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N Satake

Publications and source records attributed to N Satake.

At least 109 records · Page 6Linked to original sources
PubMed1989

[Luminol-dependent chemiluminescence of peripheral neutrophils in asthmatic patients].

To evaluate the role of the neutrophil in the pathophysiology of bronchial asthma, we examined the luminol-dependent chemiluminescence of peripheral neutrophils (CL) in steroid-dependent asthmatic patients during an acute attack (n = 18), during stable period (n = 10), and in normal controls (n = 21). When stimulated with formyl-methionyl-leucyl-phenylalanine (fMLP 0.1 microM), the CL of patients in acute attack was lower than that of normal controls. (5.29 +/- 1.25 vs. 9.29 +/- 0.84 relative light units p less than 0.01) Among 18 patients, we could examine 10 patients during the stable period after receiving steroids. The CL of those 10 patients during the stable period was significantly higher than their CL during acute attacks, when evaluated by the paired t-test (p less than 0.05), and was not very different than in normal controls. When stimulated with opsonized zymosan (5 mg/ml), CL was similar in the three groups. We also examined the CL of peripheral neutrophils of normal persons after the preincubation with serum of patients during acute attack and stable period. When stimulated with fMLP, CL after preincubation with serum of patients during acute attack was lower than CL after preincubation with the serum of patients during the stable period. It was suggested that the respiratory-burst activity of peripheral neutrophils in acute asthmatic attack was reduced to the chemotactic stimulus of fMLP.

Adult↗
PubMed1988

The mode of vasoinhibitory action of a pyridazione derivative (MCI-154), a new cardiotonic agent, on contractile responses induced by alpha-adrenoceptor agonists and 45Ca influx in isolated vascular smooth muscles.

The vasoinhibitory effects of MCI-154 (MCI), a new pyridazione derivative, on contractile responses to alpha 1- and alpha 2-adrenoceptor agonists were examined in isolated rabbit aorta. MCI (10(-8)-10(-5) M) inhibited the maximum contractile responses to clonidine and BHT-920 (BHT) in a concentration-dependent manner, but only inhibited responses to lower concentrations of methoxamine. In aortas pretreated with phenoxybenzamine however, MCI (10(-5) M) readily inhibited responses to methoxamine. MCI (10(-5) M) had no significant effect on responses to potassium or added Ca2+ in a Ca2+ free, K+-depolarizing medium. In aortas incubated in a Ca2+-free medium with EGTA, the addition of methoxamine (10(-5) M), clonidine (10(-5) M) or BHT (3 X 10(-4) M) induced a phasic contraction. The inhibitory effect of MCI (10(-9)-10(-5) M) on these phasic responses was much greater for clonidine or BHT than for methoxamine. In rabbit iliac artery caffeine (10 mM) induced a rapid phasic contraction in a Ca2+-free medium, which was inhibited by MCI (10(-7)-10(-5) M) in a concentration-dependent manner. In aortas incubated in a Ca2+-free medium with low EGTA and nifedipine (10(-6) M) in the presence of alpha-adrenoceptor agonists (methoxamine, clonidine or BHT), the addition of Ca2+ (2 mM) induced a tonic contraction. MCI (10(-8)-10(-5) M) inhibited these Ca2+-dependent, agonists-mediated responses in a concentration-dependent manner. MCI had no effect on unstimulated La3+ resistant Ca2+ binding or methoxamine-induced Ca2+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1988

The vasoinhibitory action of FR 46171, a new pyridine alcohol antianginal agent, on isolated rabbit vascular smooth muscles.

The vasoinhibitory effect of FR 46171, a new pyridine alcohol derivative, on contractile responses to alpha-adrenoceptor agonists was examined in isolated rabbit aorta. FR 46171 (10(-8)-10(-5) M) inhibited the maximum contractile response to clonidine (CL) in a concentration-dependent manner, but it only inhibited the responses to low concentrations of norepinephrine (NE) and methoxamine (MO). In the aorta pretreated with phenoxybenzamine, however, FR 46171 at 10(-5) M inhibited the residual maximum response to NE and MO. FR 46171 at 10(-5) M only inhibited the response to KCl (20 mM). FR 46171 at 10(-6) and 10(-5) M also moderately inhibited the response to added Ca2+ in a Ca2+-free medium in K+-depolarized preparations. Nifedipine at 10(-6) M, by contrast, nearly abolished the responses to potassium or added Ca2+. In a Ca2+-free medium with EGTA, an addition of NE (10(-5) M), MO (10(-5) M), or CL (10(-5) M) induced a phasic contraction. The inhibitory effect of FR 46171 (10(-8)-10(-5) M) was much greater on the response to CL than that to NE or MO. In a Ca2+-free medium with low EGTA and nifedipine (10(-6) M) in the presence of an alpha-adrenoceptor agonist (NE, MO, or CL), an addition of Ca2+ (2 mM) induced a tonic contraction. FR 46171 (10(-9)-10(-5) M) inhibited the Ca2+ response, which is activated by the agonists, in a concentration-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1988

Palytoxin-induced contraction and release of endogenous noradrenaline in rat tail artery.

1. The mechanism of the contractile effect of a potent marine toxin, palytoxin (PTX) on the rat isolated tail artery was examined. 2. PTX (10(-7) M) induced a contraction in the tail artery which was dependent on external Ca2+. This contraction was inhibited (by 75% or more) by 10(-6) M prazosin, 2.4 x 10(-5) M bretylium and 10(-4) M 6-hydroxydopamine (6-OHDA), and partially (by 40%) by 10(-5) M indomethacin. However, this contraction was not affected by 10(-6) M tetrodotoxin (TTX), 10(-6) M nifedipine or reserpine treatment. The PTX-induced contraction in reserpine-treated artery was partially inhibited by nifedipine and indomethacin but not by prazosin. 3. Transmural electrical stimulation induced a transient contraction which was dependent on external Ca2+. The contraction induced by electrical stimulation was inhibited by TTX, prazosin, bretylium, reserpine treatment and 6-OHDA but not by nifedipine or indomethacin. 4. PTX increased the release of noradrenaline from this artery. However PTX did not release noradrenaline from reserpine-treated arteries. PTX-induced noradrenaline release was only partially inhibited by TTX or by Ca2+-free solution. 5. These results suggest that PTX has pre- and postsynaptic effects in the rat tail artery. PTX may stimulate adrenergic nerves and release noradrenaline mainly by a TTX-insensitive and Ca2+-independent mechanism and partially by a TTX-sensitive and Ca2+-dependent mechanism. Further, PTX may also release prostaglandins and depolarize smooth muscle cell membrane to induce a contraction.

Acrylamides↗
PubMed1988

Inhibitory effects of nitroglycerin on contractile responses to methoxamine and clonidine in isolated rabbit renal and femoral arteries.

The inhibitory effect of nitroglycerin (NG) on contractile responses to methoxamine (MO) and clonidine (CL) was investigated in isolated rabbit renal and femoral arteries. NG (10(-7)-10(-5) mol/l) inhibited the responses to MO and CL in a noncompetitive manner and its inhibitory effect on CL-responses was much greater than that on the MO-responses. In the presence of phenoxybenzamine, however, NG (10(-5) mol/l) markedly inhibited the residual response to MO. Contractile responses to KCl or added Ca2+ in a Ca2+-free medium containing KCl were slightly inhibited by NG. In the presence of nifedipine, NG (10(-5) mol/l) markedly inhibited residual responses to CL but it only slightly inhibited the response to MO. In a Ca2+-free medium with EGTA, MO (10(-5) mol/l) or CL (10(-5) mol/l) induced a phasic contraction. NG had a greater inhibitory effect on the response to CL than MO. In a Ca2+-free medium with EGTA, nifedipine and MO (10(-5) mol/l) or CL (10(-5) mol/l), Ca2+ induced a tonic contraction. NG inhibited the Ca2+-response in the presence of CL, but it had little or no effect on the Ca2+-response in the presence of MO. These results suggest that in rabbit renal and femoral arteries, the potent inhibitory effect of NG on the responses to CL as compared to MO may be due to differences in the amount of receptor reserves that exist for both the agonists. In addition, the inhibition of voltage-dependent Ca2+ channels may not play a major role in the vasoinhibitory action of NG. Further, NG inhibits contractile responses due to mobilization of intracellular Ca2+ much more than the responses due to receptor-activated, nifedipine-insensitive Ca2+-movement.

Animals↗
PubMed1987

Differential inhibitory effects of nicorandil, a new antiangina agent, on the contractile responses to alpha-1- and alpha-2-adrenoceptor agonists in isolated rabbit renal and femoral arteries.

In the renal and femoral artery, nicorandil (10(-6)-10(-4) mol/l) had a much greater inhibitory effect on the responses to clonidine (CL) and BHT-920 than on the response to methoxamine (MO) but the inhibitory action of nifedipine on the responses was no different. In the presence of nifedipine, nicorandil further inhibited the responses to all agonists. In the tissue pretreated with phenoxybenzamine, nicorandil inhibited the residual maximum response to MO in the femoral artery but not in the renal artery. Nicorandil had no effect on the residual response to high concentrations of MO in the renal artery pretreated with phenoxybenzamine and nifedipine. Relationship between maximum contraction and percent-receptor occupancy was found to be nonlinear for MO but was close to linear for CL. The inhibitory effect (pA2) of prazosin on MO and CL was much greater than that of yohimbine. In both preparations, nicorandil had only a slight inhibitory effect on the responses to potassium and Ca2+. It is concluded that the responses induced by MO, CL and BHT are due to activation of alpha 1-adrenoceptors and that the differential effect of nicorandil on the responses to alpha 1- and alpha 2-agonists may be the result of differences in the amount of receptor reserves and/or efficacy of receptor-contraction coupling that exists for MO, CL and BHT.

Adrenergic alpha-Agonists↗
PubMed1987

The mechanism of inhibitory effects of nicorandil, a new antianginal agent, on contractile responses to alpha 1- and alpha 2-adrenoceptor agonists in isolated vascular smooth muscles.

Effects of nicorandil on contractile responses to alpha 1-(methoxamine) and alpha 2-(clonidine and BHT-920) adrenoceptor agonists were examined in isolated rabbit aortae and femoral arteries. Nicorandil (10(-6) M and 10(-5) M) had greater inhibitory effects on contractile responses to clonidine (CL) and BHT than on responses to methoxamine (MO). In tissues treated with phenoxybenzamine, nicorandil (10(-5) M) inhibited residual responses to MO. The relationship between maximum contraction and percent-receptor occupancy was nonlinear for MO, but was near linear for CL and BHT. Prazosin had much greater inhibitory effect on responses to MO and CL than did yohimbine. Nicorandil only slightly inhibited the contractile response of both aorta and femoral arteries to K+ or excess Ca2+, while nifedipine (10(-6) and 10(-5) M) nearly abolished it. In a Ca2+-free medium containing EGTA, nicorandil (10(-7)-10(-5) M) inhibited residual responses of the aorta to BHT, CL, and MO in a concentration-dependent manner. The inhibitory effect of nicorandil was much greater on responses to BHT and CL than to MO. In addition, nicorandil (10(-7)-10(-5) M) inhibited the response of the aorta to Ca2+ (2 mM) added to a Ca2+-free medium containing EGTA, nifedipine (10(-6) M), and an agonist (BHT, CL, or MO). Furthermore, in aortae pretreated with phenoxybenzamine, nicorandil nearly abolished the residual response to MO in a Ca2+-free medium containing EGTA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1987

Mode of vasorelaxing action of 5-[3-[[2-(3,4-dimethoxyphenyl)-ethyl]amino]-1-oxopropyl]-2,3,4,5- tetrahydro-1,5-benzothiazepine fumarate (KT-362), a new intracellular calcium antagonist.

In rabbit aorta, pretreatment with KT-362 (KT; 10(-6) and 10(-5) M) inhibited contractile responses to norepinephrine (NE; 3 X 10(-9)-10(-5) M) and methoxamine (10(-7)-10(-4) M) but failed to affect responses to potassium (10-70 mM). KT (10(-5) M) partially inhibited Ca++-induced contractions in K+-depolarized aorta pre-equilibrated in a Ca++-free medium. After incubation of tissues for 30 min in a Ca++-free medium containing EGTA (0.2 mM), residual responses to NE and methoxamine were inhibited by KT (10(-6)-10(-4) M) and nitroglycerin (10(-5) M), but not by nifedipine, verapamil or diltiazem (all 10(-5) M). The inhibitory action of a combined treatment with KT and nitroglycerin (both 10(-5) M) on the residual response to NE was also much greater than that of either agent alone. In a Ca++-free medium, the residual caffeine-induced contraction of rabbit iliac artery was inhibited by KT (10(-5)-10(-4) M) but not by nifedipine (10(-5) M). The inhibitory action of KT on the residual responses to methoxamine and caffeine in a Ca+-free medium was much greater than that of nitroglycerin. In a Ca++-free medium with low EGTA (0.01 mM), D600 (10(-5) M) and NE (3 X 10(-7) M), the addition of Ca++ (2 mM) resulted in a tonic contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The contractile action of palytoxin in the isolated rabbit urinary bladder.

Palytoxin at 10(-10)-10(-7) M caused contractions of the detrusor muscle from rabbit urinary bladder in a concentration-dependent manner. The response to palytoxin was markedly inhibited by indomethacin (a cyclooxygenase inhibitor) or nordihydroguaiaretic acid (a lipoxygenase inhibitor) at 10(-5) M. Indomethacin and nordihydroguaiaretic acid also inhibited the response to arachidonic acid at 10(-3) M. A Ca2+-free medium with EGTA or nifedipine at 10(-5) M, nearly abolished the responses to palytoxin and arachidonic acid. Tetrodotoxin, phentolamine, atropine and chlorpheniramine (all at 10(-5) M) had a slight or no inhibitory effect on the response to palytoxin. These results suggested that in the rabbit bladder, the contractile effect of palytoxin is mainly dependent on an increase in metabolites of arachidonic acid.

Acrylamides↗
PubMed1986

The inhibitory action of melatonin on the contractile response to 5-hydroxytryptamine in various isolated vascular smooth muscles.

The effects of melatonin on the contractile responses to 5-hydroxytryptamine (5-HT), norepinephrine (NE), angiotensin-1 (AT-1) and potassium were determined on the rabbit isolated aorta, iliac and renal arteries. Melatonin, at 10(-4) or 10(-3) M inhibited the response to 5-HT in the aorta, iliac and renal arteries. Melatonin, at 10(-3) M, had a negligible effect on the responses to NE and AT-1 in all preparations used. The potassium-induced contraction of all 3 preparations used was slightly inhibited by only the high concentration of melatonin (10(-3) M). In a Ca+-free medium with EGTA (0.1 mM), the residual response to 5-HT (10(-5) or 10(-4) M) were inhibited by melatonin (10(-4) or 10(-3) M) in all preparations used. In a Ca2+-free medium with EGTA (0.01 mM), nifedipine (10(-6) M) and 5-HT (5 X 10(-7) M), application of Ca2+ (2 mM) resulted in a tonic contraction, related to receptor operated channels, of all preparations. This Ca2+ dependent, nifedipine insensitive contraction was markedly inhibited or abolished by melatonin at 10(-5) and 10(-4) M. These results demonstrated that melatonin had a generally greater inhibitory effect on the response to 5-HT than those to NE, AT-1 and potassium in vascular smooth muscles. Also the results suggest that action of melatonin on the 5-HT induced contraction is more related to interference with Ca2+ influx through receptor operated channels than release of intracellular Ca2+ from the store site.

Angiotensin I↗
PubMed1986

Potent alpha-adrenoceptor blocking action of SGB-1534, a new quinazoline antihypertensive agent in vitro experiments.

SGB-1534 inhibited the contractile response to norepinephrine (NE), methoxamine (MO) and electrical transmural stimulation in the rabbit aorta, basilar and cat coronary arteries and only in the rabbit aorta its inhibitor action was a competitive manner. In the rabbit aorta, the potency (pA2) of SGB was greater than that of prazosin, whereas in the other preparations, the effect of SGB was comparable to that of prazosin. In the rabbit aorta, both SGB and prazosin abolished the contraction induced by transmural stimulation. In the guinea-pig vas deferens, SGB failed to affect the inhibitory effect of clonidine on the response to electrical field stimulation. SGB had no inhibitory effects on the contractile response to potassium, 5-hydroxytryptamine, PGF2 alpha and an excess Ca2+ and the relaxing response to isoproterenol in the vascular tissues. In the electrically driven left atria of guinea-pigs, SGB had no effect on the electromechanical parameters and the isoproterenol induced inotropic effect. On the specific binding of [3H]prazosin in the rabbit aorta, the inhibitory effect of SGB was greater than that of prazosin and phentolamine.

Adrenergic alpha-Antagonists↗
PubMed1986

The mode of vasorelaxant action of 2-aminoisoquinoline, 1.3 (2H.4H)-dione, a novel 'intracellular calcium inhibitor'.

In rabbit aorta, pretreatment with 2-aminoisoquinoline, 1.3 (2H.4H)-dione (AQ, 10(-5) M and 10(-4) M) shifted the concentration-response relationship to noradrenaline (NA, 10(-9) M to 10(-4) M) in a parallel manner whereas the agent (10(-4) M) failed to affect the response to potassium and only slightly depressed Ca2+-induced contractions in a Ca2+-free medium in the presence of K+ (40 mM). Ca2+-entry blockers such as nifedipine and diltiazem (10(-6) M and 10(-5) M) had very weak or no apparent effects on the response to NA but markedly attenuated or abolished the K+- and Ca2+-induced contractions. Following incubation of tissues for 15 min in a Ca2+-free medium with low EGTA (0.01 mM) and methoxyverapamil (D600, 10(-5) M), NA (3 X 10(-7) M) caused a phasic (transient) contraction and the subsequent application of Ca2+ (2mM) resulted in a tonic contraction. This NA-induced, Ca2+-dependent, D600-insensitive contraction was inhibited by AQ (10(-5) M and 10(-4) M) in a concentration-dependent manner. This suggests that the inhibitory action of AQ may be related to Ca2+ entry through specific receptor activated pathways. Following incubation of tissues for 30 min in a Ca2+-free medium with high EGTA (2.0 mM), NA (10(-5) M) caused a contraction of rabbit aorta which is dependent upon release of intracellular Ca2+, but the response was 50% to 60% less than that in a normal medium. This contraction was inhibited by AQ (10(-5) M and 10(-4) M) and nitroglycerin (10(-5) M) but not by nifedipine or diltiazem. The inhibitory action of combined treatment with AQ and nitroglycerin (10-5 M) on the response to NA was not different from that of either agent alone. 5 These results suggest that AQ may have inhibitory actions on the release of intracellular Ca2+ and also on Ca2+-entry through D600-insensitive, receptor-activated Ca2+ pathways in rabbit aorta.

Aminoquinolines↗
PubMed1986

Mechanism of barium-induced contraction in the vascular smooth muscle of rabbit aorta.

In a solution containing 1.5 mM Ca2+, cumulative application of 0.3-10.0 mM Ba2+ induced a concentration-dependent contraction of the rabbit aorta. This contraction was reduced by the Ca2+ channel inhibitors, verapamil (10(-6) M), nifedipine (10(-7) M) and lanthanum (2.0 mM), and was potentiated by the Ca2+ channel facilitator, Bay K8644 (10(-7) M). In a Ca2+-free solution containing EGTA (1.0 mM), cumulative application of Ba2+ still induced a concentration-dependent contraction, the maximum contractile tension of which was comparable to that in the presence of 1.5 mM Ca2+. The Ba2+-induced contraction which was not dependent on the external Ca2+ was also inhibited by verapamil, nifedipine and lanthanum and was potentiated by Bay K8644. A high concentration (65.4 mM) of K+ potentiated this Ba2+-induced contraction whereas noradrenaline (10(-6) M) did not have such an effect. In order to deplete the releasable Ca2+ store in the cell, the muscle strip was treated with noradrenaline (10(-6) M) and/or caffeine (20.0 mM) in a Ca2+-free solution. In such a Ca2+-depleted muscle, Ba2+ still induced a contraction of a similar magnitude to that without such treatment. Further, the second application of Ba2+ in a Ca2+-free solution induced a similar contraction to that induced by the first application of Ba2+. These results suggest that Ba2+ depolarizes the cell membrane and opens the voltage-dependent Ca2+ channels resulting in a Ca2+ influx in the presence of Ca2+. In the absence of external Ca2+, Ba2+ may enter the cell through the voltage-dependent Ca2+ channels and induce contraction without mobilizing the Ca2+ store which is sensitive to noradrenaline and caffeine.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Effect of nicorandil, N-(2-hydroxyethyl)nicotinamide nitrate, a new anti-anginal agent, on contractile responses to alpha-1- and alpha-2-adrenoceptor agonists in isolated rabbit aorta.

Effects of nicorandil on contractile responses to alpha 1- and alpha 2-adrenoceptor agonists were examined in isolated rabbit aorta. Nicorandil (10(-6) or 10(-5) M) inhibited contractile responses to clonidine (CL) and BHT-920 in a concentration-dependent manner, but had no effect on the response to methoxamine (MO). Nifedipine (10(-6) and 10(-5) M) had no significant effect on responses to CL and MO, but it had a noticeable inhibitory effect on the response to BHT-920. In tissues pretreated with phenoxybenzamine, nicorandil (10(-5) M) inhibited the residual response to MO, and nifedipine (10(-5) M) inhibited responses to MO and CL. The relationship between maximum contraction and percent receptor occupancy was found to be nonlinear for MO, but was near linear for CL and BHT-920. The inhibitory effect of prazosin (pA2 of about 9) on MO and CL was much greater than that of yohimbine (pA2 of about 6). Nicorandil had no apparent or slight inhibitory effect on responses to potassium and Ca2+, and this inhibitory effect was much less than that of nifedipine. These results indicate that the responses induced by MO, CL, and BHT-920 in the rabbit aorta are due to activation of alpha 1-adrenoceptors. It is also suggested that nicorandil minimally affects voltage-dependent Ca2+ influx and that differential effects of nicorandil on the responses to alpha 1 and alpha 2 agonists may be the result of differences in the amount of receptor reserve that exist for MO, CL, and BHT-920 in this blood vessel.

Adrenergic alpha-Agonists↗
PubMed1985

Dopamine-induced potentiation of the contractile response to arachidonic acid in guinea-pig aorta.

In guinea-pig aorta, the potentiating effect of dopamine on the response to arachidonic acid was examined. The potentiation by dopamine was completely abolished by nordihydroguaiaretic acid, but not by indomethacin, aspirin, corticosterone, haloperidol, SK & F 83566, propranolol, PGI2 or imidazole. Dopamine did not have any significant effect on the response to PGF2 alpha U-46619, KCl, 5-hydroxytryptamine or histamine.

Animals↗
PubMed1985

Inhibitory effect of ouabain on the palytoxin-induced contraction of human umbilical artery.

Palytoxin (PTX), C129H223O3N54, isolated from marine coelenterates of Palythoa tuberculosa, caused contraction of the human umbilical artery in a dose-dependent manner (10(-11)-10(-8) M). Pretreatment with ouabain (10(-5) M) abolished the PTX (10(-8) M)-induced contraction but had no effect on the serotonin- (10(-6) M) and potassium- (40 mM) induced contractions. When the muscle was exposed to a potassium-free medium, application of PTX was able to cause a contraction similar to the contraction in normal medium. In the presence of verapamil (3 X 10(-6) M) or in the calcium-free medium. PTX-induced contraction was inhibited. In the depolarized muscle with 126 mM potassium, PTX did not induce a contraction whereas serotonin did. Our results suggest that PTX causes calcium influx through the plasma membrane of the umbilical artery, causing contraction. The site of action of PTX is presumably related to the Na,K-ATPase on the plasma membrane, although the precise relation between the site of action and increase in calcium influx is not known now.

Acrylamides↗