggesting that histamine by itself may not have the ability to act on caffeine-sensitive Ca2+ release channels. Neomycin and H-7 completely abolished the histamine-induced contraction. Hence, it is suggested that histamine can contract the lingual artery via H1-receptor-coupled phospholipase C activation, and the contraction consists of a phasic response evoked by Ca2+ release from the IP3- and caffeine-sensitive Ca2+ storage site and the tonic response generated by the voltage-dependent influx of Ca2+. It is also postulated that IP3 produced by histamine may be able to produce Ca2+ release from only a part of the intracellular Ca2+ stores in the smooth muscle of rabbit lingual artery.View full abstractDownload PDF (21728K)
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