Biomedical subjects

N Satake

Publications and source records attributed to N Satake.

At least 91 records · Page 5Linked to original sources

PubMed1991

Characterization of the vasoinhibitory actions of KT2-230, a new benzothiazepine vasodilator derivative on isolated rabbit vascular smooth muscles: an alpha-adrenergic- and serotonergic-receptor antagonist.

1. Pharmacological properties of KT2-230 (benzothiazepine derivative), a newly synthesized vasorelaxing agent, were studied. 2. In the anesthetized dogs, KT2-230 increased the femoral and vertebral blood flow without effect on systemic blood pressure. 3. In rabbit aorta, KT2-230, methysergide and phentolamine inhibited contractile responses to 5-hydroxytryptamine. 4. The response to norepinephrine was also inhibited by KT2-230 and phentolamine. Responses to histamine were not affected by KT2-230. 5. Responses to KCl and Ca2+ in K+ depolarized aorta in Ca2(+)-free medium were inhibited by a high concentration of KT2-230. 6. In rabbit iliac artery, KT2-230 inhibited the response to caffeine in Ca2(+)-free medium. 7. KT2-230 decreased total La3(+)-resistant Ca2(+)-binding at high affinity sites. 8. These results indicate that KT2-230 inhibits alpha 1-adrenoceptors and 5-HT-receptors and at high concentrations it inhibits slow Ca2(+)-channels. KT2-230 may inhibit the Ca2(+) release from caffeine- and agonist-sensitive Ca2+ stores.

Adrenergic alpha-Antagonists↗

PubMed1991

The mode of vasorelaxing action of melatonin in rabbit aorta.

1. The vasorelaxing effect of melatonin on the contractile response to 5-hydroxytryptamine (5-HT) was investigated in rabbit isolated aorta. 2. Melatonin (10(-5)-10(-3) M) caused relaxation of the 5-HT (10 M) response in a concentration-dependent manner. Nifedipine (10(-6) M) did not affect the relaxing action of melatonin. 3. Pretreatment with methylene blue (10(-5) M) or nitroglycerin (3 x 10(-8) M) inhibited or potentiated, respectively, the relaxing action of melatonin. 4. Pretreatment with melatonin (10(-3) M) or M&B 22.948 (10(-3) M) potentiated the relaxing effect of nitroglycerin (10(-9)-10(-5) M) on the contraction induced by PGF2 alpha (4 x 10(-6) M). The effect of a combined treatment with melatonin and M&B 22.948 was not significantly different from that of a single treatment with M&B 22.948. 5. Melatonin (10(-5)-10(-3) M) inhibited the activity of cGMP-phosphodiesterase, in a concentration-dependent manner. 6. These results suggest that the vasorelaxing action of melatonin may be due to an increase in the level of cGMP.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1991

Vasorelaxing action of melatonin in rat isolated aorta; possible endothelium dependent relaxation.

1. Melatonin (10(-4)-10(-3) M) inhibited contractile response to 5-hydroxytryptamine (5-HT) and KCl in rat isolated aorta. 2. In the presence of verapamil but not nifedipine, melatonin failed to inhibit residual response to KCl. 3. In the aorta precontracted with 5-HT, PGF2 alpha, or KCl, melatonin (10(-6)-10(3) M) caused relaxation. Removal of endothelium only inhibited the melatonin relaxation on the 5-HT response. Methylene blue also inhibited the melatonin relaxation. 4. Nifedipine and verapamil partly inhibited the melatonin relaxation on the 5-HT response. In the absence of endothelium, verapamil but not nifedipine further inhibited the melatonin relaxation. 5. M & B 22,948 inhibited the melatonin relaxation. Melatonin potentiated the nitroglycerin relaxation. In the absence of endothelium, nitroglycerin and melatonin potentiated the relaxation by melatonin and nitroglycerin, respectively. 6. These results suggest that the mode of inhibitory action of melatonin is somewhat similar to that of verapamil. In addition, the vasorelaxing effect of melatonin on the 5-HT response is endothelium dependent and also may be related to the inhibition of cGMP metabolism.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1991

Characteristics of the vasorelaxing action of (3E)-4-ethyl-2-hydroximino-5-nitro-3-hexamide FK409, a new vasodilator isolated from microbial sources, in isolated rabbit arteries.

We examined the vasoinhibitory effect of (3E)-4-ethyl-2-hydroximino-5-nitro-3-hexamide FK409, a new vasodilator, on contractile responses in isolated rabbit arteries. FK409 (10(-8)-10(-5) M) inhibited contractile responses to norepinephrine (NE), histamine (His), and 5-hydroxytryptamine (5-HT) in rabbit aorta. The pattern of inhibition by FK409 was not competitive. The inhibitory effect of FK409 on the 5-HT response was much greater than that of nitroglycerin (NG). A high concentration of FK409 (10(-5) M) was necessary to inhibit the response to KCl (10-70 mM). The effect of combined treatment with FK409 (10(-5) M) and a subthreshold concentration of nifedipine (10(-9) M) on the KCl response was much greater than a single treatment with either agent. In addition, 3 x 10(-6) M D600, but not FK409 (10(-6) or 10(-5) M), inhibited the increase in the rate of 45Ca influx stimulated by a 40-mM KCl substituted solution. In a Ca2(+)-free medium containing EGTA and nifedipine, FK409 (10(-9)-10(-5) M) inhibited phasic responses to NE, His, and 5-HT, and subsequent sustained responses owing to addition of Ca2+. The response to caffeine in rabbit iliac arteries incubated in Ca2(+)-free medium was also inhibited by FK409 (10(-6) and 10(-5) M). In rabbit aorta precontracted with NE (10(-5) M) and partially inhibited by prior exposure to NG (10(-5) M), the relaxing effect of FK409 was slightly attenuated. Pretreatment of tissues with FK409 (10(-6) M) inhibited the relaxing action of NG much more than prior NG inhibited the relaxing action of FK409. Methylene blue (10(-5) M), but not hemoglobin (10(-6) M), inhibited the relaxing action of FK409, whereas M&B 22,948 (3 x 10(-4) M) potentiated it. FK409 caused a relaxation of precontracted aorta without endothelium that was inhibited by methylene blue. In rabbit aorta precontracted with NE, FK409 (10(-6) M) increased cyclic GMP but not cyclic AMP content. FK409 (10(-5) M) had no effect on the NE-mediated increase in tissue inositol monophosphate (IP). These results suggest that FK409 inhibits the responses attributed to both intracellular Ca2+ release and Ca2+ influx through receptor-operated channels. The inhibitory effect of FK409 on both the KCl contractile response and KCl-stimulated 45Ca influx appears to be different from that of nifedipine or D600. Furthermore, the inhibitory action of FK409 may be partially mediated by cyclic GMP.

Animals↗

PubMed1991

Positive inotropic action of veratridine in rat atria: possible involvement of prostanoids.

Veratridine caused a positive inotropic action in the electrically driven left atria of rats. Quinacrine (a phospholipase A2 inhibitor), indomethacin (a cyclooxygenase inhibitor) and aspirin (a cyclooxygenase inhibitor), but not nordihydroguaiaretic acid (a lipoxygenase inhibitor), inhibited the response to veratridine. Verapamil and nifedipine also inhibited the response to veratridine. The positive inotropic effect of arachidonic acid was abolished by aspirin and indomethacin. However, the positive inotropic effect of PGF2 alpha was not affected by indomethacin, quinacrine or aspirin. PGE2, but not STA2 and PGI2, also caused the positive inotropic effect. However, the negative inotropic effect was observed in the presence of PGE1 and PGD2. Veratridine shifted the concentration-response curve of Ca2+ to the left in a Ca(2+)-free medium. Indomethacin only inhibited the veratridine-induced potentiation of Ca2+ responses. Veratridine increased the level of PGF2 alpha in the left atria and this action was completely inhibited by indomethacin, aspirin and quinacrine. Veratridine also increased the level of PGE2. These results imply that the positive inotropic action of veratridine is partly due to stimulation of the release of arachidonic acid leading to the increase in prostaglandins in rat atria.

Animals↗

PubMed1991

[A pilot study of etoposide, split-dose cisplatin and THP in small cell lung cancer].

Sixteen untreated patients with small cell lung cancer were treated with a combination of Etoposide (70 mg/m2 i.v., day 3-5), Cisplatin (40 mg/m2 i.v., days 1 and 8) and THP (20 mg/m2 i.v., days 1 and 8). Cycles were repeated every 4 weeks and 15 patients received more than two cycles. The objective response rate was 80% (12 of 15) in complete cases, 91% (10 of 11) in limited disease and 50% (2 of 4) in extensive disease. CR rate was 33% in complete cases, 46% in limited disease. The median duration of response was 22.6 weeks. The median survival was more than 12 months in complete cases. Toxicity was primarily myelosuppression. Three of 15 patients had leukopenia of grade 4, 3 of 15 of grade 3, and 7 of 15 of grade 2. Nausea and vomiting were well tolerated by metoclopromide and methylprednisolone. The renal toxicity was minimal. There were no chemotherapy-related lethal complications. This schedule of Etoposide, split-dose Cisplatin and THP is effective and safe for patients with small cell lung cancer. However, the advantage of THP is still controversial.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1991

[A basic study on the plasma and serum levels of eosinophil cationic protein (ECP) in bronchial asthma].

A basic study on the blood eosinophil cationic protein (ECP) as an index for eosinophil activation in bronchial asthma was performed. 1) ECP concentration in the serum collected 2 hours after blood sampling and the peripheral eosinophil count were significantly higher in asthmatic patients than in normal individuals. A correlation between these two parameters was observed in normal controls but not in asthmatic patients. These findings suggest that the degree of eosinophil activation, which is reflected by the blood ECP concentration, varies with the clinical condition in asthmatic patients. 2) The plasma and serum ECP levels were compared. The serum ECP was higher than the plasma ECP in both normal controls and asthmatic patients. In asthmatic patients, however, plasma ECP levels poorly correlated with serum levels: the serum levels were markedly elevated in some cases, and only the plasma levels were significantly elevated during symptomatic periods compared with stable periods. Therefore, attention must be paid not only to the serum ECP concentration, but also to the plasma ECP concentration and the plasma-serum difference. 3) This plasma-serum difference in ECP concentration may be due to the in vitro release of ECP during coagulation after blood sampling rather than the effect of alpha 1-macroglobulin concentration, because supernatants from stimulated platelets elicited ECP release from eosinophils.

Asthma↗

PubMed1990

The inhibitory effect of quinacrine on contractile responses to norepinephrine in isolated rabbit aorta.

1. In rabbit aorta, quinacrine, but not indomethacin nor nordihydroguaiaretic acid, inhibited contractile responses to norepinephrine and KCl. Amiloride and nifedipine did not affect the effect of quinacrine. 2. In Ca2(+)-free medium, quinacrine (3 x 10(-6)-10(-4) M) inhibited the norpinephrine response less than that to a subsequent addition of Ca2+. 3. M&B 22, 948, nitroglycerin and forskolin inhibited the Ca2+ response. The effect of quinacrine was inhibited by M&B 22,948, but not by forskolin and potentiated by nitroglycerin. 4. Quinacrine and M&B 22,948 potentiated the nitroglycerin-relaxation. The effect of quinacrine plus M&B 22,948 was not different from that of quinacrine. 5. These results indicate that the effect of quinacrine may be different from that of nifedipine but is related to cGMP.

Amiloride↗

PubMed1990

Anticholinergic action of disopyramide in intestinal smooth muscle of the guinea pig: inhibition of muscarinic receptors (M1 and M2).

Antimuscarinic actions of disopyramide were investigated by measuring the contractile responses of intestinal smooth muscles and ligand binding in cardiac and intestinal membrane preparations. Disopyramide caused a parallel shift of the dose-response curves for acetylcholine, McN-A-343, and carbachol to the right in the guinea pig taenia caeci; pA2 values were 5.4 for acetylcholine, 5.5 for McN-A-343 and 5.9 for carbachol. In the guinea pig ileum, disopyramide competitively antagonized acetylcholine in the contractile responses, having the pA2 value of 6.1. In microsomal fractions of the guinea pig taenia caecum and heart, disopyramide was capable of replacing 3H-QNB; K1 values were 7 x 10(-6) M for the taenia and 2 x 10(-6) M for the heart. These results suggest that disopyramide exerts antimuscarinic action through M1 and M2 receptors with a potency approximately 3 times greater for M2 than M1.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1990

Effect of ozagrel (OKY-046), a thromboxane synthetase inhibitor, on theophylline pharmacokinetics in asthmatic patients.

The effect of ozagrel (OKY-046), a selective thromboxane A2 synthetase inhibitor, on theophylline disposition was studied in 12 asthmatic patients. Ozagrel was administered at a dose of 200 mg twice daily for 24 weeks to 4 outpatients receiving oral theophylline medication. Blood samples were drawn from each patient visiting the hospital at one to four-week intervals. There were no clinical significant changes between the time course profiles of serum theophylline concentration during the treatment and those after the cessation of ozagrel dosing. In addition, another 8 hospitalized patients received a single intravenous infusion of aminophylline (200 mg as theophylline) before and after ozagrel treatment of 200 mg twice daily for 7 days. No statistical significant alteration in elimination half-life, total body clearance or volume of distribution of theophylline was observed by the administration of ozagrel. These results suggest that ozagrel does not inhibit the metabolism of theophylline despite having an imidazole ring in its chemical structure.

Acrylates↗

PubMed1989

Bay K 8644-induced potentiation of the contractile response of rabbit iliac artery to caffeine in a Ca2+-free medium.

1. In a Ca2+-free medium caffeine (10 mM) was still able to cause a phasic contraction in rabbit iliac arteries. 2. Bay K 8644 at 10(-6) but not at 10(-7) M potentiated the residual response to caffeine in a Ca2+-free medium. In a Ca2+-free medium with or without KCl (40 mM), Bay K 8644, however, caused no contraction. 3. Nifedipine (10(-6) M) did not affect the residual caffeine-response or the potentiating effect of Bay K 8644. Verapamil (10(-6) M), however, inhibited both the caffeine response and the potentiation. 4. Bay K 8644 (10(-6) M) potentiated the contractile response to Ca2+ (0.01-2.4 mM) in a Ca2+-free medium containing KCl. The potentiation was equally inhibited by nifedipine or verapamil. 5. La#+ (1 mM), EGTA (0.1 mM), or vanadate (10(-4) M) completely inhibited the Bay K 8644-induced potentiation without affecting the residual caffeine response. 6. These results suggest that the potentiating action of Bay K 8644 on the residual caffeine response in a Ca2+-deficient medium may not be related to voltage-dependent Ca2+ channels. In addition, the activity of Ca2+-ATPase in sarcolemmal membranes may be important in this potentiation.

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

PubMed1989

Potentiating effect of Bay K 8644 on the noradrenaline-induced contraction in rabbit renal and femoral arteries.

1. In rabbit renal and femoral arteries, Bay K 8644 produced a contraction and nifedipine inhibited it. 2. Bay K 8644 potentiated the responses to noradrenaline (NA) and potassium (K+). In the presence of nifedipine, Bay K 8644 potentiated NA. 3. In a Ca2+-free medium with EGTA, NA produced a transient contraction which was not affected by Bay K 8644 or nifedipine. Bay K 8644 enhanced the Ca2+-induced contraction in a Ca2+-free medium containing EGTA, nifedipine and NA. 4. The combined treatment with nimodipine and nifedipine further inhibited the Bay K 8644 induced potentiation of Ca2+ responses in the presence of NA as compared to nifedipine alone. 5. In the presence of but not absence of Bay K 8644, Ca2+ caused contractions in a Ca2+-free medium containing EGTA, nifedipine and KCl. 6. Vanadate further enhanced the Bay K 8644 induced potentiation of the Ca2+ responses in the presence of K+ but not NA. 7. These results suggest that, in rabbit renal and femoral arteries, Bay K 8644 does not affect the intracellular translocation of Ca2+ but increases Ca2+-influx activated by K+ or NA. Bay K 8644-induced potentiation of NA responses is likely due to an increase in Ca2+-influx through voltage operated channels (VOC) activated by NA. Also, K+ activated VOC may be coupled to Ca2+-extrusion pumps more than NA activated VOC.

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

PubMed1989

Vasorelaxing action of melatonin in rabbit basilar artery.

1. In rabbit basilar arteries, melatonin (10(-5)-10(-3) M) and nifedipine (10(-10)-10(-8) M) inhibited the responses to KCl and 5-hydroxytryptamine. 2. Melatonin or nifedipine inhibited the Ca2+-responses in a Ca2+-free medium containing KCl (40 mM) or 5-HT (10(-5) M). 3. A combined treatment with nifedipine and melatonin caused no further inhibition of the Ca2+ response in the presence of K+ as compared to a single treatment with melatonin. 4. However, the combined treatment caused a greater inhibition of the Ca2+-response in the presence of 5-HT than the single treatment with either agent. 5. These results suggest that melatonin and nifedipine inhibit the same Ca2+ channels activated by KCl. Further, 5-HT-activated Ca2+ channels which are inhibited by melatonin may be different from nifedipine-sensitive Ca2+ channels activated by 5-HT.

Animals↗

PubMed1989

Inhibitory effects of TYB 3823, a new antiarrhythmic agent, on mechanical responses in the vascular smooth muscles.

1. TYB 3823 (3 x 10(-5) M to 10(-3) M) but not lidocaine (10(-4) M) inhibited the contractile response to norepinephrine in rabbit aorta in a competitive manner. On the other hand, TYB 3823 had no effect on contractile responses to histamine, 5-hydroxytryptamine, high KCl and Ca2+. 2. In rabbit aorta, TYB 3823 (10(-5) M and 10(-4) M) but not lidocaine (10(-4) M) also antagonized the ouabain-induced contraction and this action was less potent than that of phentolamine (10(-6) M). 3. In rabbit coronary arteries precontracted with KCl (40 mM), either TYB 3823 or lidocaine inhibited the isoproterenol-induced relaxation to the same levels. Propranolol at 10(-8) M shifted the relaxation curve for isoproterenol to the right and at 10(-6) M it almost completely prevented the relaxation. Further, the effect of a combined treatment with propranolol (10(-8) M) and TYB 3823 (3 x 10(-5) M) was not different from that of a single treatment with propranolol (10(-8) M). 4. In rabbit iliac arteries, TYB 3823 (3 x 10(-5) M and 10(-4) M) but not lidocaine (10(-4) M) suppressed the contractile response to caffeine in a Ca2+-free medium with EGTA and nifedipine. Nitroglycerin (10(-4) M) also inhibited the response but this action was less potent than that of TYB 3823. The combined treatment of the tissue with TYB 3823 and nitroglycerin (both 10(-4) M) further inhibited the responses to caffeine as compared to a single treatment with each drug. 5. These results suggested that TYB 3823 may interfere with the responses due to the mobilization of intracellular Ca2+ activated by caffeine and also has both alpha- and beta-adrenoceptor blocking actions on the vascular smooth muscles.

Animals↗

PubMed1989

Electrophysiological effects of FK664, a new cardiotonic agent, on preparations from guinea pig ventricle and from rabbit sino-atrial node.

Effects of the cardiotonic agent FK664, 6-(3, 4-dimethoxy-phenyl)-1-ethyl-4-mesitylimino-3-methyl-3,4-dihydro-2 (1H)-pyrimidone, on isolated guinea pig ventricular muscles and rabbit sinus node pacemaker cells were studied using micro-electrode techniques. In ventricular muscles driven at 0.5-1.0 Hz, FK664 above 3 mumol.litre-1 caused an increase in contractile force and a shortening of time to peak tension. This positive inotropic effect of FK664 was accompanied by a slight elevation of the early plateau phase of the action potential, while other action potential variables were unaffected. The change in contractile force induced by FK664 was abolished in a low Ca2+ medium (0.12 mmol.litre-1) or by treatment with ryanodine (2 mumol.litre-1), whereas it was relatively well preserved in the preparations pretreated with nefedipine (1 mumol.litre-1). The slow action potentials induced by isoprenaline (0.3 mumol.litre-1) in high K+ medium (30 mmol.litre-1) and the slow inward current measured by single sucrose gap voltage clamp at a holding potential of -40 mV were unaffected by FK664. In sinus node pacemaker cells, FK664 (1-10 mumol.litre-1) caused a dose dependent acceleration of phase 4 depolarisation and a shortening of spontaneous firing cycle length. This positive chronotropic effect of FK664 was markedly inhibited in a low Ca2+ medium (0.3 mmol.litre-1). These findings suggest that FK664 has positive inotropic and chronotropic effects on the heart, due to an enhancement of transsarcolemmal calcium influx through the low threshold, dihydropyridine insensitive Ca2+ channel population.

Action Potentials↗

PubMed1989

Differential inhibitory effects of nitroglycerin on contractile responses to the alpha-adrenoceptor agonists, methoxamine and clonidine, in rabbit aorta.

The vasoinhibitory action of nitroglycerin was examined on contractile responses to methoxamine and clonidine in isolated rabbit aorta. Nitroglycerin at 10(-5) M, but not 10(-6)-10(-8) M, shifted the concentration response curve for methoxamine to the right. Nitroglycerin (10(-8)-10(-5) M), however, noncompetitively inhibited responses to clonidine in a concentration dependent manner. Nitroglycerin (10(-5) M) had no effect on responses to potassium (10-70 mM), but slightly inhibited responses to Ca2+ (0.1-5 mM) in a Ca2+-free medium containing potassium. Nifedipine (10(-6) and 10(-5) M), however, almost abolished responses to both potassium and Ca2+ but had no effect on responses to either methoxamine or clonidine. Agonist-antagonist interactions using prazosin and yohimbine revealed that responses to both methoxamine and clonidine were due to activation of alpha 1-adrenoceptors. Results with phenoxybenzamine suggested that the aorta has more receptor reserve for methoxamine than for clonidine. Furthermore, in tissues pretreated with phenoxybenzamine, nitroglycerin (10(-5) M) inhibited the maximal contractile response to methoxamine (3 x 10(-4) M). The maximal response to clonidine in tissues pretreated with phenoxybenzamine was not affected by nitroglycerin (10(-8) M). Nitroglycerin (10(-9)-10(-4) M) had greater inhibitory effect on residual responses to clonidine (10(-5) M) than that to methoxamine (10(-5) M) in a Ca2+-free medium containing EGTA. The contractile responses to Ca2+ (2 mM) in a Ca2+-free medium containing EGTA, nifedipine, and either methoxamine (5 x 10(-7) M) or clonidine (3 x 10(-7) M) were inhibited by nitroglycerin (10(-9) - 10(-5) M). The effect of nitroglycerin was greater on responses in the presence of clonidine than methoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗

PubMed1989

Thromboxane A2 antagonistic action of a new anti-ulcer agent, azuletil sodium (KT1-32).

The TXA2/PGH2 receptor antagonistic activity of azuletil sodium (KT1-32), a new anti-ulcer agent, was examined. KT1-32 competitively antagonized the contraction of canine gastric arteries induced by U-46619, PGF2 alpha, and PGE2, whereas it had no effect on the PGF2 alpha-, PGE2- and LTD4-induced contraction of guinea-pig ileum, which was not affected by U-46619. In anesthetized dogs, KT1-32 significantly reduced the U-46619-induced decrease in gastric arterial blood flow. Gastric contraction induced by U-46619 in anesthetized rats was markedly inhibited by KT1-32. KT1-32 showed no influence on TXA2 synthetase and cyclooxygenase activities. These results indicate that KT1-32 is a competitive TXA2/PGH2 receptor antagonist, which may be important as to the effectiveness of KT1-32 against gastric ulcer.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1989

The potentiation of norepinephrine-induced contraction of rabbit aorta by Mg2+ deletion in a Ca2+-free medium.

Residual responses to norepinephrine (NE) in an Mg2+-, Ca2+-free medium with low EGTA (0.1 mM) for 15 min were potentiated following preincubation of rabbit aortas in Mg2+-free medium for 60 min. Responses to Ca2+ in a Ca2+-free medium with nifedipine and NE were not affected under a similar Mg2+-free condition. Nifedipine, theophylline, dibutyryl cAMP, 8-bromo-cGMP, methylene blue, La3+ or vanadate did not affect the residual response or the potentiation. However, high EGTA (1 mM) inhibited both the residual response and the potentiation. The residual response to NE was not potentiated following incubation in Mg2+-, Ca2+-free medium for 60 min. These results suggest that, in the rabbit aorta, Mg2+ deletion from the medium selectively potentiates the residual response to NE in a Ca2+-free medium without any effect on the response due to Ca2+-influx through receptor-operated channels. This potentiation does not appear to be related to either the levels of cAMP and cGMP or the activity of an Mg2+-dependent, Ca2+-ATPase.

Animals↗