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Biomedical subjects

K Suga

Publications and source records attributed to K Suga.

At least 235 records · Page 13Linked to original sources
PubMed1986

Phosphorylation of phosphoinositides in human platelets.

32P-labelling of phosphatidylinositol (PI), PI-4-monophosphate (PIP), PI-4,5-bisphosphate (PIP2) and phosphatidic acid (PA) in 32P-labelled intact human platelets was investigated in the presence of various agents which alter intracellular level of cAMP or Ca2+. Addition of dibutyryl cAMP to intact platelets pre- or pulse labelled with 32P resulted in increased 32P-labelling of PIP and in concomitant decreased 32P-labelling of PI without affecting that of PIP2 or PA. Similar changes were observed in intact platelets treated by prostaglandin I2 (PGI2) or a new low Km phosphodiesterase inhibitor (DN-9693). When intracellular Ca2+ was chelated by loading quin 2-AM to intact platelets, 32P-labelling of PIP was significantly increased in a dose related manner. From these observations it was concluded that PI kinase is activated by elevation of cAMP or chelation of Ca2+ in intact platelets.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1986

Inhibitory roles of the hypothalamic atrial natriuretic polypeptide on the vasopressin release in the sodium-loaded rats.

Implication of the brain atrial natriuretic polypeptide on the vasopressin release was investigated using rats fed with a high-sodium containing diet. Sodium loading increased not only the blood pressure but also the urinary output of vasopressin significantly. The plasma vasopressin concentration increased about 10 times after the intracerebroventricular injections of angiotensin II. Thereby, magnitude of the response was significantly smaller in the rat fed with a high sodium diet than in rats with the regular-diet. The hypothalamic content of both vasopressin and atrial natriuretic polypeptide was significantly larger in the high-salt group than the regular-salt. The intraventricular injections of atrial natriuretic polypeptide abolished the vasopressin release induced by the intraventricular injections of angiotensin II. These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment.

Angiotensin II↗
PubMed1986

Augmented vasodepressor and sympathetic responses to intracerebroventricular injections of diltiazem, a calcium channel blocker, in DOCA-salt hypertensive rats.

The role of the calcium ion in central cardiovascular regulation was investigated by injecting a calcium channel blocker, diltiazem, intracerebroventricularly (i.c.v.) in urethane-anaesthetized, DOCA-salt hypertensive rats. This produced a fall in blood pressure and bradycardia with corresponding decreases in abdominal sympathetic nerve activity. However, a similar amount of diltiazem injected intravenously (i.v.) did not affect abdominal sympathetic nerve activity despite an accompanying vasodepression. The responses to i.v. injections of diltiazem were not different between the two groups; however, the magnitude of the blood pressure fall, bradycardia and sympathetic inhibition with i.c.v. injections was greater in the DOCA rats than in the sham-operated animals. These results suggest that diltiazem causes the central nervous system to decrease the sympathetic nerve outflow. The augmented central vasodepressor responses to diltiazem in DOCA-salt hypertensive rats may indicate that calcium metabolism in the central nervous system is disrupted and that this is of importance in the pathogenesis of DOCA-salt hypertension in rats.

Animals↗
PubMed1986

Evidence for a digitalis-like substance in the hypothalamo-pituitary axis in rats.

The origin of an endogenous digitalis-like substance in rats was investigated. The tissue content of the substance measured by radio-immunoassay was highest in the pituitary gland, with a decreasing gradient through the hypothalamus, forebrain, cerebellum, brain stem, heart, liver and kidney. Sodium loading decreased the content in the hypothalamus and increased the urinary excretion of the substance. The urinary output of the substance decreased after electrical lesions of the anteroventral third ventricle in the brain. The content increased in the hypothalamus and decreased in the plasma when the axonal flow of neurosecretion was interrupted with intracerebroventricular injections of colchicine. These results suggest that the digitalis-like substance could be produced in the hypothalamus and secreted from the pituitary gland like vasopressin, and that sodium loading increases the turnover of the substance in the hypothalamus.

Animals↗
PubMed1985

Hydrolysis of polyphosphoinositides in human platelets.

Phospholipase C was purified 110 fold from human platelets. The activity of the enzyme was totally dependent upon Ca2+. The activity of the enzyme was markedly enhanced in the presence of arachidonic acid and was strongly inhibited by aminoglycoside antibiotics. The enzyme hydrolyzed endogenous polyphosphoinositides in addition to PI in Ca2+ dependent manner, suggesting the involvement of this enzyme in stimulus-linked rapid hydrolysis of polyphosphoinositides in platelets. The stimulation by thrombin of 32P-labelled human platelets induced about 30% decrease in 32P-TPI and about 220% increase in 32P-PA at the first 10 sec. The degree of hydrolysis of TPI was dependent upon the amount of agonist and it was not affected by the extracellular concentration of Ca2+. The changes in 32P-phospholipids in thrombin-stimulated platelets in the absence of Ca2+ were inhibited in a dose dependent manner by preincubation with relatively higher amount of quin 2 AM. The inhibition was completely overcome by an addition of CaCl2 to the suspending buffer. By such treatment in the absence of extracellular Ca2+, the intracellular Ca2+ concentration was significantly lowered below the basal level (less than 100 nM). Those observations suggest that TPI breakdown in thrombin-stimulated platelets is primary mediated by the agonist receptor coupling and requires at least the basal level of intracellular Ca2+.

Aminoquinolines↗
PubMed1985

Ca2+ requirement in hydrolysis of phosphatidylinositol-4,5-bisphosphate in human platelets.

The activity of partially purified phospholipase C from human platelets was totally dependent on Ca2+, and approximately 800 microM Ca2+ was required for half-maximal activity. The enzyme hydrolyzed endogenous substrates in the order DPI greater than TPI greater than PI in a Ca2+-dependent manner. Hydrolysis of TPI in thrombin-stimulated platelets was dependent on the amount of the agonist, and it was not affected by the presence or absence of extracellular Ca2+. Hydrolysis was inhibited by preincubation with Quin-2AM in the absence of extracellular Ca2+. The intracellular Ca2+ concentration was significantly lowered below the basal level by such treatment. These observations suggested that TPI breakdown in thrombin-stimulated platelets is mediated by agonist-receptor coupling and requires at least the basal level of intracellular Ca2+.

Blood Platelets↗
PubMed1984

Cellular immune response to infection with respiratory syncytial virus and influence of breast-feeding on the response.

Virus-specific lymphocyte transformation (LTF) activity in vitro was examined in 78 infants with various forms of illness due to respiratory syncytial virus (RSV) infection. In 73 subjects with lower respiratory tract disease, significant LTF activity was often detected within one week after onset of initial symptoms, and responses characteristic for each clinical form were observed in the subsequent rise. Thus, mean activity in subjects with tracheobronchitis increased gradually, with the maximum response being detected at the fourth week after the onset of illness. In subjects with pneumonia the response was rather low during the first week of illness, and then a sharp increase of activity was observed at the second week. Although patients with bronchiolitis elicited similar levels of the activity until the first week, the response was significantly suppressed during the subsequent two weeks. The response at the second week in this group was significantly lower than those of corresponding specimens obtained from patients with pneumonia (p less than 0.01) or tracheobronchitis (p less than 0.05), suggesting a close association of the responsiveness with underlying mechanisms of bronchiolitis induced by RSV. The present study further indicated a possibility that breast-feeding of RSV-infected infants may alter levels of the LTF activity in these subjects.

Adult↗
PubMed1984

Quantitation of apolipoprotein A-I in pooled human serum by single radial immunodiffusion and sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

Apolipoprotein A-I was released from human HDL particles by treatment with 8 M urea, and the free apolipoprotein exhibited identical antigenicity and the same low mobility as purified apolipoprotein A-I in electrophoresis. Treatment of serum with 8 M urea enabled enabled quantitation of apolipoprotein A-I by single radial immunodiffusion assay, as judged by comparison with sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

Apolipoprotein A-I↗
PubMed1984

[Intracarotid arterial infusion with CDDP in combination with angiotensin II].

Intracarotid CDDP infusion in combination with angiotensin II was performed in two patients with metastatic brain tumor, lung carcinoma (LC) and ovarian carcinoma (OC). The patient with OC received 40 mg/m2 CDDP while the other patient with LC was administered intra-arterially with 50 mg/m2 CDDP, 30 mg/m2 ADM and 2.5 mg/m2 MMC. 50% or greater reduction in the size of metastatic lesions was observed in both patients in whom no neurological toxicities developed. Intra-arterial infusion of CDDP either alone or in combination with ADM or MMC seems to present an aggressive approach in dealing with other metastatic neoplasms without increasing toxicity, especially if intra-arterial angiotensin II is infused concomitantly.

Adenocarcinoma, Papillary↗