Search PubMed⌕ Search

Biomedical subjects

T Satake

Publications and source records attributed to T Satake.

At least 73 records · Page 4Linked to original sources
PubMed1990

[The role of endothelium-derived contracting factor (EDCF) and endothelium-derived relaxing factor (EDRF) in the aorta of the rat: identification of EDCF].

The present experiment was performed to identify endothelium-derived contracting factor produced by acetylcholine stimulation in the aorta of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The rings of the thoracic aorta were obtained from age-matched SHR and WKY, and changes in isometric tension were recorded. The relaxant responses to acetylcholine in the rings from SHR were significantly weaker than those obtained in WKY. The relaxant responses to acetylcholine were significantly enhanced by pretreatment with a cyclooxygenase-inhibitor (indomethacin) or thromboxane A2/prostaglandin H2 receptor antagonist (ONO-3708) both in the SHR and WKY rings. A thromboxane A2 synthetase inhibitor (OKY-046) did not affect the acetylcholine-induced relaxation in the rings from SHR or WKY. In the organ bath solution, following acetylcholine stimulation, prostaglandin E2 and 6-keto-prostaglandin F1 alpha concentrations increased, but prostaglandin F2 alpha and thromboxane B2 concentrations did not increase. Exogenous prostaglandin H2, a stable analogue of thromboxane A2 (STA2) and prostaglandin F2 alpha induced contractions of the SHR rings at a lower concentration than prostaglandin E2, prostaglandin D2 and prostaglandin I2. These contractile responses to various prostaglandins were markedly inhibited by pretreatment with ONO-3708. A prostacyclin synthetase inhibitor did not affect the relaxant responses to acetylcholine in the SHR rings. These results show that endothelium-derived contracting factor is produced and released by acetylcholine stimulation not only in the aorta of SHR but also in that of WKY. The results also suggest that prostaglandin H2, a precursor of the released prostaglandins, is a strong candidate for endothelium-derived contracting factor produced by acetylcholine stimulation.

Animals↗
PubMed1990

[Inhalation therapy for bronchial asthma. A. Bronchodilator--beta 2-stimulant].

In the treatment of bronchial asthma, usefulness of beta 2-agonists aerosol inhalation are emphasized as well as sustained theophylline tablets recently. In this study, the effectiveness of procaterol metered dose inhalor on asthmatic patients were examined compared with procaterol tables. The effect of procaterol inhalor together with sustained-theophylline on Holter ECG were also examined. When procaterol was exchanged to inhalation from tablets, 41% of the patients were improved symptomatically. Procaterol inhalor had no effect on Holter ECG. Procaterol inhalation regularly was expected to be more useful in treating asthmatic patients than tablets.

Administration, Inhalation↗
PubMed1990

Interaction between terbutaline and ethyl 2-(4'-carboxybenzamido)-4-propionamidobenzoate sodium salt in tracheal smooth muscle relaxation of guinea pig.

Ethyl 2-(4-carboxybenzamido)-4-propionamidobenzoate sodium salt (AM-682) is a new, orally active, antiallergic compound which has been reported to inhibit the release of histamine and leukotrienes from mast cells more than disodium cromoglycate (DSCG) or Tranilast. In the present study, the interaction between terbulatine, a beta 2-receptor agonist, and AM-682 or met-A, AM-682's main metabolite in humans, in guinea pig tracheal smooth muscle was investigated by measuring the isometric tension in vitro. Combinations of terbutaline and AM-682 or met-A produced more than additive relaxant effects. Comparing the combined effects with the calculated algebraic sums of single drug effects, the differences were statistically significant for terbutaline 10(-9) mol/l and AM-682 3 X 10(-6) mol/l, 10(-5) mol/l and 3 X 10(-5) mol/l (p less than 0.01) or met-A 3 X 10(-6) mol/l, 10(-5) mol/l (p less than 0.05) on the spontaneous tone of tracheal smooth muscle, and for terbutaline 10(-9) mol/l and AM-682 10(-5) mol/l (p less than 0.01), 3 X 10(-5) mol/l (p less than 0.05) on the tension of tracheal smooth muscle induced by 5.4 X 10(-7) mol/l carbachol. Thus the tracheal smooth muscle relaxant effects of AM-682 and the beta 2-receptor agonist terbutaline were synergistic. It is suggested that the combination of AM-682 and a beta 2-receptor agonist, rather than administration of each drug separately, may provide the therapeutic advantage in the treatment of bronchial asthma.

Aminobenzoates↗
PubMed1990

Effects of phospholipase A2 on numbers of histamine H1 receptors in guinea pig lungs.

Effects of phospholipase A2 on numbers of histamine H1 receptors and muscarinic acetylcholine receptors were estimated in guinea pig lungs. Histamine H1 and muscarinic acetylcholine receptors in lung membranes were studied by the direct binding technique using 3H-pyrilamine and 3H-quinuclidinyl benzilate, respectively. The control group had two orders (high-affinity and low-affinity) of binding sites of histamine H1 receptors. Pretreatment of lung membranes with phospholipase A2 destroyed high-affinity binding sites, and these sites could not be detected after treatment. Low-affinity sites were not affected by the treatment. In contrast, the numbers of muscarinic acetylcholine receptors did not change significantly in spite of the addition of phospholipase A2. These results indicate that resistance of receptors against phospholipase A2 treatment varies among receptors and even between the binding sites in the same receptor. These variations might modulate pathological conditions associated with inflammation in which phospholipase is activated. Easy establishment of histamine tachyphylaxis might be explained by this mechanism.

Animals↗
PubMed1989

Changes in myocardial mitochondrial electron transport activity in rats administered with acetylcholinesterase inhibitor.

This study was designed to elucidate harmful effects of acetylcholine on myocardial mitochondrial electron transport activity. Rats were cervically dislocated 3 h and 6 h after oral administration of pyridostigmine, an acetylcholinesterase inhibitor. The myocardial mitochondrial electron-transport activity (NADH-cytochrome c reductase, succinate-cytochrome c reductase and cytochrome c oxidase), and myocardial acetylcholine and norepinephrine concentrations were measured. Activities of cytochrome c oxidase were significantly decreased in the pyridostigmine-3h and the pyridostigmine-6h groups compared with untreated rats. Activity of NADH-cytochrome c reductase was significantly decreased 6 h after administration. No significant changes were observed in those of succinate-cytochrome c reductase among all groups. Pyridostigmine increased significantly myocardial acetylcholine concentration, however, no significant changes of myocardial norepinephrine concentrations were observed among all groups. It is indicated that these mitochondrial injuries might be dependent on an increase in acetylcholine level and independent of norepinephrine.

Acetylcholine↗
PubMed1989

5-Hydroxytryptamine receptor subtypes participating in pulmonary edema in dogs.

The present study was undertaken to evaluate the effects of 5-hydroxytryptamine on pulmonary vascular resistances and vascular permeability with respect to the 5-hydroxytryptamine receptor subtypes. Left lower lobe of lungs isolated from the dog was perfused with constant heights of arterial and venous blood reservoirs and was maintained at zone III condition (pulmonary venous pressure greater than airway pressure). Drugs were administered into blood reservoir (1 l of total blood volume). Infusion of 5-hydroxytryptamine (100 micrograms/min) increased the pulmonary pre- and post-capillary resistances, but did not change the filtration coefficient. In the presence of ketanserin (10 mg), the infusion of 5-hydroxytryptamine caused an increase in filtration coefficient that was prevented by methysergide (30 mg). ICS 205-930 (10 mg) did not prevent such an increase in filtration coefficient. Infusion of 5-carboxamidotryptamine (100 micrograms/min) increased the filtration coefficient as well as both pre- and post-capillary resistances. These results suggested that the 5-HT1-like receptor mediates the increase in pulmonary vascular permeability.

Animals↗
PubMed1989

Increased Ca2+ influx into platelets induced by thromboxane A2 analog in patients with ischemic heart disease.

We compared platelet aggregation and intracellular free calcium concentrations [( Ca2+]i) following stimulation with STA2, an analog of thromboxane A2 between patients with ischemic heart disease (IHD) showing significant stenosis in coronary angiograms and controls. In the presence of extracellular calcium, platelet aggregation and intracellular Ca2+ increase were enhanced by STA2 stimulation in a dose-dependent fashion and were higher in the IHD patients than in the controls. However, in the absence of extracellular calcium, no difference in intracellular Ca2+ increase was observed due to its total dependence on release from intracellular stores. These results suggest that thromboxane A2 increases platelet intracellular Ca2+-inducing aggregation, and this increase and aggregation, which is enhanced by thromboxane A2 in IHD patients, is due to promotion of Ca2+ influx by thromboxane A2. IHD patients appear to have an abnormality in the platelet membrane which may explain such thromboxane A2-dependent increased permeability to Ca2+.

Adult↗
PubMed1989

Cardioprotective and antiarrhythmic effects of beta-blockers, propranolol, bisoprolol, and nipradilol in a canine model of regional ischemia.

Cardioprotective and antiarrhythmic effects of three beta-blockers with different pharmacological properties were investigated in 33 anesthetized dogs with a 2-h coronary occlusion. Dogs were divided into 4 groups and received physiological saline or one of the following drugs using a 10-min infusion at 25 min before the occlusion: saline or control (n = 12), propranolol (0.3 mg/kg, n = 7), bisoprolol (0.05 mg/kg, n = 7), and nipradilol (0.2 mg/kg, n = 7) groups. Blood pressure did not significantly differ among the 4 experimental groups throughout the entire observation period. On the contrary, the postocclusion change (fall) in heart rate from the preocclusion value was significantly (P less than 0.05-0.01) greater in the drug-treated groups than in the control group. Each of the beta-blockers effectively prevented the development of ventricular arrhythmias associated with the 2-h coronary occlusion. In terms of assessing a cardioprotective effect, the respiratory control index and rate of oxygen consumption in State III in mitochondria, and lysosomal enzyme activities (N-acetyl-beta-glucosaminidase or beta-glucuronidase) in myocardial tissues, all prepared from both ischemic and non-ischemic areas, were measured using the respective, established methods. The 2-h coronary occlusion induced a mitochondrial dysfunction and leakage of lysosomal enzymes in the control group, whereas each beta-blocker significantly (P less than 0.05-0.01) protected mitochondria against ischemia and prevented the lysosomal enzyme leakage. The results indicate that the antiarrhythmic effects of beta-blockers on ischemic myocardium are, at least in part, due to their cardioprotective action, and these effects appear to be unrelated to the ancillary pharmacological properties of these drugs.

Acetylglucosaminidase↗
PubMed1989

Forskolin inhibits the Gs-stimulated adenylate cyclase in rat ascites hepatoma AH66F cells.

Forskolin increased intracellular cyclic AMP and augmented cyclic AMP formation by prostaglandin E1 (PGE1) in normal rat hepatocytes and ascites hepatoma AH66 cells. However, in AH66F cells which were derived from the AH66 cell line, the diterpene only slightly increased the cyclic AMP level, and dose-dependently inhibited the accumulation caused by PGE1. Forskolin dose-dependently activated adenylate cyclase in these membranes, and the magnitude of activation by forskolin was largest in the following order: hepatocytes, AH66 cells, and AH66F cells. This difference may be based on the number of forskolin-binding sites. The binding affinity of forskolin for each cell membrane was similar. The number and affinity of forskolin-binding sites in these cells were not influenced by 5'-guanylylimidodiphosphate [Gpp(NH)p]. In hepatocytes and AH66 cells, forskolin and other adenylate cyclase activators such as PGE1, GTP, Gpp(NH)p, F-, and Mn2+ synergistically increased the enzyme activity. In AH66F cells, the forskolin-stimulated activity was hardly influenced by the GTP analog, and forskolin diminished the activities induced by the GTP analog in a manner similar to that of diterpene alone. Forskolin (10 microM) also significantly inhibited the activities induced by PGE1, GTP, and F-. The effect of forskolin with Mn2+ was additive in AH66F cells. The data suggest that forskolin promotes the interaction between the stimulatory guanine nucleotide-binding protein and the catalytic unit in the membrane of normal hepatocytes and AH66 cells, but it interferes with the coupling in AH66F cells.

Adenylyl Cyclases↗
PubMed1989

Effect of reperfusion on the cardiac acetylcholine and norepinephrine contents in rat hearts.

The effects of ischemia, reperfusion and hypoxia on the cardiac acetylcholine, choline, norepinephrine and cyclic AMP contents were investigated in isolated, spontaneously beating rat hearts perfused under constant pressure (100 cm H2O) with Krebs-Henseleit solution gassed with 95% O2-5% CO2. Acetylcholine, choline and norepinephrine were determined by high performance liquid chromatography with electrochemical detection. Cyclic AMP was determined by radioimmunoassay. One min reperfusion following 15 min ischemia (termination of perfusion) caused a significant decrease in both cardiac acetylcholine (P less than 0.05) and norepinephrine (P less than 0.01) contents, but had no significant effect on the cardiac norepinephrine/acetylcholine content ratio, or choline or cyclic AMP content. By contrast, 16 min ischemia did not significantly affect the cardiac acetylcholine, norepinephrine, choline or cyclic AMP content. Also, 16 min hypoxia (perfusion with Krebs Henseleit solution gassed with 95% N2 5% CO2) decreased the cardiac norepinephrine content significantly (P less than 0.01) and norepinephrine/acetylcholine content ratio slightly but not significantly. However, hypoxia had no significant effect on the cardiac acetylcholine, choline or cyclic AMP content. Pre-treatment with 10 microns atropine sulfate prevented the decrease in the cardiac acetylcholine content caused by reperfusion but caused a significant depletion in the cardiac norepinephrine content in the control (P less than 0.01) and ischemia (P less than 0.05) groups and a significant decrease in the norepinephrine/acetylcholine content ratio in all three groups (all, P less than 0.05). Extending the reperfusion period to 5 and 10 min following 15 min ischemia also caused a significant decrease in both cardiac acetylcholine and norepinephrine contents compared with the control groups. However, no significant difference in these contents was found between 1 min reperfusion group and 5 or 10 min reperfusion group. Twenty or 25 min ischemia alone did not significantly affect these contents. These findings suggest that reperfusion disturbs both the sympathetic and parasympathetic nervous systems in the heart and that pre-treatment with atropine adversely affects the balance of the autonomic nervous system.

Acetylcholine↗
PubMed1989

Disappearance and appearance of isoenzymes of creatine kinase, lactate dehydrogenase and aspartate aminotransferase in the myocardium undergoing infarction.

Recent investigations have shown that cardiac isoenzymes change with mechanical overload and possibly with myocardial ischaemia. This complicates the interpretation of serum enzyme changes in acute myocardial infarction. We have therefore investigated the rate of release of isoenzymes from necrosing myocardium and the effect of ischaemia per se. Discrete myocardial infarction was produced in 35 male Wistar rats by ligation of left coronary artery. Six (n = 7), 12 (n = 6), 24 (n = 9), 72 (n = 7) h and 3 weeks (n = 6) after surgery, total and isoenzyme activities of creatine kinase (CK), lactate dehydrogenase (LD) and aspartate aminotransferase (AST) were measured in the infarcted myocardium. Untreated rats (n = 12) were used as the control (time 0). Sham operation was performed in 36 rats. During the early period (0 to 12 or 24 h) of infarction, each (iso)enzyme disappeared monoexponentially from the myocardium (mean r = 0.88) with different disappearance rates. Cytosolic isoenzyme fractions decreased more rapidly than mitochondrial fractions. CK MB and the LD-H subunit decreased faster than CK MM and the LD-M subunit. Such differences in the disappearance rate may be related to subcellular localisation of each isoenzyme. In the late period (72 h and 3 weeks), CK BB and the LD-M subunit showed significant reaccumulation in the infarcted myocardium. Although inflammatory cells can be responsible for the reaccumulation of LD-M subunit, the origin of CK BB is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Biochemical and morphological changes in myocardium during coronary occlusion and reperfusion in canine hearts: effects of propranolol on myocardial damage.

To clarify the mechanism of irreversible myocardial damage, we studied the relationship between ischaemic mitochondrial dysfunction and leakage of lysosomal enzymes, and the effects of propranolol on myocardial damage. Open chest anaesthetised dogs were divided into six groups: 30 min occlusion of the left anterior coronary artery (LAD); 2 h LAD occlusion; 2 h LAD occlusion after premedication with 0.3 mg.kg-1 propranolol; 30 min LAD occlusion/l h reperfusion; 2 h LAD occlusion/l h reperfusion; and 2 h LAD occlusion/l h reperfusion after propranolol premedication. After occlusion or reperfusion, heart mitochondria were prepared from normal and occluded or reperfused areas, and mitochondrial function (rate of oxygen consumption in State III, and respiratory control index) was measured polarographically. Myocardial tissue was fractionated and activities of lysosomal enzymes (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were measured. Electron microscopic studies were performed. Thirty min occlusion induced mitochondrial dysfunction without leakage of lysosomal enzymes. Reperfusion for 1 h reversed these changes. However occlusion for 2 h induced mitochondrial dysfunction associated with the leakage of lysosomal enzymes, and mitochondrial dysfunction was not reversed by 1 h reperfusion. Propranolol reduced mitochondrial dysfunction after 2 h occlusion and prevented leakage of lysosomal enzymes. Mitochondrial function was fairly well maintained after 1 h reperfusion in dogs premedicated with propranolol. Structural changes in mitochondria were observed in the 2 h occlusion/l h reperfusion group, and were reduced by premedication with propranolol. These results suggest that irreversible injury of ischaemic mitochondria is closely linked with instability of lysosomal membranes, and that propranolol prevented irreversible myocardial mitochondrial dysfunction.

Animals↗
PubMed1989

Effect of colforsin on human neutrophil superoxide production and intracellular calcium mobilization.

1. The effects of dibutyryl cyclic AMP (cAMP), isoproterenol and colforsin (forskolin) were evaluated on respiratory burst in human polymorphonuclear neutrophils (PMN). 2. Dibutyryl cAMP showed a dose-dependent inhibition of n-formyl-methionyl-leucyl-phenylalanine (FMLP)-induced superoxide production by human PMN. 3. Administration of isoproterenol induced a dose-dependent inhibition of FMLP-induced superoxide production by human PMN, and the inhibition was blocked by propranolol. 4. Administration of colforsin induced a dose-dependent inhibition of FMLP-induced superoxide production by human PMN, and the inhibition could not be blocked by propranolol. 5. Incubation with colforsin caused a significant increase in the cAMP level in human PMN. 6. Pretreatment with colforsin caused a dose-dependent inhibition in the elevation of intracellular free calcium (monitored by fura-2 fluorescence), which was observed in human PMN stimulated with FMLP. 7. These results suggest that cAMP is an inhibitory factor of superoxide production and intracellular calcium mobilization in human PMN stimulated with FMLP.

Adult↗
PubMed1989

Mechanism of xanthine-induced relaxation of guinea-pig isolated trachealis muscle.

1. Four 3-alkylxanthines (3-methylxanthine, 3-n-propylxanthine (enprofylline), 3-n-butylxanthine and 3-iso-butylxanthine) and four 1-methyl-3-alkylxanthines (1-methyl-3-methylxanthine (theophylline), 1-methyl-3-n-propylxanthine, 1-methyl-3-n-butylxanthine and 1-methyl-3-iso-butylxanthine (IBMX], were compared in terms of cyclic AMP phosphodiesterase (PDE) inhibition and trachealis muscle relaxation. The relationship between xanthine structure and cyclic AMP PDE inhibition was also studied. 2. Xanthine induced relaxation of guinea-pig isolated trachealis muscle was measured against spontaneous tone. 3. The four 1-methyl-3-alkylxanthines were each significantly more potent than the corresponding 3-alkylxanthines in relaxing the isolated trachealis muscle. The 1-methyl-3-alkylxanthines were similarly more potent than the corresponding 3-alkyl derivatives in inhibiting low Km cyclic AMP PDE. There was a strong positive correlation between low Km cyclic AMP PDE inhibition and the tracheal smooth muscle relaxation evoked by the xanthine derivatives. 4. Since methylation of the 1-position of each 3-alkylxanthine increased the potency of the derivative in inhibiting low Km cyclic AMP PDE and in relaxing trachealis muscle and since a strong positive correlation was observed between the relaxant EC50 and the Ki value of each xanthine derivative, it is suggested that low Km cyclic AMP PDE inhibition by xanthines plays an important role in their tracheal relaxant effect.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1989

Capsaicin-sensitive nerves exert an inhibitory effect on the development of fibrin-induced pulmonary edema in rats.

This study was undertaken to evaluate the role of vagal nerves in the development of neurogenic pulmonary edema. We injected fibrinogen and thrombin into the cisterna magna of rats, a model of neurogenic pulmonary edema. When the vagal nerves were left intact, pulmonary edema occurred (fibrin-induced pulmonary edema) at a rate of 33%. Vagotomy at the midcervical portion increased the incidence of pulmonary edema to a rate of 100%, whereas pretreatment with atropine did not affect the incidence. These results suggested that vagal afferent nerves or nonadrenergic-noncholinergic efferent nerves played an important role in inhibiting the development of fibrin-induced pulmonary edema. Furthermore, in vagotomized and vagal nerve-intact rats pretreated with capsaicin, the incidence of pulmonary edema was 100%. Pretreatment with a substance P antagonist, [D-Pro2, D-Trp7,9]-SP, also increased the incidence to 100% in the vagal nerve-intact rats. On the other hand, intravenous administration of some neuropeptides that may be released from the capsaicin-sensitive nerves (e.g., substance P or calcitonin gene-related peptide) inhibited the development of pulmonary edema in vagotomized rats. We concluded that the vagal capsaicin-sensitive nerves exerted an inhibitory effect on the development of fibrin-induced pulmonary edema.

Animals↗
PubMed1989

Central nervous system-mediated glucagon secretion is enhanced by alpha 2-adrenoreceptor activation.

We assessed the response of the adrenergic receptor in pancreatic glucagon secretion to central nervous system stimulation. Injection of neostigmine (5 x 10(-8) mol) into the third cerebral ventricle in intact rats resulted in increased epinephrine and norepinephrine secretion associated with glucagon secretion. This glucagon secretion was still observed in bilateral adrenalectomized (ADX) rats, although its concentration was significantly lower than that in the intact rats. This glucagon rise was significantly inhibited by ip treatment of ganglionic blocker with hexamethonium. Intraperitoneal injection of alpha-adrenergic receptor antagonist phentolamine (5 x 10(-7) mol), but not of beta-adrenergic receptor antagonist propranolol (1 x 10(-6) mol), reduced the hyperglucagonemic effect of a subsequent neostigmine injection in intact and ADX rats, although these antagonists did not influence epinephrine or norepinephrine secretion in intact rats. In addition, ip injection of the selective alpha 2-receptor antagonist yohimbine (5 x 10(-7) mol), but not of the selective alpha 1-receptor antagonist prazosin (1 x 10(-6) mol), inhibited the neostigmine-induced glucagon secretion in intact and ADX rats. From this evidence it is suggested that central nervous system-mediated glucagon release is enhanced by alpha 2-adrenoreceptor stimulation by either catecholamines or the autonomic nervous system.

Adrenalectomy↗
PubMed1989

Stimulatory and inhibitory effects of forskolin on adenylate cyclase in rat normal hepatocytes and hepatoma cells.

Forskolin synergistically potentiated adenosine 3',5'-cyclic monophosphate formation by prostaglandin E1 (PGE1) in rat normal hepatocytes freshly prepared by collagenase digestion and rat ascites hepatoma AH66 cells, but dose-dependently inhibited the accumulation by PGE1 in AH66F cells. Forskolin activated adenylate cyclase in a dose-dependent manner in homogenates of all cell lines. In normal hepatocytes and AH66 cells, simultaneous addition of forskolin and other adenylate cyclase activators [isoproterenol (IPN), PGE1, guanosine 5'-triphosphate sodium salt (GTP), 5'-guanylylimidodiphosphate sodium salt (Gpp (NH)p), NaF, cholera toxin, islet activating protein and MnCl2] gave greater than additive responses. On the other hand, in AH66F cells, the effect of forskolin on adenylate cyclase was hardly influenced by GTP, but forskolin diminished the activities induced by high concentrations of GTP to that by the diterpene alone. Forskolin also significantly inhibited the PGE1-stimulated and the guanine nucleotide binding regulatory protein-stimulated activities. Because AH66F cells were insensitive to IPN, the combination with forskolin and IPN gave similar activity to that obtained with the diterpene alone. The effect of forskolin on the activation by manganese ion was neither synergistic nor inhibitory but was additive in AH66F cells. These results suggest that forskolin promotes the interaction between the stimulatory guanine nucleotide binding regulatory protein and the catalytic unit in normal hepatocytes and AH66 cells, but in AH66F cells forskolin interferes with the coupling of the two components of adenylate cyclase.

Adenylate Cyclase Toxin↗