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Biomedical subjects

H Moritoki

Publications and source records attributed to H Moritoki.

At least 55 records · Page 3Linked to original sources
PubMed1986

Ketanserin potentiates the prejunctional inhibitory effect of 5-hydroxytryptamine on rat vas deferens.

5-Hydroxytryptamine (5-HT) slightly inhibited the twitch contractions of rat vas deferens caused by single pulse field stimulation at 0.1 Hz. The inhibitory effect of 5-HT was much less in the epididymal portion than in the prostatic portion of the vas deferens. Ketanserin potentiated the prejunctional inhibitory effect of 5-HT and attenuated its stimulatory effect. This potentiation was observable only in the epididymal portion, of the vas deferens. Cyproheptadine and mianserin, but not methysergide, had essentially similar potentiating effects to those of ketanserin. These results suggest that the 5-HT receptor that mediates prejunctional inhibition is not of the 5-HT2 type, and that ketanserin acts by suppressing the 5-HT-induced stimulatory effect, which is possibly mediated by a postjunctional 5-HT2 receptor, thus unmasking the inhibitory effect of 5-HT.

Animals↗
PubMed1985

Possible mechanism of action of diazepam as an adenosine potentiator.

Diazepam (10(-5)-3 X 10(-4) M) selectively enhanced the negative inotropic responses of guinea-pig atria and the relaxation of guinea-pig taenia coli caused by adenosine and ATP. In the atria, the effect of 2-chloroadenosine, a stable analog of adenosine, was not affected by diazepam. Segments of guinea-pig atria or taenia coli took up 3H-activity during incubation with [3H]adenosine but did not take up 32P-activity from [32P]ATP. Diazepam at concentrations sufficient to enhance the in vitro responses reduced by half the uptake of 3H-activity into the preparations. Adenosine (10(-6) M) and ATP (10(-6) M) were degraded to inactive inosine during incubation with atrial segments and their degradation was inhibited by diazepam. In contrast, in rat atria, diazepam did not enhance the negative inotropic effects of adenosine and ATP, and did not prevent the uptake of adenosine. These results suggest that in guinea-pig atria and taenia coli, diazepam like dipyridamole, acts as an adenosine potentiator by preventing the uptake and degradation of adenosine.

2-Chloroadenosine↗
PubMed1985

Opioid receptor types on adrenergic nerve terminals of rabbit ear artery.

Methionine enkephalin, leucine enkephalin, [D-Ala2, D-Leu5] enkephalin, alpha-neoendorphin, beta-endorphin, dynorphin (1-13) and ethylketocyclazocine inhibited the contractions of rabbit ear artery ring segments elicited by transmural nerve stimulation at 8 Hz. Ethylketocyclazocine, dynorphin (1-13) and leucine enkephalin produced partial inhibition, their apparent intrinsic activities (alpha) being 0.57, 0.75 and 0.66, respectively. Morphine and normorphine, which are agonists at mu-receptors, did not inhibit the response of the artery. Naloxone antagonized the actions of opioids and ethylketocyclazocine, and was more effective against methionine enkephalin, leucine enkephalin and [D-Ala2, D-Leu5] enkephalin than against alpha-neoendorphin, ethylketocyclazocine and dynorphin (1-13). The pA2 values of naloxone against so-called delta-agonists were approx. 8.5, and against so-called kappa-agonists were approx. 7.7. The supposed kappa-antagonist, Mr2266, was more effective than naloxone in antagonizing the actions of alpha-neoendorphin, and the kappa-agonists dynorphin (1-13) and ethylketocyclazocine. The pA2 values of Mr2266 against kappa-agonists were 8.5-9.0, and against delta-agonists were 7.8 or less. The opioid peptides and opioids tested did not cause dilatation of the artery previously contracted with histamine. These results suggest that the opioid peptides and ethylketocyclazocine acted on opioid receptors at adrenergic nerve terminals in the ear artery. The opioid receptors appear to be of the delta- and kappa-types, not the mu-type.

Animals↗
PubMed1984

Tripeptides acting on opioid receptors in rat colon.

The tripeptides SD-34 and SD-25 induced atropine-, guanethidine-, antihistaminics-resistant but naloxone-sensitive contractions of isolated rat distal colon. They appeared to act on an opioid receptor, probably of the mu subtype, distinct from those for methionine enkephalin and morphine, because the pA2 values of naloxone for the peptides were similar to those for mu-agonists but different from those for methionine enkephalin and morphine, and because the peptides caused contractions of colon that had been desensitized to morphine. Mr 2266, a supposed kappa-antagonist, inhibited the actions of the peptides, ethylketocyclazocine and dynorphin at concentrations much lower than those inhibiting the actions of methionine enkephalin and morphine. Thus these peptides seem to act on the mu- and/or kappa-receptors. The actions of the tripeptides were inhibited by methysergide and methylergometrine, but not by the 5-HT2 antagonist ketanserin, and were not affected by 5-HT or substance P autodesensitization . Thus their actions do not seem to involve 5-HT, histamine, ACh or substance P. It seems likely that the tripeptides, through opioid receptors, directly activate the muscle, or remove some inhibitory modulation of myogenic activity, thus causing contractions.

Animals↗
PubMed1984

Papaverine enhances the effect of adenosine in guinea-pig atria.

Papaverine, while enhancing the force of contraction of guinea-pig atria, remarkably and dose-dependently enhanced the negative inotropic response of the atria to adenosine. It also enhanced the actions of ATP and other adenine nucleotides, but not those of 2-chloroadenosine and ACh. At similar concentrations, papaverine inhibited the uptake of adenosine by the atrial tissue during incubation with adenosine. Adenosine in the medium was degraded to inactive inosine during incubation with the atrial tissue, and papaverine reduced its degradation. The enhancing effect of papaverine on the action of adenosine on guinea-pig atria was like those of dipyridamole, 6-(2-hydroxy-5-nitrobenzyl)thioguanosine and cinepazide. The effect seemed to be due mainly to inhibition of adenosine uptake into the tissue. Inhibition of adenosine degradation may also have contributed to the action of papaverine, but this action was probably much less important than inhibition of adenosine uptake.

Adenine Nucleotides↗
PubMed1982

Further evidence for a muscarinic component to the neural vasodilator innervation of cerebral and cranial extracerebral arteries of the cat.

Transmural electrical stimulation of segments of lingual and cerebral (basilar, middle and posterior cerebral) and also other cranial arteries of the cat results after a long latency in a dilator response. The response may be resolved into two components--an initial transient atropine-sensitive component and a slower more ponderous one that is atropine-resistant. The variability in pattern of dilation responses from segments of different vessels or even those from the same segment of different cats is considerable. Some responses are entirely atropine-sensitive and others atropine-resistant; however the vast majority show a dilation that can be considered to be made up of both components. The latencies of the atropine-sensitive and atropine-resistant components are not different. The effect of atropine on the lingual but not the cerebral arteries is frequency dependent, being proportionately greater at low than at high frequencies. In both vessels, the effect of atropine is independent of train length at 1 Hz. Physostigmine potentiates significantly the dilation of the lingual artery but not that of the cerebral arteries. The potentiation is reversed by atropine. The endogenous acetylcholine level was measured in a series of vessels. It can be correlated with the activity of choline acetyltransferase and the presence of neurogenic dilation. It is proposed that there are two transmitters released in parallel from nerve(s) in the walls of cerebral, lingual, and possibly, other cranial arteries to cause vasodilation. It seems that one of these is acetylcholine.

Acetylcholine↗
PubMed1981

Potentiating effects of 5-hydroxytryptamine and histamine on nerve stimulation-induced contractions of the rabbit mesenteric artery.

Contractions of the rabbit mesenteric artery induced by transmural adrenergic nerve stimulation at a frequency of 8 Hz were augmented by 5-hydroxytryptamine (5-HT), quipazine, methysergide, tolazoline, histamine, angiotensin II and 4-aminopyridine. The potentiating effect of 5-HT was partly reduced by cyproheptadine and by prolonged treatment with methysergide. After treatment with a histamine H1-antagonist, chlorpheniramine, histamine failed to augment but contrarily inhibited the response. This inhibition was reversed after subsequent administration of an H2-antagonist, metiamide. These results indicate that H1- and H2-receptors mediate the potentiation and inhibition, respectively, and that the effect medicated by H1-receptors normally predominates. It seems unlikely that the potentiation by these agents is due to prevention of norepinephrine metabolism, augmentation of norepinephrine release or prostaglandin formation. It is suggested that 5-HT and histamine act on postjunctional 5-HT and histamine receptors, respectively, to modulate the transmitter effect and that norepinephrine, methysergide and tolazoline may also act through the 5-HT receptors.

4-Aminopyridine↗
PubMed1980

Potentiation by dilazep on the negative inotropic effect of adenosine on guinea-pig atria.

1 Dilazep, a coronary dilator, has been reported to potentiate the negative inotropic and negative chronotropic responses of guinea-pig atria to adenosine. Studies were made on the mechanism of the potentiating action of dilazep with special reference to the degradation and uptake of adenosine. 2 The negative inotropic actions of adenosine and adenine nucleotides, such as ATP, ADP, AMP and cyclic AMP, on guinea-pig atria were selectively and dose-dependently augmented by dilazep at concentrations insufficient to produce any effect alone (0.01 to 1 microM). 3 Incubation of atrial tissue with 8.8 nM adenosine, containing 0.1 microCi of [3H]-adenosine, resulted in accumulation of [3H]-adenosine in the tissue; dilazep (0.01 to 1 microM) inhibited this accumulation. 4 Adenosine (10 microM to 10 mM) was degraded to inosine and hypoxanthine during incubation with atrial tissue; dilazep (0.1 to 10 microM) retarded the disappearance of adenosine and the formation of inosine and hypoxanthine. 5 These results suggest that dilazep potentiates the negative inotropic effect of adenosine on guinea-pig atria by preventing both its accumulation by atrial tissue and degradation by deaminase.

Adenosine↗
PubMed1980

Interaction of cinepazide with adenosine on guinea-pig atria.

The negative inotropic effects of adenosine and adenine nucleotides, such as ATP and cAMP, on guinea-pig atria were selectively and dose-dependently augmented by cinepazide in concentrations insufficient to produce any effect alone (3 X 10(-5) M-3 X 10(-4)M). Adenosine (10(-5) M, 10 microCi) was degraded to inosine and hypoxanthine during incubation with atrial tissue. Cinepazide (3 X 10(-4) M) retarded the degradation of adenosine, and the formation of inosine and hypoxanthine. Incubation of the atrial tissue with adenosine (8.1 X 10(-9) M, 0.1 microCi) resulted in accumulation of 3H-activity. Cinepazide (3 X 10(-5) M-3 X 10(-4) M) inhibited this accumulation. These results suggest that cinepazide potentiates the negative inotropic effect of adenosine on guinea-pig atria by preventing both its degradation by deaminase and its accumulation by atrial tissue.

Adenosine↗
PubMed1979

Possible involvement of prostaglandins in the action of ATP on guinea-pig uterus.

ATP and other adenine derivatives, such as AMP and adenosine, at concentrations above 10(-6) M induced dose-dependent contractions of guinea-pig uterine strips. Treatment of the strips with nonsteroidal anti-inflammatory drugs, such as indomethacin, aspirin and phenylbutazone, at concentrations of 10(-6) to 10(-4) M irreversibly inhibited the contractions, without affecting those caused by acetylcholine and bradykinin. Arachidonic acid (10(-8)-10(-6) g/ml) and prostaglandins (E1, E2 and F2 alpha, 10(-9)-10(-7) g/ml) restored the inhibited uterine response to ATP, but the inhibition was reinstated on washing out of the arachidonic acid or prostaglandins. Furthermore, the prostaglandin antagonists polyphloretin phosphate (3 x 10(-5)-3 x 10(-4) g/ml) and SC 19220 (10(-6)-3 X 10(-5) M) selectively suppressed the action of ATP. In addition to the prostaglandin antagonists, 2,2'-pyridylisatogen, reported to be an ATP antagonist, at concentrations of 10(-6) to 3 x 10(-5) M selectively inhibited the response of uterine strips to ATP. These results suggest the involvement of prostaglandins in the actions of ATP and other adenine derivatives on guinea-pig uterine tissue and provide further evidence for ATP-stimulated prostaglandin formation in smooth muscle.

Adenine Nucleotides↗
PubMed1978

Effects of cholinesterase inhibitors on the spasmogenic action of acetate esters on rat uterus.

Acetate esters, such as phenyl acetate and aspirin, induced atropine-sensitive contractions of isolated uterus only when choline was present. These contractions were selectively and reversibly inhibited by carbamate-type cholinesterase inhibitors, such as neostigmine and eserine, and quaternary ammonium compounds, such as tetraethylammonium and decamethonium. After treatment with organophosphorus cholinesterase inhibitors, such as di-isopropyl fluorophosphate and tetraethyl pyrophosphate, the uterus failed to respond to the acetate esters, even when high concentrations of choline were present. The inhibition of the response of the uterus by organophosphates was effectively removed by pyridine-2-aldoxime methiodide. Pretreatment of the uterus with neostigmine or simultaneous addition of high concentrations of quaternary ammonium compounds prevented the inhibition by organophosphates. The inhibition produced by neostigmine was also reduced by simultaneous addition of quaternary ammonium compounds. These findings suggest that some esterase having an anionic site and an esteratic site, probably cholinesterase, may mediate in the uterine contractions induced by acetate esters in the presence of choline, and that inhibition by organophosphates, carbamates and quaternary ammonium compounds of cholinesterase activity in the preparation may impede the initiation of contractions by the acetate esters in the presence of choline.

Acetates↗
PubMed1978

Potentiation by dipyridamole of the inhibition of guinea-pig ileum twitch response caused by adenine derivatives.

The inhibition actions of adenosine and adenine nucleotides, such as ATP, AMP and cyclic AMP, on contractions of guinea-pig from ileum induced by transmural stimulation were potentiated by dipyridamole, whereas those of inosine, morphine and tetrodotoxin were not affected. Tritium activity, accumulated during incubation of the ileal segments with [3H]adenosine, was reduced by dipyridamole. The adenosine added was degraded to inosine and then hypoxanthine during incubation, with the ileal segments, thereby restoring the twitch response of the ileal segments. In the presence of dipyridamole, the degradation of adenosine and the recovery of the twitch response was retarded. Thus, dipyridamole may potentiate the inhibitory actions of adenosine and adenine nucleotides on the twitch response of the ileum by inhibiting both the accumulation and the degradation of adenosine.

Adenine Nucleotides↗
PubMed1977

Aspects of the spasmogenic effects of acetate esters on ileal smooth muscle.

Acetate esters, such as aspirin methylester, aspirin and resorcinol monoacetate, induced contractions of guinea-pig ileum. Their actions were selectively antagonized by atropine, but were not affected by ganglion blocking agents, conduction blockers, aging with cooling, anoxia or antihistaminics. On the other hand, N-acetates, such as acetanilide and p-acetaminophenol, and no contractile action on the ileum. These acetate esters thus seemed to have a cholinergic action, and not a direct action on muscle or other known specific receptors for endogenous active substances. The contractions induced by the acetate esters were selectively potentiated by low concentrations of choline, whereas those induced by acetylcholine, nicotine, 5-hydroxytryptamine and histamine were not. However, N-acetates did not induce the contractions even in the presence of choline. Organophosphorus cholinesterase inhibitors, such as diisopropyl fluorophosphate and paraoxon, selectively and irreversibly inhibited the actions of aspirin and N,O-diacetyl-p-aminophenol with or without choline. From these results, it is concluded that the acetate esters with or without choline act through the cholinergic system. However, their actions cannot be explained in terms of known mechanisms, such as acetylcholine release, cholinesterase inhibition or a direct muscarinic action. Therefore, the acetate esters, including phenyl acetate which was supposed to be a releaser of acetylcholine, seem to have a hitherto undescribed type of cholinergic action whose mechanism is unknown. It seems that organophosphate-sensitive esterase(s) in the preparation may be essential for initiation of the actions of the acetate esters with or without choline, but the mechanism of the effect of choline is unknown.

Acetates↗