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Biomedical subjects

N Toda

Publications and source records attributed to N Toda.

At least 325 records · Page 18Linked to original sources
PubMed1980

Effects of 5-hydroxytryptophol, a 5-hydroxytryptamine metabolite, on isolated cerebral arteries of the dog.

5-Hydroxytryptophol (5-HTOL) caused a dose-dependent contraction of helically-cut strips of dog cerebral arteries. The 5-HTOL-induced contraction was suppressed by cinanserin, as was the contraction induced by 5-hydroxytryptamine (5-HT). Treatment with 5-HTOL shifted the dose-response curve for 5-HT to the right and downward in a dose-dependent manner, but did not attenuate the contractile response to prostaglandin F2a. It may be concluded that 5-HTOL elicits cerebroarterial contractions by activating tryptaminergic receptors and also interferes with the action of 5-HT on the receptors.

Animals↗
PubMed1980

Responsiveness to vasoactive agents of cerebral and mesenteric arteries isolated from control and reserpine-treated dogs.

1 Pretreatment of dogs for 20 to 24 h before the start of experiments with reserpine (0.5 mg/kg) depleted noradrenaline from cerebral and mesenteric arteries, the diminution being greater in the latter arteries. 2 Contractile responses of helically-cut strips of cerebral and mesenteric arteries to noradrenaline were unaffected by pretreatment with reserpine. Tyramine-induced contractions of mesenteric arteries were markedly attenuated by reserpine-pretreatment, whereas the contraction of cerebral arteries was not influenced. The contractile response of mesenteric arteries to transmural nerve stimulation or nicotine was abolished by reserpine-pretreatment, but the relaxation induced by nicotine of cerebral arteries contracted with prostaglandin F2 alpha was not affected. Pretreatment with reserpine attenuated the contractions of mesenteric arteries induced by angiotensin II, but did not alter the response of cerebral arteries to 5-hydroxytryptamine. 3 In prostaglandin-contracted cerebral and mesenteric arterial strips, relaxant effects of acetylcholine, isoprenaline and K+ were not significantly influenced by reserpine-pretreatment. 4 It appears that tyramine and nicotine do not release noradrenaline from dog cerebral arteries in amounts sufficient to cause significant contractions. Attenuation of the response to angiotensin II by pretreatment with reserpine is not the result of depletion of noradrenaline from the mesenteric arterial wall but may be due to interference with the mechanism specific to actions of angiotensin II.

Acetylcholine↗
PubMed1980

Responses to prostaglandins H2 and I2 of isolated dog cerebral and peripheral arteries.

In helical strips of cerebral and peripheral arteries isolated from dogs and contracted with prostaglandin F2 alpha (PGF2 alpha), PGH2 produced a slight transient contraction followed by a relaxation. The relaxation was greater and persisted longer in mesenteric and renal than in cerebral and coronary arteries. Following tranylcypromine or 15-hydroperoxy arachidonic acid, both PGI2 synthetase inhibitors, the relaxation was reversed to a contraction. The contraction was abolished by polyphloretin phosphate, a prostaglandin antagonist. Concentrations of PGI2Na sufficient to produce the same magnitude of relaxations as those induced by PGH2 were greater in mesenteric arteries. PGI2Na or PGI2 methylester caused a dose-related relaxation of the strips contracted with PGF2 alpha or K+, the relaxation being in the order: mesenteric greater than renal greater than coronary greater than cerebral. 6-Keto PGF1 alpha relaxed only mesenteric arteries. It may be concluded that PGH2 is rapidly converted to PGI2 and causes a marked relaxation in dog cerebral and peripheral arteries, the conversion being greater in mesenteric arteries. PGH2, PGE2, and PGF2 alpha all appear to share the same site of excitatory action on arterial smooth muscles. Responses of a variety of isolated dog arteries to vasodilating prostaglandins apparently differ.

Animals↗
PubMed1980

Mechanisms of ouabain-induced arterial muscle contraction.

Ouabain caused dose-related contractions in helically cut strips of cerebral, mesenteric, renal, and femoral arteries isolated from dogs and monkeys; the contractions were elicited at lower concentrations in cerebral than in the peripheral arteries. Contractions induced by ouabain were abolished by exposure of cerebral arteries to Ca2+-free media. Contractions induced by Ca2+ in Ca2+-free media were potentiated by ouabain. Substitution of LiCl for NaCl and reduction of [K+]0 suppressed the contractile response of cerebral arteries to ouabain. Pretreatment of dogs with reserpine abolished the response of peripheral arteries to ouabain but not the cerebroarterial response. Phentolamine also abolished the response of peripheral arteries. Once oubain-induced contractions were stabilized, the alpha-antagonist caused a marked relaxation in peripheral but not in cerebral arteries. Ouabain-induced contractions appear to be mediated by an increase in the Ca2+ influx that results mainly from an inhibition of the electrogenic Na+ pump in low concentrations (cerebral arteries) and from a release of norepinephrine from nerves in high concentrations (mesenteric, renal, and femoral arteries).

Animals↗
PubMed1980

Mechanism of cerebral arterial contraction induced by blood constituents.

In helically cut stips of cerebral, coronary, mesenteric, and renal arteries from dogs, a test solution containing hemoglobin (Hb) and soluble constituents, obtained by exposure of blood clot to distilled water, produced a dose-related contraction. The contraction of cerebral arteries was greater than that of the other arteries. Methemoglobin (metHb) caused only a slight contraction. The contractile response of cerebral arteries to the Hb-containing test solution was attenuated by aspirin (10(-5) to 2 X 10(-4) M), polypholretin phosphate (PPP, 3 X 10(-5) gm/ml), a prostaglandin (PG) antagonist, and cinanserin (10(-7) M), a serotonin antagonist. Combined treatment with these antagonists suppressed the response to the test solution, but only slightly attenuated contractions induced by K+. Phentolamine was ineffective. Contractions of measenteric arterial strips induced by the test solution were potentiated by aspirin, but were attenuated by PPP and cinanserin. Serum also produced contractions of cerebral and mesenteric arteries, which were attenuated by treatment with cinanserin or PPP. Contractile responses to Hb-containing solution and serum obtained from dogs pretreated with reserpine were weaker than those to the solutions obtained from control dogs. It may be concluded that the Hb-containing test solution releases vasoconstricting PG's from the cerebral arterial wall but vasodilating PG's from mesenteric arteries. The test solution appears to contain vasconstricting PG's and serotonin. Serum-induced contractions appear to be mediated mainly by serotonin.

Animals↗
PubMed1980

Age-related alterations in the response of rabbit tracheal smooth muscle to agents.

In tracheal muscle strips isolated from rabbits of different ages (3-360 days), median effective concentrations of acetylcholine and K+ increased with age. Nicotine (10(-4) M)-induced contractions decreased with increasing age. Concentrations of acetylcholine sufficient to elicit the same contraction as that induced by nicotine also decreased with age. The contractile response to histamine was reduced with age. Tracheas from mature rabbits, contracted with acetylcholine, relaxed in response to histamine in a dose-dependent manner. The histamine-induced contractions were suppressed by cholorpheniramine, while the relaxations were attenuated by cimetidine. The relaxing response to isoproterenol of tracheal strips contracted with acetylcholine was related inversely to age, whereas the response to prostaglandin E1 was increased at day 360. It may be concluded that the amount of acetylcholine released from cholinergic nerves by nicotine decreases with age and that excitatory processes related to H1-receptor stimulation in the tracheal smooth muscle decrease with age, whereas inhibitory processes related to H2-receptor stimulation are enhanced. The beta adrenoceptor mechanism apparently deteriorates with age.

Aging↗
PubMed1979

Antagonism by droperidol of dopamine-induced relaxation in isolated dog arteries.

Dopamine caused a dose-related relaxation in helically cut strips of dog coronary and renal arteries treated with phenoxybenzamine andcontracted with prostaglandin F2 alpha. The dose-response curve to dopamine was shifted to the right by droperidol in concentrations above 3 X 10(-5) M. Adenosine-induced relaxations were not attenuated by droperidol. The dose--relaxation curve to isoproterenol was also shifted to the right by droperidol. Propranolol (10(-6) M) failed to significantly alter the dose response curve to dopamine, and in propranolol-treated preparations the antagonism by droperidol of dopamine actions was practically identical with that in control preparations. Droperidol appears to act as a reversible, surmountable antagonist to dopamine actions on dog arterial smooth muscles, and such evidence supports the hypothesis of specific dopamine receptors in dog arteries.

Animals↗
PubMed1979

Inhibition of dog renin activity by pepstatin A.

The inhibitory effect of pepstatin A, an isovaleryl pentapeptide isolated from streptmyces, was studied. Pepstatin A inhibited the action of dog renin on homologus substrate. The Ki value was 7.7 X 10(-7) M and the mode of the inhibition was non-competitive. Pestatin A suppressed angiotensin I generation in dog plasma. Dose-dependent hypotensive effect of pepstatin A was observed in rats with sustained increase in blood pressure during continuous infusion of dog renin. It is concluded that pepstatin A inhibits the dog renin activity in vitro and in vivo.

Angiotensin I↗
PubMed1979

Structure-activity relationship of 5-hydroxykynurenamine analogues in isolated dog cerebral arteries.

In helically-cut strips of cerebral arteries isolated from dogs, analogues of 5-hydroxykynurenamine (5-HK), including 2-(3'-aminopropyl)-aniline (Cpd. I), 2'-amino-3-dimethylamino-3'-hydroxypropiophenone(CPD. II), 2'-amino-3-dimethylamino-5'-hydroxypropiophenone (Cpd. III) and 2',3-diamino-propiophenone (kynurenamine), caused a dose-related contraction which was antagonized by treatment with methysergide. The potency for inducing contractions was in the order of 5-hydroxytryptamine greater than 5-HK greater than Cpd. III greater than kynurenamine, Cpd. I and Cpd. II. Treatment with the 5-HK analogues antagonized the contractile response to 5-hydroxytryptamine in a dose-dependent manner, the antagonistic potency being in the order of 5-HK greater than Cpd. III greater than kynurenamine, Cpd. II greater than Cpd. I. Alterations in the hydroxy group on the benzene ring and/or radicals of long side chain of 5-HK attenuated the agonistic and antagonistic actions of 5-HK; however, the attenuation of these actions differed. Thus, the radicals appear to be involved in the agonistic and antagonistic actions to a different extent.

Aniline Compounds↗
PubMed1979

Age-dependent alteration in the response of isolated rabbit basilar arteries to vasoactive agents.

Responses to vasoactive agents were compared in helical strips of basilar arteries isolated from rabbits, 15 to 360 days of age, which were stretched under optimal resting forces. Contractions induced by serotonin, histamine, norepinephrine, angiotensin II and K+ increased with increasing age. However, the maximum forces developed by these drugs relative to those by 50 mM K+ as well as ED50 values of these drugs were not significantly different in the arteries from mature and immature rabbits; only the response to serotinin at day 360 was significantly less. Basilar arteries contracted with histamine relaxed in response to isoproterenol; the relaxing effect was suppressed by treatment with 10-6 M propranolol and was inversely related to age. On the other hand, relaxations induced by adenosine and prostaglandin E1 did not significantly differ in the arteries from rabbits of different ages. Relaxations induced by small amounts of K+ (0.5-10 mM) increased with age; the relaxations were suppressed by ouabain. It may be concluded that the cerebroarterial relaxation related specifically to the beta adrenergic mechanism is reduced with increasing age. The electrogenic Na+ pump mechanism appears to mature in rabbit basilar arteries during an early postnatal period.

Aging↗
PubMed1978

Modifications by stretches of the mechanical response of isolated cerebral and extracerebral arteries to vasoactive agents.

Length-tension relationship was compared in helically cut strips of canine cerebral, coronary, mesenteric, renal, and femoral arteries. Tension developed progressively by increasing the stretch; with the same strain, a greater passive tension developed in cerebral than in extracerebral arteries. The peak active tension developed by serotonin (cerebral, coronary), norepinephrine (mesenteric, renal and femoral) or K+ (coronary) was obtained at a resting tension of 1.5 g (other than coronary) or 2.0 g (coronary). Papaverine (10(-4) M) caused a relaxation in cerebral arterial strips contracted with serotonin to a level lower than that prior to the addition of serotonin, the relaxation from the initial level of tension being related directly to the stretch applied. The relaxing effect of adenosine was related directly to stretches of cerebral arterial strips. It seems likely that a rise of intra-arterial pressure effects a greater increase in the wall stiffness in cerebral than in extracerebral arteries. The responsiveness to vasoconstricting and vasodilating agents of both cerebral and extracerebral arteries appears to increase when the arteries are distended.

Adenosine↗
PubMed1978

Age-related changes in the response of rabbit isolated aortae to vasoactive agents.

1 In helically-cut strips of aortae from rabbits of different ages (2 to 360 days old), responses to vasoconstrictor and vasodilator agents were compared. 2 The passive tension developed by the same magnitude of stretch was markedly less in aortae from immature rabbits than in aortae from mature rabbits. 3 Contractile responses to noradrenaline and K+ increased with age in the range from 2 to 90 days. High concentrations of noradrenaline (10(-5) and 5 X 10(-5) M) produced relaxation of aortic strips from immature rabbits (2 to 30 days). The response to histamine was not altered with age. Age-dependent reductions (90 to 360 days) in the response to 5-hydroxytryptamine were observed. 4 Relaxations induced by isoprenaline of aortic strips contracted with prostaglandin F2alpha increased with age in the range from 2 to 30 days but decreased with age from 30 to 360 days. Similar age-related alterations in the relaxant response to adenosine were observed. 5 It is concluded that aortae from immature rabbits are more distensible than those from mature rabbits; alpha-adrenoceptors mature during an early postnatal period (2 to 30 days), and 5-hydroxytryptamine receptor mechanisms deteriorate with age (older than 90 days). The beta-receptor mechanism does not seem to alter greatly with age.

Aging↗
PubMed1978

Mechanical responses of isolated dog cerebral arteries to reduction of external K, Na, and Cl.

Reduction of the extracellular potassium concentration ([K+]0) caused a significant contraction in helical strips of dog cerebral arteries, but only a slight contraction, or none, in peripheral (coronary, mesenteric, renal, and femoral) arteries. The cerebroarterial contraction was abolished by treatment with ouabain or by substitution of Li+ for Na+, and suppressed by exposure to Ca2+-free media or verapamil. When one-half of the NaCl of the bathing solution was substituted with choline chloride a moderate, sustained contraction was produced in cerebral and peripheral arteries. Ouabain potentiated this contraction, whereas exposure to Ca2+-free media abolished it. Substitution of Na propionate, NaI, or Na acetylglycinate for one-half of the NaCl elicited a marked, transient contraction in only the cerebral arteries. This contractile response was potentiated by ouabain and markedly attenuated by exposure to Ca2+-free media. It may thus be concluded that cerebroarterial contractions induced by a reduction in [K+]0 are due to inhibition of the electrogenic Na+ pump, which results in depolarization of smooth muscle cells. Substitution of Cl- with less permeant anions appears to produce cerebroarterial contraction in association with depolarization of smooth muscle cells.

Animals↗
PubMed1978

[Influence of indapamide on isolated rabbit arteries (author's transl)].

The effect of indapamide, a high ceiling diuretic, antihypertensive drug, was investigated in helically-cut strips of rabbit cerebral, coronary, renal, mesenteric and femoral arteries and aortae. The addition of indapamide in concentrations higher than 3 X 10(-5)M relaxed those arterial strips contracted with prostaglandin F2alpha; the relaxation being greater in cerebral, coronary and renal arteries. Atropine propranolol and aminophylline did not reduce the relaxing effect. Hydrochlorothiazide produced fewer incidences of relaxation. Treatment for 20 min with indapamide (3 X 10(-5) or higher) significantly attenuated the contractile response of mesentric arteries to nicotine and tyramine. Contractile responses to transmural electrical stimulation were not reduced but rather potentiated. The dose-response curve of norepinephrine was not significantly affected by indapamide. The contractile response of nictitating membranes of anesthetized cats to stimulation of preganglionic sympathetic nerves was not influenced by indapamide but was abolished by hexamethonium. It may be concluded that arterial relaxations induced by indapamide are due to a direct action on smooth muscles. Indapamide appears to attenuate the response to nicotine and tyramine by interfering with the mechanism of neuronal amine uptake. However, such does not involve a ganglionic blockade nor a reduction of the release of norepinephrine from adrenergic nerve terminals.

Animals↗