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Biomedical subjects

J Yamanishi

Publications and source records attributed to J Yamanishi.

At least 19 recordsLinked to original sources
PubMed1991

Calcium supplementation in salt-dependent hypertension.

To clarify the mechanism of the antihypertensive effect of oral Ca loading, we studied the effect of Ca supplementation on salt-induced blood pressure elevations in patients with essential hypertension and DOCA-salt hypertensive rats. When the diet was changed from low to high salt (300 mEq/day), the percent increase in mean blood pressure was smaller (p less than 0.01) in the Ca-supplemented (2,160 mg/day) patients than in the Ca-restricted (250 mg/day) ones. Oral Ca loading resulted in a smaller weight gain, a greater urinary sodium excretion, and an increase in red cell Mg. In the experimental study, high Ca (4% CaCl2) intake attenuated the blood pressure elevation in DOCA-salt-treated rats, accompanied with an increase in urinary sodium excretion, with the resultant attenuation in intra- and extracellular sodium retention. The decrease in catecholamine contents of hearts was improved, and a higher survival rate was observed in Ca-supplemented DOCA-salt rats. The results suggest that Ca supplementation may prevent a rise in BP in salt-dependent hypertension by inducing natriuresis with the resultant attenuation in sodium retention. The altered intracellular Mg level in hypertensive patients and the normalization of enhanced sympathetic nervous activity in DOCA-salt rats may, in part, be involved in its mechanism.

Adult↗
PubMed1987

The role of chloride on deoxycorticosterone acetate-salt hypertension.

Selective sodium loading attenuated the development of hypertension in the deoxycorticosterone acetate (DOCA) treated rat. The DOCA treated rat fed a diet equimolar in sodium to a 7% sodium chloride diet and in chloride to a standard diet, differed in various parameters from the DOCA treated rat fed a 7% sodium chloride diet: it had higher sodium concentration in both erythrocytes and muscles, a higher erythrocyte ouabain sensitive 22Na efflux rate constant (Kos), and a lower norepinephrine turnover rate in the heart and the spleen. These results suggest that the suppressed sympathetic nervous system activity and the activated cell membrane sodium pump contribute in part to the mechanism for the suppression of the development of hypertension in the DOCA-selective sodium loaded rat.

Animals↗
PubMed1986

Enhanced red cell sodium permeability in patients with borderline hypertension.

Red cell membrane sodium permeability was studied in 41 untreated patients with essential hypertension (20 borderline hypertensives and 21 established hypertensives) and 21 age matched normotensive subjects by means of the measurement of unidirectional passive influx of 22Na+ into ouabain-treated erythrocytes. The mean value (+/- SD) of 22Na+ influx was greater in the hypertensives than in the normotensives (0.183 +/- 0.047 vs 0.152 +/- 0.047 mmol/l . cells/hr, respectively, p less than 0.02). Among the patients with essential hypertension, the borderline hypertensives demonstrated a higher 22Na+ influx than the established hypertensives (0.207 +/- 0.043 vs 0.160 +/- 0.038 mmol/l . cells/hr, respectively, p less than 0.001), and 22Na+ influx positively correlated with plasma renin activity (r = 0.44, p less than 0.005). In 16 of 20 borderline hypertensives, 5 year blood pressure changes were examined retrospectively, and a positive correlation was observed between mean blood pressure increase and 22Na+ influx value in these subjects (r = 0.64, p less than 0.01). These results suggest that passive sodium influx may be altered in the course of the development of hypertension in relation to the changes in blood pressure level and that enhanced sodium permeability may be a characteristic of the early stage of essential hypertension.

Adult↗
PubMed1986

A circulating Na+-K+ATPase inhibitor, erythrocyte sodium transport and hypertension in patients with chronic renal failure.

The level of circulating Na+-K+ATPase inhibitor (% inhibition), erythrocyte ouabain-sensitive 22Na+ efflux rate constant (Kos) and erythrocyte sodium content (RBC Na) were measured in 11 undialysed patients with chronic renal failure, 16 patients on chronic hemodialysis and 16 age-matched normotensive healthy controls. In uremics, % inhibition was significantly higher than that in the controls (p less than 0.001). There were significant correlations between % inhibition and both mean blood pressure (r = 0.74, p less than 0.001) and Kos (r = -0.47, p less than 0.005) for all the groups combined. Hypertensive uremics showed significantly higher % inhibition, lower Kos and higher RBC Na compared with normotensive ones. These data suggest that the elevated level of circulating Na+-K+ ATPase inhibitor may, at least in part, account for the pathogenesis of hypertension in patients with chronic renal failure.

Adult↗
PubMed1985

Plasma concentrations of platelet-specific proteins in different stages of essential hypertension: interactions between platelet aggregation, blood lipids and age.

Plasma beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) were significantly higher in a group of 116 hypertensive men than in a normotensive group of 142 men. They increased with the stage of hypertension but the level did not correlate with the age of the subjects. Platelet aggregation was similar in the two groups and positively correlated with the age of the subjects in the normotensive group but not in the hypertensive group. A strong positive correlation was observed between the levels of plasma beta TG and PF4 and between platelet aggregation to ADP and that to epinephrine in both the hypertensive and normotensive groups. However, there was no correlation between the level of plasma beta TG or PF4 and platelet aggregation. Plasma antithrombin III was lower in the hypertensive group than in the normotensive group. These studies suggest that plasma levels of beta TG and PF4 are closely related to the stage of hypertension and are better indicators than aggregation of in vivo platelet activation in hypertensive subjects. Enhanced platelet activation may be involved in the acceleration of hypertensive arteriovascular damage and atherosclerosis.

Adenosine Diphosphate↗
PubMed1984

Inhibitory action of guanosine 3',5'-monophosphate on thrombin-induced calcium mobilization in human platelets.

During thrombin-induced serotonin release from platelets, phosphorylation of myosin light chain was increased. This protein phosphorylation, which is initiated by Ca2+ mobilization, and serotonin release were inhibited progressively by increasing concentrations of sodium nitroprusside, a potent stimulator of platelet guanylate cyclase, or 8-bromo-cyclic GMP. Thrombin-induced increase in cytoplasmic free Ca2+, which was also inhibited by these drugs in a dose-dependent manner. These results provide evidence that an increase in platelet cyclic GMP inhibits thrombin-induced Ca2+ mobilization and prevents platelet activation.

Blood Platelets↗
PubMed1984

Protein phosphorylation and mechanism of action of tumor-promoting phorbol esters.

The phorbol ester TPA may be intercalated into the membrane phospholipid bilayer and selectively binds to every molecule of C-kinase in exhibiting its full enzymatic activity. Available evidence suggests that C-kinase is the receptive protein of this tumor promoter, and the results presented seem to provide clues for clarifying the mechanism of controlling cell growth and differentiation.

Animals↗
PubMed1983

Elevation of cytoplasmic free calcium concentration by stable thromboxane A2 analogue in human platelets.

9, 11-Epithio-11, 12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, caused a rapid rise in cytoplasmic free Ca2+ concentration ([Ca2+]i) in human platelets as measured with the fluorescent Ca2+ indicator quin2. Concomitantly, this compound induced phosphorylation of myosin light chain which is catalyzed by Ca2+, calmodulin-dependent protein kinase. These reactions were fast enough to trigger serotonin release. 13-Azaprostanoic acid, a receptor level antagonist of thromboxane A2 inhibited STA2-induced elevation of [Ca2+]i, phosphorylation of myosin light chain and serotonin release. These results provide evidence that STA2 interacts with a thromboxane A2 receptor which leads to elevation of [Ca2+]i.

Blood Platelets↗
PubMed1983

Effect of cyclic AMP on cytoplasmic free calcium in human platelets stimulated by thrombin: direct measurement with quin2.

With the fluorescent Ca2+ indicator quin2, we measured directly cytoplasmic free Ca2+ [( Ca2+]i) in washed human platelets stimulated by thrombin and examined the effect of cyclic AMP on [Ca2+]i levels and 14C-serotonin release. Thrombin (0.2 U/ml) evoked a rise in [Ca2+]i from the basal level of about 100 nM to integral of 3 microM which was fast enough to trigger serotonin release. This rise was inhibited in a dose-dependent manner by preincubation with prostaglandin E1 (PGE1) (0.1-10 microM) or dibutyryl cyclic AMP (0.01 -1 mM). Parallel to this, serotonin release was also inhibited by these drugs. When added to platelets after stimulation by thrombin, PGE1 caused the rapid decrease of elevated [Ca2+]i. These results provide direct evidence that [Ca2+]i levels in platelets are regulated by cyclic AMP.

Aminoquinolines↗
PubMed1983

Protein phosphorylation and diglyceride production during serotonin release induced by epinephrine plus ADP in human platelets.

Epinephrine (1 microM) plus ADP (5 microM) induced serotonin release from human platelets although neither epinephrine nor ADP alone brought about such a release. During this release reaction, the phosphorylation of 40K-dalton protein was induced to an extent similar to that induced by 0.5 unit/ml thrombin. The amount of diglyceride (DG) produced by epinephrine plus ADP, however, was much smaller than that produced by thrombin. The reaction velocities of these reactions induced by epinephrine plus ADP were slower than those induced by thrombin. Epinephrine or ADP alone hardly produced any DG and induced 40K-dalton protein phosphorylation only slightly. Indomethacin (1 microgram/ml), a cyclooxygenase inhibitor, remarkably inhibited epinephrine plus ADP induced serotonin release, 40K-dalton protein phosphorylation and DG production although this agent had little effect on the same reactions induced by thrombin. These results suggest that prostaglandin endoperoxides or thromboxane A2 may be involved in serotonin release, 40K-dalton protein phosphorylation and DG production induced by epinephrine plus ADP.

Adenosine Diphosphate↗
PubMed1983

Synergistic functions of phorbol ester and calcium in serotonin release from human platelets.

In human platelets, thrombin activates Ca2+-activated, phospholipid-dependent protein kinase (protein kinase C) and mobilizes Ca2+ concomitantly, whereas 12-O-tetradecanoylphorbol-13-acetate (TPA) may be intercalated into membranes and directly activates protein kinase C without mobilization of Ca2+ in sufficient quantities. A series of experiments with TPA and Ca2+-ionophore (A23187) indicates that activation of protein kinase C is a prerequisite requirement for release of serotonin, and that this enzyme activation and Ca2+ mobilization act synergistically to elicit a full cellular response. Both cyclic AMP and cyclic GMP inhibit activation of protein kinase C by prohibiting the signal-dependent breakdown of inositol phospholipid to produce diacyl-glycerol, but none of these cyclic nucleotides prevents the TPA-induced activation of this enzyme.

Blood Platelets↗
PubMed1983

A role of calcium-activated phospholipid-dependent protein kinase in human platelet activation. Comparison of thrombin and collagen actions.

In human platelets stimulated by thrombin and collagen, diacylglycerol is rapidly produced from phosphatidylinositol. Concurrently, an endogenous protein having a molecular weight of about 40,000 (40K protein) is phosphorylated, and serotonin is released. These reactions are all inhibited by a prior treatment of platelets with prostaglandin E1, dibutyryl cyclic AMP, sodium nitroprusside, or with 8-bromo-cyclic GMP, which are known as potent inhibitors for platelet activation. Ca2+-activated phospholipid-dependent protein kinase (protein kinase C) preferentially phosphorylates 40K protein. As judged by fingerprint analysis, the sites in 40K protein that are phosphorylated during the platelet activation appear to be identical with those phosphorylated by protein kinase C in a purified cell-free system. 12-O-Tetradecanoylphorbol-13-acetate, which directly activates protein kinase C by substituting for diacylglycerol, stimulates 40K protein phosphorylation and release reaction without inducing diacylglycerol formation. Tetracaine, which inhibits protein kinase C by competing with phospholipid, blocks 40K protein phosphorylation and serotonin release without inhibiting the receptor-linked diacylglycerol formation. The results indicate that thrombin and collagen activate platelets in almost similar mechanisms and that protein kinase C may lie on a common pathway which leads to the release of serotonin. However, analysis with indomethacin indicates that the role of thromboxane A2 appears to be more predominant for the action of collagen, and it is suggestive that this arachidonate metabolite activates platelets in an analogous mechanism to thrombin.

Blood Platelets↗
PubMed1983

Membrane phospholipid turnover in signal transduction; protein kinase C and mechanism of action of tumor promoters.

Protein kinase C distributed widely in tissues and organs has the potential to play a crucial role in signal transduction for a variety of biologically active substances including growth factors, which elicit activation of cellular functions and proliferation. When cells are stimulated, this protein kinase is transiently activated by diacylglycerol which is produced in the membrane during the signal-induced turnover of inositol phospholipids. Tumor-promoting phorbol esters are intercalated into the membrane, substitute for diacylglycerol, and permanently activate protein kinase C irrespective of the feedback control by cyclic AMP. Under normal conditions in many tissues this cyclic nucleotide blocks the signal-induced inositol phospholipid breakdown and thereby prevents the activation of this protein kinase. Available evidence suggests that protein kinase C is most likely a receptor protein of tumor promoters, and exploration of the roles of this enzyme may provide clues for understanding better the biochemical basis of cell growth and differentiation.

Animals↗