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Biomedical subjects

K Sumikawa

Publications and source records attributed to K Sumikawa.

At least 145 records · Page 8Linked to original sources
PubMed1988

Synergistic interaction of alpha 1- and beta-adrenoceptor agonists on induction arrhythmias during halothane anesthesia in dogs.

The authors investigated the role of alpha 1- and beta-adrenoceptors on the induction of arrhythmias during halothane anesthesia in the dog. The arrhythmogenic doses (ADs) of various combinations of alpha 1- and beta-adrenoceptor agonists were determined in dogs (N = 105) during halothane anesthesia. Isoproterenol (ISP) and phenylephrine (PHE) administered separately failed to induce arrhythmias in doses up to 4 micrograms/kg and 200 micrograms/kg, respectively. The interaction between ISP and PHE in inducing arrhythmias showed typical hyperbolic isoboles. At a systolic pressure of 140 mmHg, the AD of ISP in the presence of PHE was significantly lower than that in the presence of angiotensin II (ANG II). At a systolic pressure of 150, 160, 170, or 180 mmHg, there was no significant difference between the AD of ISP in the presence of PHE and that in the presence of ANG II. Increasing heart rate by electrical pacing did not replace ISP in the arrhythmogenic interaction between ISP and PHE. The results indicate that both alpha 1- and beta-adrenoceptor agonists are important for producing arrhythmias during halothane anesthesia, and that these agonists synergistically interact on the heart by different mechanisms.

Adrenergic alpha-Agonists↗
PubMed1988

Quantitative analysis of the contribution of hepatic, renal and portal circulation to the clearance of exogenous catecholamines.

The contribution of hepatic, renal and portal circulation to the clearance of exogenous catecholamines was analyzed quantitatively. During infusion of clinical doses of norepinephrine, epinephrine and dopamine in dogs, the plasma level of catecholamine and the plasma flow were measured simultaneously. Percentage of contribution was calculated from the following equation; transorgan difference of plasma catecholamine (ng/ml) x plasma flow (ml/min) x 100/dose (ng/min). This value means the percentage of the amount of catecholamine cleared by an organ to the amount of catecholamine administered into the body. Significant transorgan gradients of plasma levels of norepinephrine, epinephrine and dopamine were observed in each of hepatic, renal and portal circulation. The calculated contribution values indicate that hepatic circulation clears 15.9% of norepinephrine, 24.2% of epinephrine and 9.0% of dopamine administered exogenously. The corresponding figures for renal circulation are 8.7, 22.0 and 9%, and those for portal circulation are 11.5, 21.5 and 10.4%.

Animals↗
PubMed1987

Hydrolysis of phosphatidate by human placental alkaline phosphatase.

Highly purified alkaline phosphatase of human placenta catalyzed the hydrolysis of phosphatidate with quantitative formation of almost stoichiometric amounts of diglyceride and inorganic phosphate. In the presence of sodium deoxycholate, the activity was maximal at pH 8.8. The activity was strongly inhibited by L-phenylalanine but scarcely affected by NaF. These results show that alkaline phosphatase hydrolyzes phosphatidate under different conditions from those for activity of phosphatidate phosphohydrolase.

Alkaline Phosphatase↗
PubMed1987

Activation of a common effector system by different brain neurotransmitter receptors in Xenopus oocytes.

Xenopus oocytes possess 'native' muscarinic receptors, which give rise to oscillatory chloride currents; similar responses are elicited by activation of foreign receptors to serotonin, glutamate and noradrenaline, expressed in oocytes after injection of messenger RNA from rat brain. When low concentrations of two agonists are applied together, the combined response is greater than would be expected from the sum of the responses to each agonist applied alone. Potentiation of acetylcholine by serotonin is blocked by the serotonin antagonist methysergide; conversely, the potentiation of serotonin by acetylcholine is blocked by the muscarinic antagonist atropine. This indicates that each agonist acts on a distinct receptor. The interactions between serotonin, acetylcholine and other agonists provide further evidence that the different receptors may all 'link in' to a common receptor-channel coupling system, in which phosphoinositide metabolism and calcium liberation lead to the opening of chloride channels in the oocyte membrane.

Acetylcholine↗
PubMed1987

A novel alkaline phosphatase isozyme in human adipose tissue.

A novel alkaline phosphatase (AP) isozyme was found in human adipose tissue. Adipose tissue alkaline phosphatase differed in enzymatic properties from liver, placental and intestinal alkaline phosphatases. On electrophoresis it showed the same mobility as intestinal alkaline phosphatase, but after treatment with neuraminidase its mobility was decreased to the same as or slightly less than that of neuraminidase-treated liver alkaline phosphatase. Its inhibition by amino acids, inactivation by urea and activation by Mg2+ were almost the same to those of liver alkaline phosphatase. However, at 56 and 65 degrees C it was more stable than liver alkaline phosphatase. Alkaline phosphatase activity was demonstrated histochemically in adipose tissue with naphthol AS-MX phosphate as substrate. It was localized in the wall of blood capillaries, but not present in adipocytes.

Adipose Tissue↗
PubMed1987

Oscillatory chloride current evoked by temperature jumps during muscarinic and serotonergic activation in Xenopus oocyte.

1. Membrane currents were recorded from voltage-clamped oocytes of Xenopus laevis, during temperature jumps imposed by a heating light. Resting oocytes usually showed little response, but large oscillatory membrane currents developed in response to cooling steps applied during activation of 'native' muscarinic receptors. 2. Similar temperature jump (Tjump) currents were seen during activation of oscillatory chloride currents mediated by muscarinic acetylcholine (ACh), serotonin, glutamate and noradrenaline receptors, expressed in the oocyte following injection with messenger ribonucleic acid (mRNA) from rat brain. The Tjump response during muscarinic activation was selectively blocked by atropine, and that during serotonergic activation by methysergide. In contrast, the 'smooth' membrane currents elicited by nicotinic ACh, kainate and gamma-aminobutyric acid (GABA) were not accompanied by Tjump responses. 3. Rapid cooling of the oocyte gave larger Tjump currents than a gradual cooling over a few seconds. The size of the Tjump current elicited by a fixed cooling step increased linearly with the preceding time of warming, becoming maximal at intervals greater than about 100 s. 4. The Tjump current was inward at a clamp potential of -60 mV and reversed direction at about -22 mV, which corresponds to the chloride equilibrium potential in the oocyte. In low-chloride solution the reversal potential was shifted to more positive potentials, but it was almost unchanged by changes in potassium and sodium concentration. The size of the Tjump current decreased as the membrane potential was made more negative than about -40 mV. 5. The period of oscillation of the Tjump current increased with decreasing temperature, following a Q10 of 3.15. Depolarization also caused a small increase in period. 6. The Tjump current was not abolished in calcium-free solution, or by addition of manganese or lanthanum to the bathing solution. However, it was abolished by intracellular injection of the calcium-chelating agent EGTA. 7. Intracellular injection of inositol 1,4,5-trisphosphate evoked an oscillatory membrane current, during which Tjump responses developed similar to those after muscarinic activation. Intracellular injection of calcium evoked a chloride current, but this was not accompanied by Tjump responses. 8. We conclude that the oscillatory currents evoked by temperature jumps arise from chloride channels activated by intracellular calcium. This calcium is probably mobilized from intracellular stores by inositol trisphosphate which is liberated as a result of activation of muscarinic receptors, and also receptors for serotonin and glutamate.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1987

Calorigenic action of circulating epinephrine during pentobarbital, halothane and morphine anesthesia in dogs.

The calorigenic action of circulating epinephrine was analyzed quantitatively in the dog during pentobarbital, halothane and morphine anesthesia. The whole body oxygen consumption (VO2) was measured by an on-line analysis of breath-by-breath respiratory gas exchange. Epinephrine was infused at various doses and the plasma concentrations of epinephrine were measured by semiautomated fluorimetric analysis. During pentobarbital anesthesia, the basal VO2 was 5.26 ml/kg/min and was increased by epinephrine in a dose dependent manner at plasma concentrations between 3.9 ng/ml (VO2 = 5.68 ml/kg/min) and 36.5 ng/ml (VO2 = 6.47 ml/kg/min). Epinephrine exerted a similar effect during halothane anesthesia, but it failed to affect VO2 during morphine anesthesia. Morphine also inhibited dibutyryl cyclic AMP-induced increase in VO2, suggesting that morphine inhibits the calorigenic action of epinephrine at the intracellular site distal to beta-receptors.

Anesthesia↗
PubMed1987

Selective inhibition by dantrolene of caffeine-induced catecholamine release from perfused dog adrenals.

Effects of dantrolene sodium on catecholamine (CA) release from the perfused dog adrenal medulla was investigated in relation to it's therapeutic action on malignant hyperthermia (MH), in which CAs would play a significant pathophysiological role. Acetylcholine (ACh)-induced CA release was not affected, whereas caffeine-induced CA release was inhibited by dantrolene in a dose-dependent manner (84% inhibition at 10 microM). Dantrolene had no effect on the CA release induced by lasalocid or Na+ deprivation. On the other hand halothane inhibited ACh-induced CA release markedly, Na+ deprivation-induced CA release slightly, but not caffeine-induced CA release at all. The results indicate that dantrolene selectively inhibit caffeine-induced CA release, and that the therapeutic action of dantrolene on MH would be, at least in part, due to inhibition of abnormal release of Ca2+ in the adrenal medullary cells.

Adrenal Glands↗
PubMed1986

Neurotensin and substance P receptors expressed in Xenopus oocytes by messenger RNA from rat brain.

Xenopus oocytes were induced to acquire sensitivity to neurotensin and substance P, by injecting them with a fraction of poly(A)+ mRNA from rat brain. Non-injected oocytes, and oocytes injected with other brain mRNAs, failed to show responses, suggesting that receptors to these peptides were expressed by specific brain mRNAs. Responses to substance P and neurotensin comprised an oscillatory chloride current, and a smooth current having different ionic basis. These currents resembled those seen during activation of muscarinic and serotonergic receptors, but were not blocked by the corresponding antagonists atropine and methysergide. The responses to substance P, and to a lesser extent to neurotensin, showed a long-lasting desensitization. Similarities between the oscillatory currents evoked by the peptides acetylcholine and serotonin suggest that all these receptors may 'link in' to a common intracellular messenger pathway.

Animals↗
PubMed1986

Ketamine inhibits 45Ca influx and catecholamine secretion by inhibiting 22Na influx in cultured bovine adrenal medullary cells.

The effects of ketamine, an intravenous anesthetic, on 22Na influx, 45Ca influx and catecholamine secretion were investigated in cultured bovine adrenal medullary cells. Ketamine inhibited carbachol-induced 45Ca influx and catecholamine secretion in a concentration-dependent manner with a similar potency (IC50 40 microM). Ketamine also reduced veratridine-induced 45Ca influx and catecholamine secretion (IC50 260 microM) but did not affect high K-induced 45Ca influx and catecholamine secretion. The influx of 22Na caused by carbachol or by veratridine was suppressed by ketamine with a concentration-inhibition curve similar to that of 45Ca influx and catecholamine secretion. Inhibition by ketamine of the carbachol-induced influx of 22Na, 45Ca and secretion of catecholamines was not reversed by the increased concentrations of carbachol. These observations indicate that ketamine, at clinical concentrations, can inhibit nicotinic receptor-associated ionic channels and that the inhibition of Na influx via the receptor-associated ionic channels is responsible for the inhibition of carbachol-induced Ca influx and catecholamine secretion. At higher concentrations, the anesthetic also inhibits voltage-dependent Na channels but has no effect on voltage-dependent Ca channels.

Adrenal Medulla↗
PubMed1986

Mechanism of the inhibitory effect of thiopentone on stimulus-secretion coupling in chromaffin cells.

This study was undertaken to clarify the mechanism of action of thiopentone on stimulus-secretion coupling in cholinergic postsynaptic cells using cultured bovine adrenal chromaffin cells. Thiopentone (20-100 microns) inhibited carbachol-induced Ca2+ uptake into, and catecholamine release from the cells in a concentration-dependent manner. The inhibition of catecholamine release was almost parallel to the inhibition of Ca2+ uptake. The inhibitory effect of thiopentone was not overcome by an increase in the concentration of carbachol, whereas that of alcuronium was. Contrary to the inhibition by diltiazem, which was reversed by increasing the Ca2+ concentration, the inhibition by thiopentone was not overcome by a high Ca2+ concentration. Compared with the inhibition of carbachol-induced catecholamine release, a higher concentration of thiopentone was required to inhibit high K+ (56 mM KCl)-induced catecholamine release (200 microns thiopentone exhibited 32% inhibition). The results suggest that thiopentone blocks the stimulus-secretion coupling in the chromaffin cells as a result of inhibiting Ca2+ uptake through nicotinic receptor-linked channels. The linkage between receptor stimulation and Ca2+ channel activation seems to be the process most susceptible to inhibition by the barbiturate.

Animals↗
PubMed1986

Quantitative analysis of the contribution of pulmonary and hind limb circulation to the clearance of exogenous catecholamines.

The contribution of pulmonary and hind limb circulation to the clearance of exogenous catecholamines was analyzed quantitatively. During infusion of clinical doses of norepinephrine, epinephrine and dopamine in dogs, the plasma level of catecholamine and the plasma flow were measured simultaneously. Percentage of contribution was calculated from the following equation; transorgan difference of plasma catecholamine (nanograms per milliliter) X plasma flow (milliliters per minute) X 100/dose (nanograms per minute). This value means the percentage of the amount of catecholamine cleared by an organ to the amount of catecholamine administered into the body. Small but significant transpulmonary gradients of plasma levels of norepinephrine, epinephrine and dopamine and large translimb gradients of plasma levels of these catecholamines were observed. The plasma flow of pulmonary circulation was increased by infusion of epinephrine and dopamine, whereas it remained unchanged by infusion of norepinephrine. The plasma flow of hind limb circulation showed no significant change by infusion of catecholamines. The calculated contribution values indicate that pulmonary circulation clears 35.7% of norepinephrine (at 0.2 ng X kg-1 X min-1), 27.1% of epinephrine (0.2 ng X kg-1 X min-1) and 21.5% of dopamine (10 micrograms X kg-1 X min-1) administered exogenously, and that the corresponding figures for hind limb circulation are 8.2, 7.8 and 4.5%.

Animals↗
PubMed1985

Messenger RNA from bovine retina induces kainate and glycine receptors in Xenopus oocytes.

The retina contains several types of nerve cells that communicate through chemical synapses. The transmitter and receptor molecules that mediate signal transmission across these synapses need further characterization. For this purpose, poly (A)+ mRNA was isolated from bovine retinas and injected into Xenopus laevis oocytes. Translation of the foreign mRNA induced the oocyte membrane to acquire functional receptors to kainate and, to a lesser extent, also receptors to glycine, gamma-aminobutryic acid (GABA), aspartate and glutamate. Thus, the cells in the retina must contain different messengers coding for these neurotransmitter receptors. Activation of the kainate receptors opens membrane channels, generating an ionic current which has an equilibrium potential close to 0 mv. The current is well maintained during prolonged application of kainate, and hence these receptors may be involved in the neurotoxic effects produced by kainate in the retina.

Animals↗
PubMed1985

Mechanism of the effect of droperidol to induce catecholamine efflux from the adrenal medulla.

The study was undertaken to determine whether droperidol had an effect to induce catecholamine efflux from the adrenal medulla as a mechanism for the possible pressor effect of droperidol in patients with pheochromocytoma and, if so, to ascertain the site of action of this compound. The efflux of catecholamines from perfused dog adrenals was increased from control level, 0.15 micrograms/min, to 0.66 micrograms/min by the administration of droperidol 6.6 microM. This effect of droperidol was not dependent on extracellular Ca++, in contrast to acetylcholine. The concomitant secretion of catecholamines and dopamine-beta-hydroxylase was observed in response to acetylcholine and caffeine. However, droperidol-, histamine-, and reserpine-induced catecholamine efflux was not accompanied by dopamine-beta-hydroxylase release. In additional studies, chromaffin granules were isolated with a Millipore filter technique from the bovine adrenal medulla and were incubated for 10 min in an isotonic medium to examine the direct effects of droperidol. Droperidol did not enhance the efflux of catecholamines from the granules in contrast to histamine. The uptake of 14C-norepinephrine into the granules was inhibited by droperidol in a manner comparable to reserpine. The results suggest that droperidol induces catecholamine efflux from adrenal medullary cells and the efflux probably is caused by a nonexocytotic mechanism. A contributing mechanism was an inhibition of catecholamine uptake into chromaffin granules, resulting in an increased diffusion of catecholamines out of the cell.

Acetylcholine↗
PubMed1984

Messenger RNA from rat brain induces noradrenaline and dopamine receptors in Xenopus oocytes.

Xenopus oocytes were induced to acquire sensitivity to noradrenaline and dopamine, by injecting them with poly(A)+ mRNA isolated from rat brain. In mRNA-injected oocytes, both neurotransmitters elicited a smooth inward membrane current on which was superimposed an oscillatory inward current, which was carried mainly by chloride ions. This contrasts with the native responses that are sometimes seen in non-injected oocytes, where noradrenaline and dopamine both elicit smooth outward currents that are carried mainly by potassium ions. The serotonin antagonist methysergide blocked the induced responses to both noradrenaline and dopamine, and the noradrenaline response was blocked by propranolol.

Animals↗
PubMed1984

Separate fractions of mRNA from Torpedo electric organ induce chloride channels and acetylcholine receptors in Xenopus oocytes.

Poly(A)+ mRNA extracted from the electric organ of Torpedo was fractionated by sucrose density gradient centrifugation. After injection into Xenopus oocytes one mRNA fraction induced the appearance of chloride channels in the oocyte membrane. Many of these channels were normally open, and the ensuing chloride current kept the resting potential of injected oocytes close to the chloride equilibrium potential. When the membrane was hyperpolarized, the chloride current was reduced. A separate fraction of mRNA induced the incorporation of acetylcholine receptors into the oocyte membrane. When translated in a cell-free system this fraction directed the synthesis of the alpha, beta, gamma, and delta subunits of the acetylcholine receptor. In contrast, the mRNA fraction that induced the chloride channels caused the synthesis of the delta subunit, a very small amount of alpha, and no detectable beta or gamma subunits. This suggests that the size of the mRNA coding for the chloride channel is similar to the preponderant species of mRNA coding for the delta subunit of the acetylcholine receptor.

Animals↗