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Biomedical subjects

K Terada

Publications and source records attributed to K Terada.

At least 271 records · Page 15Linked to original sources
PubMed1989

[Immunohistochemical studies of putative neurotransmitters in the lower urinary tract].

Putative neurotransmitters of the lower urinary tract were investigated in apes, rabbits and cats using immunohistochemical techniques of PAP (Peroxidase antiperoxidase) staining and IGSS (Immunogold silver staining) methods for Neuron specific enolase (NSE), Acetylcholine (Ach), Noradrenaline (NA), Vasoactive intestinal polypeptide (VIP), Substance P (SP) and Calcitonin gene related peptide (CGRP). 1) The localization of pelvic ganglions exhibited more striking evidence of species difference. Huge pelvic ganglions were found particularly in the dorsolateral area of the prostate in apes. On the other hand, in cats and rabbits, many ganglion cells were found around the uretero-vesical junctions. 2) In the pelvic ganglions of the apes, Ach immunoreactives were detected in nearly 70 percent of the cell bodies. 10-15 percent were NA immunoreactive cells. In addition, 15-20 percent VIP and a smaller percentage of SP immunoreactive cells were detected in the same ganglions. Axons extending from the ganglion cells showed the intense neurotransmitters immunoreactivity. 3) In the apes, varicose fibers containing SP were widely distributed in the epithelium, submucosa, muscle layer, and around the vessels of the bladder. SP immunoreactive cell bodies were found in the dorsal root ganglion at levels of L7, S1 and at the same levels in the posterior horn. On the other hand, the bulbourethral gland and the seminal vesicle contained SP immunoreactive cell bodies. 4) CGRP containing fibers were distributed in similar locations as SP containing fibers in the bladder. 5) VIP immunoreactive fibers were also widely distributed, being most dense at the base of the bladder.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of inositol phosphates on the membrane activity of smooth muscle cells of the rabbit portal vein.

The effects of intracellular perfusion of inositol 1,4,5-trisphosphate (InsP3) or inositol 1,3,4,5-tetrakisphosphate (InsP4) on electrical responses of smooth muscle cell membranes of the rabbit portal vein were studied using the whole cell voltage clamp technique. Depolarisation to 0 mV from a holding potential of -60 mV, evoked inward Ca (Ica), transient outward (ISO), oscillatory outward (IOO) and sustained outward (ISO) currents. Generation of IOO was dependent on the [Ca]o, but it was also generated in 0 mM Ca solution for over 10 min. From amplitude histograms, IOO was divided into two components. Reduction in [Ca]o inhibited the appearance of but not the amplitudes of both IOO components. However, the larger component of IOO was more resistant to a reduction in [Ca]o than the smaller one. InsP3 (10 microM) increased the frequency of both IOO components to a greater extent than their amplitude, but the larger component was more sensitive to InsP3 than the smaller one. The increase in the occurrence of IOO induced by InsP3 did not occur following pretreatment with 3 mM caffeine or 1 nM A23187. In normal PSS, InsP3 was evoked by a depolarising pulse positive to -40 mV, whereas following perfusion with InsP3 (10 microM), IOO was evoked at -60 mV. In normal PSS, intracellular perfusion with 10 microM InsP4 changed neither the frequency nor the amplitude of IOO, and the amplitudes of ICa, ITO and ISO were also unchanged. However, in 10 mM Ca solution, 10 microM InsP4 generated IOO at a membrane potential of -60 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Ryanodine inhibits the Ca-dependent K current after depletion of Ca stored in smooth muscle cells of the rabbit ileal longitudinal muscle.

1. Effects of ryanodine on the membrane currents were investigated on dispersed smooth muscle cells of rabbit ileal longitudinal layer using voltage and patch clamp procedures. 2. With voltage clamp, membrane depolarization to 0 mV from the holding potential of -60 mV produced an inward Ca current (ICa) which was followed by transient and sustained outward currents (ITO and ISO, respectively). Prolonged depolarization of the membrane produced spontaneous oscillations of the outward current (oscillatory outward current; IOO) on ISO. 3. Ryanodine (30 microM) modified neither the basal membrane current recorded at the holding potential (-60 mV) nor ISO. Ryanodine inhibited both ITO and IOO in a concentration-dependent manner (IC50 = 5.5 and 4.5 microM, respectively, measured 12 min after application of ryanodine). These values were much higher than that observed in skeletal muscle for Ca release. 4. The time course of the ryanodine-induced inhibition of IOO was slow and the inhibition was irreversible. Caffeine (3 mM) enhanced the amplitudes of ITO and IOO in the presence of Ca, and only transiently enhanced IOO in the absence of Ca. However, following application of 10 microM ryanodine, 3 mM caffeine did not increase IOO. 5. Ryanodine (3-30 microM) slightly enhanced the amplitude of ICa evoked by depolarization pulses at potentials more negative than O mV but not that induced by larger depolarizations (positive potentials). 6. With patch clamp procedure, single Ca-dependent K channel currents were recorded in cell free and cell attached configurations. Application of 30 microM ryanodine transiently enhanced the Ca-dependent K current without any detectable changes in the amplitude of the single channel current recorded in the cell attached condition. In the inside-out membrane patch, when the intracellular membrane side was superfused with 1 microM Ca buffered with 10 mM EGTA, bath application of 10 microM ryanodine had no effect on the Ca-dependent K current. 7. It was concluded that both ITO and IOO are generated by Ca released from intracellular stores, mainly sarcoplasmic reticulum. Ryanodine appears to open irreversibly the Ca channel in the store and to inhibit the Ca-dependent K channel due to depletion of the stored Ca.

Alkaloids↗
PubMed1988

[Ginsenoside-Rb1 as a suppressor in central modulation of feeding in the rat].

Ginsenosides, the main component of Panax ginseng root, have been reported to show several pharmacological actions on the peripheral metabolism of glucose and lipid and on endocrine secretion. The present study aimed to clarify the effects of ginsenoside-Rb1 on feeding behavior and endogenous chemical substances. Rb1 infusion into the rat third cerebroventricle was started at 1930 hr, and ingestive behavior was recorded in a soundproof room illuminated daily from 0800 to 2000 hr. Rb1 at doses of 0.05, 0.10 and 0.20 mumol potently decreased food intake dose-dependently during the first dark period after infusion. Analysis of meal patterns revealed that the suppressive effect was due to decreasing meal size, but not to postprandial intermeal interval and eating speed. Drinking episodes decreased concomitantly with feeding suppression only at the highest dose of 0.20 mumol. Ambulatory activity was not affected in the doses tested. Infusion of Rb1 increased plasma glucose, leaving insulin unaffected. Microinjection of 0.01 mumol Rb1 into the hypothalamic ventromedial nucleus (VMH) decreased food intake, but injection into the lateral hypothalamic area did not. Taking these data together, Rb1 was found to have a suppressive effect on feeding partly through the VMH.

Animals↗
PubMed1987

Blocking actions of Ca2+ antagonists on the Ca2+ channels in the smooth muscle cell membrane of rabbit small intestine.

Actions of Ca2+ antagonists, verapamil, nicardipine and diltiazem, were investigated on the Ca2+ inward current in the fragmented smooth muscle cell membrane (smooth muscle ball; SMB) obtained from the longitudinal muscle layer of the rabbit ileum, by enzymatic dispersion. All Ca2+ antagonists inhibited the inward current, in a dose-dependent manner. The ID50 value on the maximum amplitude of the inward current of nicardipine was 24 nM, and this value was roughly 50 times lower than values obtained with verapamil and diltiazem, when the inward current was provoked by 0 mV command pulse from the holding potential of -60 mV. Lowering the holding potential to -80 mV shifted the dose-response curve to the right. When depolarizing pulses (100 ms, stepped up to 0 mV from -60 mV or -80 mV) were applied every 20 s, the peak amplitude of the inward current remained unchanged, but nicardipine immediately, and diltiazem and verapamil slowly reduced the peak amplitude. These slow inhibitions by the latter two drugs depended on the frequency or number of stimulations. Nicardipine but not diltiazem and verapamil shifted the voltage-dependent inactivation curve to the left (3 s duration of the conditioning pulse). However, with a longer conditioning pulse (10 s) verapamil and diltiazem shifted the voltage-dependent inactivation curves to the left. Therefore, the inhibitory actions of these Ca2+ antagonists differ. Namely, diltiazem and verapamil inhibit the Ca2+ channels, mainly in a frequency- or use-dependent manner while nicardipine does so in a voltage-dependent manner.

Animals↗
PubMed1987

Different inhibitions of the voltage-dependent K+ current by Ca2+ antagonists in the smooth muscle cell membrane of rabbit small intestine.

Actions of Ca2+ antagonists (verapamil, nicardipine and diltiazem) on the voltage-dependent K+ current, obtained from the fragmented smooth muscle cell membrane (smooth muscle ball; SMB) of the rabbit small intestine, were investigated using voltage clamp techniques. To eliminate the influence of the Ca2+-dependent K+ current, the voltage-dependent K+ current was recorded in 2.5 mM Mn2+ (Ca2+ omitted) solution. These three Ca2+ antagonists inhibited the peak amplitude of the K+ current, in a dose-dependent manner. During application of a long command pulse (duration, 3 s), the amplitude of the voltage-dependent K+ current decreased slowly with time. Diltiazem inhibited the K+ current with a slight prolongation of the 20% decay time, while TEA (tetraethyl-ammonium), a K+ channel blocker, inhibited the current, without affecting the decay. By contrast, verapamil and nicardipine accelerated inactivation. In the control, the voltage-dependent inactivation was also seen in the K+ current. This inactivation curve below 0 mV was not modified by 10 microM diltiazem, 5 microM verapamil nor 3 microM nicardipine. These results indicate that inhibition of the voltage-dependent K+ current by verapamil or nicardipine differed from that by diltiazem.

Animals↗
PubMed1987

D600 blocks the Ca2+ channel from the outer surface of smooth muscle cell membrane of the rabbit intestine and portal vein.

The voltage dependent Ca2+ inward current in single smooth muscle cells dispersed from the longitudinal muscle layer of the rabbit ileum and rabbit portal vein was recorded using the whole-cell voltage clamp technique. D600 added to the bathing solution inhibited the Ca2+ current, while the intracellular perfusion of this agent did not reduce the amplitude of this current. Thus, D600 probably acts from the outer surface of the membrane. The nature of the Ca2+ channel in smooth muscle cells seems to differ from that in cardiac muscle cells.

Animals↗
PubMed1987

Action of the 1,4-dihydropyridine derivative, KW-3049, on the smooth muscle membrane of the rabbit mesenteric artery.

1. The effect of 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridine-dicarboxylic acid methyl 1-(phenylmethyl)-3-piperidinyl ester hydrochloride (KW-3049) on the smooth muscle membrane of the rabbit mesenteric artery was investigated using microelectrode and single electrode voltage clamp methods. 2. In whole tissue preparations KW-3049 did not alter the resting membrane potential of the artery, but did inhibit the action potential evoked by a depolarizing current in the presence of 10 mM tetraethylammonium (TEA). 3. Using the voltage clamp technique, the effects of KW-3049 on the inward current evoked in solution containing 100 mM BaCl2 were observed. When the membrane was held at -60 mV, KW-3049 inhibited the inward current in a concentration-dependent manner. The inward current evoked by a larger depolarizing pulse was inhibited to a larger extent than that evoked by a smaller one. 4. When the membrane was held at -80 mV, the inward current evoked at test potentials of -10 and 0 mV was enhanced by low concentrations of KW-3049 (below 100 nM). 5. KW-3049 accelerated the rate of inactivation of the inward current and shifted the voltage-dependent inactivation curve to the left. 6. KW-3049 has a long-lasting inhibitory action on smooth muscle cells, since the inhibition of the inward current persisted for over 1 h after the removal of KW-3049. 7. Our results suggest that KW-3049 has a selective and long-lasting action on the Ca channels of the smooth muscle cell membrane of the rabbit mesenteric artery. This agent has both facilitatory and inhibitory actions on the Ca channel, depending on the values of the holding and command potentials.

Action Potentials↗