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Biomedical subjects

N Toda

Publications and source records attributed to N Toda.

At least 361 records · Page 20Linked to original sources
PubMed1976

Serotonin antagonism in isolated canine cerebral arteries.

In helically-cut strips of canine cerebral arteries, the dose-response curve of serotonin was not influenced by 10(-7) M phentolamine but was slightly moved to the right and downward at 10(-6) M. The contractile response to serotonin was unaffected by cocaine (3 X 10(-6)M), atropine (10(-6) M) and propranolol (10(-6) M). The addition of lysergic acid diethylamide (LSD), ergotamine and methysergide caused a dose-dependent contraction. Treatment with LSD (10(-9) and 10(-8) M), ergotamine (10(-10) to 10(-8) M) and methysergide (10(-8) to 10(-6) M) shifted the dose-response curve of serotonin to the right and downward in a dose-dependent manner. The inhibitory effect of methysergide was reversed by washing, while that of ergotamine was not reversed. Apparent pA2 values of LSD, ergotamine and methysergide were 9.17, 9.63 and 7.92, respectively. Contractile responses to 20 mM K+ were not significantly influenced by these blocking agents even in the highest concentrations used. It may be concluded that an alpha-adrenergic mechanism is not involved in the genesis of serotonin-induced contractions and that serotonin acts directly on serotonergic receptors in canine cerebral arteries.

Animals↗
PubMed1975

Effects of dopamine on isolated canine coronary arteries.

Dopamine contracted isolated canine coronary arteries at initial concentrations of 5 times 10(-6) mol/l. In the presence of phentolamine or phenoxybenzamine and after contraction of the arteries with K+ or prostaglandin F2alpha, dopamine caused dose-related relaxation at initial concentrations of 5 times 10(-6) mol/l and 10(-6) mol/l. Propranolol, 10(-6) mol/l, and haloperidol, 10(-5) mol/l, did not antagonize the relaxation.

Animals↗
PubMed1975

Comparison of the relaxing effect of dopamine with that of adenosine, isoproterenol and acetylcholine in isolated canine coronary arteries.

Isolated canine coronary arteries were contracted with prostaglandin F2a and the relaxing effects of dopamine, adenosine, isoproterenol and acetylcholine were compared. Relaxation induced by dopamine in phenoxybenzamine-treated arteries was not significantly influenced by propranolol and atropine in concentrations sufficient to shift dose-respone curves of isoproterenol and acetylcholine, respectively, to the right. Dose-response curves of isoproterenol were shifted significantly to the left by 2 x 10(-5) M aminophylline. In contrast, the relaxing effect of adenosine was significantly attenuated by aminophylline (5 x 10(-6)-10(-4) M) in a dose-dependent manner. Kinetic analysis showed that aminophylline competitively antagonized the effect of adenosine, and the pA2 was 5.57. At these concentrations, aminophylline did not alter the relaxing action of dopamine and acetylcholine. It may be concluded that dopamine produces relaxation at a different site and with a different mechanism of action from those of isoproterenol, the effect of the latter being presumably mediated by cellular cyclic AMP, and that dopamine also does not share the site of action with adenosine and acetylcholine. It appears that receptive sites specific for adenosine are present in canine coronary arteries.

Acetylcholine↗
PubMed1975

Dopamine induced relaxation of isolated canine renal, mesenteric, and femoral arteries contracted with prostaglandin F2-alpha.

The purpose of this investigation was to develop a system for studying the effects of dopamine on isolated blood vessels. Canine renal, mesenteric, and small femoral arteries (less than 1 mm outside diameter) were exposed to phenoxybenzamine 10-5 M for one hour and contracted with prostaglandin F2-alpha. Cumulative concentrations of dopamine ranging from 10-6 to 10-4 M caused dose-related relaxation of the arteries. Propranolol 10-6 M did not affect the relaxation in concentrations which markedly antagonized the effects of isoproterenol. Large femoral arteries (greater than 1 mm outside diameter) did not relax with similar concentrations of dopamine. N-methyldopamine (epinine) produced similar relaxation; 3-methoxytyramine was inactive. Specific antagonism could not be demonstrated by the postulated dopamine antagonists-haloperidol, chlorpromazine, apomorphine, or bulbocapnine-in concentrations up to 10-5 M. Higher concentration of these agents could not be used because they caused the arteries to relax. This study demonstrated that PGF2-alpha-contracted arteries pretreated with phenoxybenzamine are suitable for further investigations of putative dopamine agonists and antagonists.

Adrenergic beta-Antagonists↗
PubMed1975

Nicotine-induced relaxation in isolated canine cerebral arteries.

Nicotine in concentrations ranging from 5 times 10- minus 6 to 10- minus 4 M caused a transient relaxation in strips of isolated canine basilar, middle cerebral and posterior cerebral arteries contracted with prostaglandin F2a (PGF). Transmural neural stimulation did not produce changes in the tension of these arteries. Tyramine contracted the arterial strips. Relaxation induced by nicotine was markedly attenuated by hexamethonium (10- minus 5 M), cocaine (10- minus 5M), bretylium (2 times 10- minus 5 M), sotalol (5 times 10- minus 5 M), propranolol (10- minus 6 M) and removal of Ca-++ from the bathing media. Relaxation was not significantly influenced by atropine, physostigmine, ouabain, tetrodotoxin, aminophylline and sotalol (10- minus 5 M). In cerebral arterial strips, the addition of K-+ also elicited a transient relaxation which was abolished by treatment with ouabain but not with other blocking agents. In mesenteric arterial strips, nicotine caused a transient contraction as did transmural stimulation. The nicotine-induced contraction was markedly attenuated or completely abolished by hexamethonium, cocaine, bretylium and phentolamine and also high concentration of sotalol (5 times 10- minus 5 M), and propranolol. Tetrodotoxin did not affect the contractile response to nicotine but did abolish the response to transmural stimulation. It is strongly suggested that relaxation induced by nicotine in cerebral arterial strips is the result of a specific action on nicotinic receptors as is the contraction observed in mesenteric arteries. It appears that beta adrenergic and cholinergic mechanisms do not play major roles in the genesis of nicotine-induced relaxation nor does it appear that an electrogenic Na-+ pump mechanism is involved.

Animals↗
PubMed1975

Analysis of the effect of 5-hydroxykynurenamine,, a serotonin metabolite, on isolated cerebral arteries, aortas and atria.

In helically cut strips of dog and human cerebral arteries, the addition of 5-hydroxykynurenamine (5-HK) caused dose-related contractions, and this contractile response was attenuated by methysergide and lysergic acid diethylamide (LSD). Treatment of the strips with 5-HK in concentrations higher than 2 X 10- minus 6 M shifted the dose-response curve of serotonin to the right and downward. The inhibitory effect of 5-HK was reversed only partially by repeated washings, whereas the inhibition caused by methysergide and LSD was completely reversed. The contractile response to K-+ (30 mM) was reduced only slightly even at the highest concentration of 5-HK used (5 X 10-minus 5 M). In strips of rabbit aortas, the contractile effect of serotonin was markedly attenuated by 5-HK, whereas that of norepinephrine was reduced only slightly. In isolated rabbit right atria, 5-HK produced a transient increase in the rate as did serotonin, 5-HK being approximately 1/20 as potent as serotonin. The positive effect was not influenced by methysergide but was markedly attenuated or abolished by 10-minus 6 M propranolol and 3 X 10-minus 6 M cocaine. Treatment with 5-HK (5 X 10-minus 5 M) did not modify the chronotropic response to isoproterenol. It appears that 5-HK produces vascular contractions via serotonergic receptors, inhibits specifically the contractile response of arteries and aortas to serotonin and causes a tachycardia in rabbit atria by liberating catecholamines from adrenergic nerves.

Adult↗
PubMed1974

Effects of 5-hydroxykynurenamine, a new serotonin metabolite, on isolated dog basilar arteries.

Serotonin and 5-hydroxykynurenamine caused dose-related contractions in the spiral strips of dog basilar arteries. The potency of 5-hydroxykynurenamine was approximately 1/100 that of serotonin, the former frequently causing a transient relaxation preceding the contraction. The contractile responses to 5-hydroxykynurenamine and serotonin were attenuated by methysergide. Treatment with 5-hydroxykynurenamine inhibited the response to serotonin, and this inhibitory effect was not completely reversed by removal of 5-hydroxykynurenamine from the bathing medium. The contractile response to K(+) was only slightly attenuated by high concentrations of 5-hydroxykynurenamine. It appears that 5-hydroxykynurenamine and serotonin share receptors in dog basilar arteries and that the effect of serotonin is specifically antagonized by 5-hydroxykynurenamine.

Amines↗