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Biomedical subjects

N Toda

Publications and source records attributed to N Toda.

At least 181 records · Page 10Linked to original sources
PubMed1991

Prevention by nicardipine of dog basilar artery spasm caused by oxyhemoglobin in vivo and in vitro.

Intravenous infusions of nicardipine in a dose insufficient to lower blood pressure prevented the generation of the basilar artery spasm provoked by oxyhemoglobin (oxyHb) injected intracisternally in anesthetized dogs. The plasma concentration of nicardipine was comparable to that sufficient to suppress the oxyHb-induced contraction in isolated dog basilar arteries. Nicardipine appears to be similarly effective in antagonizing the vasoconstrictor action of oxyHb in vivo and in vitro.

Animals↗
PubMed1991

Analysis of the potentiating action of N(G)-nitro-L-arginine on the contraction of the dog temporal artery elicited by transmural stimulation of noradrenergic nerves.

Dog temporal artery strips without endothelium responded to transmural electrical stimulation with a contraction which was potentiated by NG-nitro-L-arginine (L-NNA). The noradrenaline-induced contraction and the release of 3H-noradrenaline were not affected. The stimulation-induced contraction was reversed to a relaxation by phentolamine. The relaxation was not influenced by timolol and atropine but inhibited by L-NNA; L-arginine abolished the inhibition. Transmural stimulation released NOx from the arteries, the release being abolished by L-NNA. Potentiation by L-NNA of the neurally-induced contraction appears to be due to elimination of NO produced by non-adrenergic, non-cholinergic vasodilator nerve activation.

Animals↗
PubMed1991

Reactivity to vasoactive agents of canine basilar arteries exposed to experimental subarachnoid hemorrhage.

Autologous blood was injected into the cisterna magna of mongrel dogs twice with an interval of 48 hours. They were killed 3 days, 1 week, or 4 weeks after the first injection of blood, and helical strips of the basilar artery were prepared. Contractions induced by 5-hydroxytryptamine, noradrenaline, prostaglandin F2 alpha, and oxyhemoglobin were significantly potentiated. Relaxations caused by nicotine, K+, arachidonic acid, and prostaglandin I2 were suppressed, but the relaxant response to calcium ionophore A23187 and substance P did not change significantly. These results suggest that contractions mediated via activation of alpha, 5-hydroxytryptamine, and prostaglandin F2 alpha receptors are potentiated, and relaxations caused by stimulation of vasodilator nerves and by endogenous and exogenous prostaglandin I2 are attenuated in dog basilar arteries exposed to subarachnoid clot. On the other hand, certain relaxations possibly mediated by endothelium-derived relaxing factor do not appear to be significantly influenced.

Animals↗
PubMed1991

Suppression of the cerebral vasospastic actions of oxyhemoglobin by ascorbic acid.

Oxyhemoglobin (Oxy-Hb) produced a concentration-dependent contraction of monkey, dog, and bovine cerebral artery strips. Treatment of Oxy-Hb with ascorbic acid suppressed the ability of Oxy-Hb to contract the arteries, especially in the monkey arteries. The ability of intracisternally applied Oxy-Hb to constrict the basilar artery in anesthetized dogs was diminished when Oxy-Hb was treated previously with ascorbic acid (AsA-Hb). The contraction caused by Oxy-Hb was suppressed by treatment with indomethacin and aspirin in isolated bovine cerebral arteries. Endothelium-dependent relaxations elicited by substance P and relaxations induced by stimulation of the vasodilator nerves with nicotine were suppressed by treatment with Oxy-Hb and AsA-Hb; however, the inhibitory effect of AsA-Hb was markedly less. Oxy-Hb attenuated nitroglycerin-induced relaxations in a dose-dependent fashion, whereas AsA-Hb in concentrations up to 1.6 x 10(-5) M did not significantly influence the relaxations. It is concluded that incubation of Oxy-Hb with ascorbic acid alters markedly the biological activity of Oxy-Hb; the vasoconstrictor activity is suppressed, and the ability to diminish vasodilator actions is minimized. These findings provide a rationale for the use of ascorbic acid in cisternal irrigation to prevent the development of cerebral vasospasm after a subarachnoid hemorrhage.

Animals↗
PubMed1991

Comparison of endothelium-dependent responses of monkey cerebral and temporal arteries.

1. Endothelium-dependency of vasodilator responses was compared in helical strips of monkey cerebral and superficial temporal arteries contracted with prostaglandin F2 alpha. Acetylcholine produced an endothelium-dependent relaxation in the temporal arteries, but did not consistently alter the tone of cerebral arteries. 2. Adenosine 5'-triphosphate (ATP) produced a transient contraction followed by a relaxation in the temporal and cerebral arteries; removal of the endothelium partially attenuated the relaxation of the cerebral arteries and markedly suppressed the relaxation in the temporal arteries. The dependency of adenosine 5'-diphosphate (ADP)-induced relaxations on the endothelium was also greater in temporal arteries than in cerebral arteries. 3. Histamine-induced relaxations in the temporal arteries were independent of the endothelium and were reversed to contractions by cimetidine. Cerebral arterial relaxations induced by histamine were partly dependent on the endothelium. Relaxations caused by substance P were reversed to contractions by removal of the endothelium in the temporal arteries, whereas the peptide did not consistently alter the tone of cerebral arteries. 4. The Ca2+ ionophore, A23187, relaxed the temporal and cerebral arteries to a similar extent; removal of the endothelium abolished these relaxations. Glyceryl trinitrate elicited similar relaxation of cerebral and temporal arteries, and these were independent of the endothelium. 5. These findings clearly indicate heterogeneity in the endothelium-dependency of several vasodilator responses in monkey intra- and extracranial arteries, although the ability of these arteries to respond to A23187 and glyceryl trinitrate does not appear to differ. The heterogeneous responses observed so far could therefore be due to different distributions of receptors or to variation in receptor-effector coupling in endothelial cells.

Acetylcholine↗
PubMed1991

Constrictor action of oxyhemoglobin in monkey and dog basilar arteries in vivo and in vitro.

Angiographic studies on anesthetized dogs and Japanese monkeys showed that oxyhemoglobin (HbO2) injected into the cisterna magna produced a constriction of the basilar artery; the maximal constriction was attained 2-4 h later. Intracisternal injections of autologous blood, prostaglandin (PG) E2 and PGF2 alpha also constricted the artery to a similar extent, although the peak response was obtained much later (approximately 1 wk) with blood and was earlier (approximately 20 min) with PGs. The vasoconstrictor action of HbO2 was almost abolished by treatment for 5 h with aspirin in dogs and monkeys, whereas treatment of dogs with OKY 046, a thromboxane A2 synthesis inhibitor, did not significantly alter the action. In isolated monkey basilar arteries, HbO2 elicited a concentration-related contraction, which was suppressed by treatment with aspirin and by endothelium denudation. The basilar arteries responded to PGE2 and PGF2 alpha with contractions comparable to those caused by elevated external K+. Levels of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha in the nutrient solution bathing dog and monkey cerebral arteries were increased by HbO2; the increment was depressed by endothelium denudation and by treatment with indomethacin. These findings suggest that cerebral artery constriction caused by HbO2 in vivo and in vitro is associated mainly with the release of vasoconstrictor PGs, such as PGE2 and PGF2 alpha. Endothelium appears to play an important role in the release of PGs. Cerebral vasospasm elicited by intracisternal injections of HbO2 may be a useful model for the analysis of mechanisms underlying the provocation of delayed vasospasm after subarachnoid hemorrhage.

Animals↗
PubMed1991

Age-related changes in responses to nerve stimulation and catecholamines in isolated monkey cerebral arteries.

Mechanical responses to transmural electrical stimulation, nicotine, norepinephrine, and isoproterenol were compared in cerebral artery strips obtained from Japanese monkeys of different ages (1 mo, 1 yr, 4-7 yr, and greater than 7 yr old). Transmural electrical stimulation produced a contraction in the baby and juvenile monkey arteries contracted with prostaglandin F2 alpha, whereas the older monkey arteries responded to the stimulation with a relaxation. The stimulation-induced contraction was abolished or reversed to a relaxation by phentolamine; the relaxation was not influenced by propranolol and atropine but was abolished by tetrodotoxin, as was the response of the mature monkey arteries. Contractions caused by norepinephrine were greater in baby cerebral arteries than in the older monkey arteries; however, the apparent median effective concentration values did not differ. Middle cerebral artery contractions were greater than those of basilar arteries. The norepinephrine-induced contraction was suppressed by prazosin but not influenced by yohimbine. Isoproterenol (up to 10(-6) M) produced a greater relaxation in the baby arteries than in the older monkey arteries. It is suggested that adrenergic nerves innervating immature monkey cerebral arteries contribute to the regulation of vascular tone predominantly over nonadrenergic, noncholinergic vasodilator nerves, whereas the vasodilator nerves play a major role in the mature monkey arteries. alpha 1-Adrenoceptor subtype appears to be mainly involved in the norepinephrine-induced contraction of baby monkey cerebral arteries, as it is in that of the adult monkey arteries.

Aging↗
PubMed1991

Reciprocal regulation by putatively nitroxidergic and adrenergic nerves of monkey and dog temporal arterial tone.

In monkey and dog superficial temporal artery strips denuded of the endothelium, transmural electrical stimulation and nicotine produced a contraction that was abolished by phentolamine and potentiated by NG-nitro-L-arginine (L-NNA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. The arteries treated with phentolamine and contracted with prostaglandin F2 alpha responded to the electrical stimulation and nicotine with relaxations that were abolished by tetrodotoxin and hexamethonium, respectively, and were markedly inhibited by L-NNA but not by D-NNA, atropine, and timolol. The L-NNA-induced inhibition was reversed by L-arginine. Nicotine increased the level of guanosine 3',5'-cyclic monophosphate in the monkey arteries; the increment was prevented by L-NNA. It is concluded that the monkey and dog temporal arterial tone appears to be reciprocally regulated by adrenergic vasoconstrictor and nonadrenergic noncholinergic vasodilator nerves. The neurogenic relaxation would be mediated by NO that is possibly released from the vasodilator nerve and transmits information to smooth muscle; therefore the nerve may be called "nitroxidergic."

Animals↗
PubMed1991

Different modulation by cyclooxygenase inhibitors of the response to angiotensin II in monkey arteries and veins.

In coronary, renal and femoral arteries and mesenteric veins isolated from Japanese monkeys, tachyphylaxis to angiotensin (ANG) II (10(-7) M)-induced contraction rapidly developed. Contractions caused by ANG II in coronary arteries were attenuated by treatment with indomethacin and aspirin and also by endothelium denudation. Indomethacin inhibited the response of the arteries with and without endothelium to a similar extent. OKY 046, a thromboxane A2 synthesis inhibitor, failed to inhibit the response. In contrast, contractions of renal arteries were potentiated and prolonged by the cyclooxygenase inhibitors. ANG II-induced contractions of mesenteric veins were prolonged but those of femoral arteries were not altered by indomethacin. It is concluded that ANG II contracts monkey coronary arteries, possibly due to the release of vasoconstrictor prostanoids but not thromboxane A2 from endothelial and subendothelial tissues and also due to its direct action on smooth muscle, whereas contractions of renal arteries and mesenteric veins are blunted by vasodilator prostanoids, possibly PGI2. Cyclooxygenase products even if released do not appear to regulate femoral artery contractions produced by ANG II.

Angiotensin II↗
PubMed1991

Suppression by NG-nitro-L-arginine of relaxations induced by non-adrenergic, non-cholinergic nerve stimulation in dog duodenal longitudinal muscle.

In dog duodenal longitudinal muscle strips, transmural electrical stimulation (10 Hz, 15 sec) elicited a transient contraction, which was abolished by tetrodotoxin and atropine but potentiated by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enantiomer. Acetylcholine-induced contractions were not influenced by L-NA. After treatment with atropine, the electrical neural stimulation relaxed the muscle strips partially contracted with bradykinin, the relaxation being abolished by tetrodotoxin and suppressed by L-, but not D-, NA. L-arginine reversed the L-NA-induced inhibition. Oxyhemoglobin abolished the relaxation caused by nerve stimulation and NO. The neurally-induced relaxation was not attenuated by adrenoceptor antagonists and indomethacin. It is concluded that electrical stimulation of non-adrenergic, non-cholinergic nerves relaxes dog duodenal smooth muscle, due possibly to NO produced upon neural excitation, and potentiation by L-NA of the contractile response to cholinergic nerve stimulation, would be derived from elimination of the neurally-induced relaxation.

Animals↗
PubMed1991

Role of nitric oxide in neurally induced cerebroarterial relaxation.

Transmural electrical stimulation and nicotine produced a relaxation of dog cerebral artery strips denuded of endothelium, which was abolished by tetrodotoxin and hexamethonium, respectively, and also suppressed by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The inhibition was reversed by L-arginine but not by the D-enantiomer. L-NA also suppressed the endothelium-dependent relaxation by substance P but not the response to NO and nitroglycerin. Treatment with high concentrations of nitroglycerin or sodium nitroprusside markedly inhibited the relaxant response to nicotine, substance P and NO but not the response to papaverine. Slight, slowly developing relaxations caused by L-arginine in the endothelium-denuded arteries were not potentiated by repeated applications of the amino acid or by exposure of the strips for 24 hr to the bathing medium. Ca++ ionophore-induced contractions in the denuded strips were not potentiated by L-NA. Nicotine significantly increased the level of cyclic GMP in the arteries without endothelium; the increment was abolished by treatment with L-NA and hexamethonium. NO does not seem to be synthesized in smooth muscle in an amount sufficient to produce significant relaxation. It may be concluded that NO liberated from vasodilator nerves activates guanylate cyclase in smooth muscle and produces cyclic GMP, resulting in cerebroarterial relaxation.

Animals↗
PubMed1991

An overview of biological signal processing: non-linear and non-stationary aspects.

The elucidation of biological systems will be one of great keys to scientific advance. However, it is difficult to analyze such biological systems because of their non-linear and non-stationary characteristics. This paper reviews newly developed methods for analysing such non-linear and non-stationary characteristics.

Neural Networks, Computer↗
PubMed1990

Isolated bovine cerebral arteries from rostral and caudal regions: distinct responses to adrenoceptor agonists.

Responsiveness to norepinephrine and related agents was compared in isolated bovine anterior cerebral (ACA). middle cerebral (MCA), intracranial internal carotid (ICA), posterior communicating (PCOM), posterior cerebral (PCA) and basilar arteries (BA). Norepinephrine contracted the strips from ACA, MCA and ICA, but relaxed those from PCOM, PCA and BA. In the presence of propranolol, the amine-induced contractions tended to be potentiated in ACA, MCA and ICA, and the relaxations in PCOM, PCA and BA were reversed to contractions. The maximum contractions induced by norepinephrine in ICA and ACA treated with propranolol were significantly greater than those in PCA and BA, but the EC50 values did not differ among arteries. In ACA and MCA, the contractions induced by phenylephrine were greater than those induced by clonidine. The contractions induced by norepinephrine and phenylephrine were attenuated by prazosin but not influenced by yohimbine in ACA and MCA treated with propranolol. These findings indicate that the responses to norepinephrine evidently differ in bovine cerebral arteries of rostral (ACA, MCA and ICA) and caudal regions (PCOM, PCA and BA), possibly due to different functioning of alpha/beta receptors. The amine-induced contraction predominantly seen in the rostral arteries appears to be associated with activation of the alpha 1 adrenoceptor subtype.

Adrenergic alpha-Agonists↗
PubMed1990

Possible role of nitric oxide in transmitting information from vasodilator nerve to cerebroarterial muscle.

Treatment with L-NG-monomethyl arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis from L-arginine, suppressed the relaxant response of dog cerebral artery strips to transmural electrical stimulation and nicotine, as did oxyhemoglobin. The inhibition by L-NMMA was reversed or prevented by L-, but not D-, arginine. It is concluded that NO or an NO-related compound may play a crucial role in transmitting information from excited vasodilator nerves to cerebroarterial smooth muscle.

Animals↗
PubMed1990

Mechanism of inhibitory action of peptide YY on cholecystokinin-induced contractions of isolated dog ileum.

In isolated canine ileal longitudinal muscle preparations, cholecystokinin-octapeptide (CCK-8) produced a concentration-dependent contraction, which was suppressed by peptide YY (PYY) and was abolished by tetrodotoxin and atropine. PYY was approximately 2200-times as potent as CR1505, a CCK-receptor antagonist. PYY opposed the action of CCK-8 to a greater extent than that of nicotine and transmural electrical stimulation. Acetylcholine-induced contractions were not influenced by PYY. It seems likely that the CCK-8-induced ileal muscle contraction is associated with an activation of CCK receptors in cholinergic nerves, which generates nerve action potentials and releases acetylcholine, whereas CCK-8 acts on CCK receptors in gallbladder smooth muscle, producing contractions. It may be concluded that PYY inhibits the action of CCK-8 on ileal muscle strips, by inhibiting the release of acetylcholine from cholinergic nerve terminals. On the other hand, in the gallbladder, PYY does not appear to block cholinergic nerve function.

Animals↗
PubMed1990

Inhibitory effects of L-NG-nitro-arginine on the synthesis of EDRF and the cerebroarterial response to vasodilator nerve stimulation.

Treatment with L-NG-nitro-arginine (L-NA) inhibited the brady-kinin-induced relaxation, mediated via EDRF, in dog coronary artery strips partially contracted with prostaglandin F2 alpha; the inhibition was prevented by L-, but not D-, arginine. Relaxation caused by nitroglycerin was not altered by L-NA. The release of EDRF, as assayed using dog coronary artery strips without endothelium, from perfused femoral artery segments with endothelium in response to acetylcholine and substance P was significantly reduced by treatment of the femoral artery with L-NA. The inhibitory effect was reversed by L-arginine. Relaxant responses of dog cerebral artery strips with and without endothelium to electrical stimulation of non-adrenergic, non-cholinergic nerves were suppressed by L-NA, whereas relaxation of coronary arteries with and without endothelium by the stimulation of adrenergic nerves was not influenced. The L-NA-induced inhibition was reversed by L-arginine. It is speculated that L-NA inhibits the synthesis of EDRF, as does L-NG-monomethyl arginine, and NO-like substance(s) produced plays an important role in transferring information from vasodilator nerves to smooth muscle in cerebral arteries.

Animals↗
PubMed1990

Conversion of angiotensin I to angiotensin II in dog isolated renal artery: role of two different angiotensin II-generating enzymes.

The functional role of the endothelium in conversion of angiotensin (Ang) I to Ang II was studied in helical strips of dog renal arteries. In the arteries precontracted with PGF2 alpha, Angs I and II caused a moderate relaxation, which was abolished by treatment with saralasin and reversed to a contraction by indomethacin. Removal of the endothelium attenuated the response to Ang I but did not abolish it. The Ang I-induced relaxation in the arteries without endothelium was not significantly attenuated by an Ang-converting enzyme inhibitor, SA446, but was markedly suppressed by chymostatin. On the other hand, in the arteries with endothelium, the relaxation was suppressed but not abolished by SA446, and the remaining relaxation was abolished by additional treatment with chymostatin. Relaxation induced by prostaglandin I2 was unaffected by these enzyme inhibitors. These results strongly suggest that the conversion of Ang I to Ang II is due mainly to the Ang-converting enzyme in the endothelium and to the chymostatin-sensitive Ang II-generating enzyme in subendothelial tissues.

3-Mercaptopropionic Acid↗