[Combination effect of H2-receptor antagonist and mucosal protective agent on hemodynamics in the gastric mucosa].
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Animals↗
Biomedical subjects
T Ogihara
Publications and source records attributed to T Ogihara.
[The esophageal mucosal hemodynamics in patients with liver cirrhosis].
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Adult↗
[Enzyme immunoassay for serum 18-hydroxycorticosterone and its clinical application].
An enzyme immunoassay for serum 18-hydroxycorticosterone was established using alkaline phosphatase as a label. The antiserum for 18-hydroxycorticosterone was produced by immunization of rabbits with 18-hydroxycorticosterone 3-(o-carboxymethyl) oxime conjugated to bovine serum albumin. Sephadex LH-20 column chromatography was used to separate 18-hydroxycorticosterone from other steroids in serum samples. The minimal detectable amount of 18-hydroxycorticosterone was 50 pg/tube, and the measurable range was from 5 to 1000 ng/dl when a 1.0 ml serum sample was used. Intra- and inter-assay coefficients of variance were 5.0% (n = 6), and 5.8% (n = 6), respectively. In normal controls the serum 18-hydroxycorticosterone level was 4.8 approximately 34.0 ng/dl (mean +/- S.D. = 17.1 +/- 9.0 ng/dl) on an unrestricted diet. Seven out of 8 patients with aldosterone-producing adenoma had above-normal serum 18-hydroxycorticosterone levels. Serum 18-hydroxycorticosterone increased and decreased significantly following ACTH and dexamethasone administration, respectively. In essential hypertensive patients, serum 18-hydroxycorticosterone was high during a low-sodium diet and was suppressed remarkably by captopril. These observations support the previous reports that adrenal 18-hydroxycorticosterone synthesis is dependent on both ACTH and the renin-angiotensin system. The present method is sufficiently sensitive and producible, avoids the use of radioisotopes and is quite satisfactory for clinical use.
18-Hydroxycorticosterone↗
Effects of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet activating factor) on cardiac function in perfused guinea-pig heart.
The direct cardiac action of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF) was studied in isolated perfused guinea-pig heart preparations. PAF produced a fall in left ventricular pressure, decreases in the rate of rise of the left ventricular pressure (dp/dt) and coronary flow, but had no effect on heart rate. These results indicate that PAF is a cardiodepressant with inotropic selectivity and this effect on heart is blocked by CV-3988, a specific PAF antagonist.
Animals↗
Renal vein prostaglandins in renovascular hypertensive patients.
To investigate the role of intrarenal prostaglandins in the pathophysiology of renovascular hypertension, we measured bilateral renal vein prostaglandins (PGE2, 6-keto-PGF1 alpha) and plasma renin activity (PRA) of nine patients with renovascular hypertension caused by fibromuscular dysplasia. Both PGE2 and PRA on the stenotic side were significantly higher than those on the non-stenotic side. The difference in 6-keto-PGF1 alpha levels between the stenotic and the non-stenotic sides was not significant. PGE2 ratio of the stenotic and the non-stenotic sides was significantly correlated with PRA ratio of the stenotic and contralateral sides. These results suggest that renal PGE2 plays an important role in the maintenance of renal blood flow through modulation against vasoconstriction in the renal vasculature and that renal PGE2 may be closely associated with renal renin secretion in the renovascular hypertension.
6-Ketoprostaglandin F1 alpha↗
Hypotensive mechanism of acetyl glyceryl ether phosphorylcholine (AGEPC) in dogs. Effects on hemodynamics and humoral factors.
One-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphorylcholine (AGEPC) was intravenously administered to anesthetized dogs to study the effects on hemodynamics and several endocrine factors. The effect of AGEPC on local blood flow was also studied by direct intra-arterial injection. Following intravenous injection, blood pressure and cardiac output decreased significantly (p less than 0.001). Changes in total peripheral resistance (TPR) and heart rate were biphasic. TPR increased significantly (p less than 0.01) after an initial slight reduction. Heart rate decreased significantly (p less than 0.01) with only a transient slight elevation. Femoral blood flow was increased (p less than 0.001) by intraarterial injection and decreased (p less than 0.05) by intravenous administration. Plasma norepinephrine (p less than 0.001), epinephrine (p less than 0.01), thromboxane B2 (p less than 0.001), 6-0-PGF1 alpha (p less than 0.01), aldosterone (p less than 0.001) and cortisol (p less than 0.001) were elevated, but plasma renin activity did not change. These results suggest that the hypotensive mechanism of AGEPC is due to both cardiosuppression and vasodilation. AGEPC increased plasma catecholamines, thromboxane A2, PGI2, aldosterone and cortisol which, in turn, may modify hemodynamics.
Aldosterone↗
Calmodulin levels in hypertensive rats.
Intracellular calmodulin levels were measured by direct radioimmunoassay in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Decreased calmodulin levels were demonstrated in the brain, heart, aorta and kidney of spontaneously hypertensive rats compared with those in Wistar-Kyoto rats. Calmodulin levels in the brain were also decreased in deoxycorticosterone acetate (DOCA)-salt rats, but not changed significantly in the heart, aorta and kidney compared with those in Wistar-Kyoto rats. These findings suggest that intracellular calcium-dependent regulatory systems are genetically disrupted in spontaneously hypertensive rats, but this is probably not an important factor in the development of hypertension.
Animals↗
Sensitive assay and kinetic property of urinary inhibitor of Na+, K+-ATPase in sodium-loaded patients with essential hypertension.
A sensitive assay method to evaluate the inhibitor of Na+, K+-ATPase in human urine was developed by measuring the inorganic phosphate liberated from ATP in vitro using Na+, K+-ATPase from porcine cerebral cortex. Ouabain inhibited the Na+, K+-ATPase by competing with the potassium ion (an apparent Ki = 2.6 +/- 0.89 X 10(-8) M, n = 8) under the condition of 100 mM NaCl, 4.5 mM MgSO4 and 0.56 mM ATP. The apparent Km value of KCl was 0.4 mM. Factors inhibiting Na+, K+-ATPase were detected in the post-salt fraction on Sephadex G-15 chromatography following the ethanol extraction of lyophilized fresh urine of sodium loaded human subjects (300 meq Na+/day, for 4 days) with essential hypertension. Two active fractions around the 400 daltons following salt were eluted on Sephadex G-15 chromatography. The slower eluted factor competed kinetically with potassium ion, but the inhibitory activity was lost within two days during storage at 4 degrees C. The faster-eluted inhibitor lost its activity within a day. These results indicate that the unstable inhibiting factors of Na+, K+-ATPase exist in human urine and one of these factors inhibits ouabain sensitive Na+, K+-ATPase by binding to the potassium binding site (or very close to it), which exists at the outer surface of the cell membrane of this enzyme.
Binding Sites↗
Involvement of endogenous prostaglandins in salt-induced hypertension.
Insufficient production of prostaglandins, which are possible antihypertensive agents, may be a pathogenetic factor in hypertensive patients on salt loading. We compared the levels of plasma PGE2, plasma renin activity (PRA) and urinary 6-keto-PGF1 alpha (6-O-PGF1 alpha), a major stable metabolite of PGI2, on day 5 of salt deprivation and also on day 5 of subsequent salt loading in 17 patients with essential hypertension. Salt loading decreased plasma PGE2, and slightly increased urinary 6-O-PGF1 alpha. On salt loading, a positive correlation was found between the levels of plasma PGE2 and urinary sodium excretion. On salt deprivation, PRA was significantly correlated with plasma PGE2. The per cent change in mean blood pressure on changing from salt restriction to salt loading was inversely correlated with the per cent change in PGE2, and positively correlated with the per cent change in 6-O-PGF1 alpha excretion. These findings suggest that on salt restriction, PGE2 is involved in the renin-angiotension system and that on salt loading, PGE2 is produced to compensate for the excessive sodium. The finding that PGE2 production was attenuated progressively as the mean blood pressure increased on salt loading in patients with essential hypertension suggests that insufficient compensatory PGE2 production is a pathogenetic factor in salt-induced hypertensive patients. In contrast, PGI2 may be produced adaptively to regulate blood pressure during changes in salt balance.
Adult↗
[A case of idiopathic retroperitoneal fibrosis associated with localized swelling and pain on bilateral lower legs].
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Female↗
Comparative changes in plasma and RBC alpha-tocopherol after administration of dl-alpha-tocopheryl acetate and d-alpha-tocopherol.
Changes in plasma and RBC alpha-tocopherol after intravenous and oral administration of dl-alpha-tocopheryl acetate were investigated using vitamin E-deficient rats and were compared with those following the administration of d-alpha-tocopherol, which is the most active and natural form of tocopherol. Intravenous administration: By the administration of dl-tocopheryl acetate, the elevated plasma tocopherol levels were higher at 6 h than those elevated by d-tocopherol, but the RBC tocopherol was lower 6 h after the infusion of dl-tocopheryl acetate than after d-tocopherol infusion. The tocopheryl acetate incorporated into the RBCs remained for 24 h after the administration of tocopheryl acetate, the acetate then becoming undetectable in plasma. Oral administration: The tocopherol elevated in plasma and RBC was only the alpha-form and not tocopheryl acetate. In both plasma and RBCs, tocopherol levels were higher after the administration of d-tocopherol than after dl-tocopheryl acetate administration, and more was found in RBCs.
Administration, Oral↗
Hypotensive mechanism of potassium supplementation in salt-loaded patients with essential hypertension.
To investigate the hypotensive mechanism of potassium supplementation, blood pressure responses and hormonal changes were measured during KCl supplementation in salt-loaded patients with essential hypertension. Ten patients with essential hypertension were placed on low sodium intake, high sodium intake, and high sodium intake with KCl supplementation. Blood pressure increased during NaCl loading and decreased during KCl supplementation. The levels of urinary sodium and fractional sodium excretion increased after KCl supplementation. Reduction in blood pressure after KCl supplementation was correlated with an increase in blood pressure after NaCl supplementation, i.e., potassium sensitivity and sodium sensitivity were correlated. Plasma PGE2 and norepinephrine increased after KCl loading. Increases in plasma PGE2 were correlated with a reduction of blood pressure by KCl. These results indicate that natriuresis and hypotensive action of KCl are associated with increased PGE2 production, and the sympathetic nerve activity suggests a compensatory increase for the decrease in blood pressure.
Blood Pressure↗
Structure of angiotensin II-binding site probed with diaminoalkanes.
The nature of the hormone-binding site of detergent-solubilized angiotensin II receptor from the bovine adrenal cortex has been characterized using diaminoalkanes. Their affinity for the hormone-binding site showed a dramatic alteration depending on their chain length; at the hexamethylene stage, a maximum and competitive inhibition was observed. These results indicate that the angiotensin II receptors have a definite hydrophobic binding groove limbed with diagonally located two negative charges, and those hydrophobic and electrostatic forces may play an important role in the proper register between the receptor and hormone.
Adrenal Cortex↗
Synergic effects of kallikrein-kinin and prostaglandins on renin release on infusion of isolated hog kidney with aldosterone.
The effects of infusion of a large amount of aldosterone into the renal artery of isolated perfused hog kidney on the release of renin, prostaglandins (PG) and kinin and the excretion of urinary kallikrein were investigated. Infusion of aldosterone at a rate of 100 ng/min (100 to 800 ng/ml of perfusate) resulted in significant releases of renin, PG (PGE2 , 6-0-PGF1 alpha), and kinin and increase in urinary kallikrein. Infusion of aldosterone and an inhibitor of kallikrein, aprotinin, decreased the releases of renin, PG and kinin and infusion of aldosterone with indomethacin decreased the release of PG but increased that of kinin and urinary kallikrein without significant change in renin releases. These findings suggest that the release of renin by aldosterone may result from synergic effects of renal PG and the kallikrein -kinin system.
Aldosterone↗
Effect of 1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine inhibitor on the reduction of one-kidney, one clip hypertension after unclipping in the rat.
The role of 1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine in regulating blood pressure was studied in one-kidney, one clip hypertensive rats using 3-(N-n-octadecylcarbamoyloxy)-2-methoxypropyl-2-thiazolio ethylphosphate, which specifically inhibited the hypotensive activity of exogenously injected 1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine. The blood pressure of rats with established hypertension produced by clipping one renal artery and contralateral nephrectomy normally decreases rapidly after unclipping the artery, but this rapid decrease was significantly inhibited by intravenous infusion of 3-(N-n-octadecylcarbamoyloxy)-2-methoxypropyl-2-thiazolio ethylphosphate. This shows that endogenous 1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine participates in the rapid decrease of blood pressure after unclipping the kidney in one-kidney, one clip hypertensive rats.
Animals↗
PGE2, 6-O-PGF1 alpha and sodium balance in essential hypertensive patients.
Insufficient production of PGE2 has been thought to be a pathogenic factor in hypertensive patients on salt loading. However, the inter-relationship between PGE2 and sodium is still uncertain. Essential hypertensive patients participated in a salt balance study for two consecutive 5-day periods of restriction and repletion. Urinary PGE2 increased on the second or the third day of salt balance, but subsequently declined and remained stable. On the fifth day, PGE2 excretion on salt loading was lower than on salt deprivation. Changes in urinary PGE2 during salt loading paralleled those in urinary sodium excretion. Urinary 6-O-PGF1 alpha did not show any significant change. On salt deprivation PGE2 excretion was correlated with plasma renin activity (PRA). These results suggest the possibility that PGE2 is involved in sodium excretion on salt loading and that on salt depletion PGE2 excretion increases in association with activation of the renin-angiotensin axis.
6-Ketoprostaglandin F1 alpha↗
The role of antihypertensive polar renomedullary lipid in the pathogenesis of hypertension.
One-0-hexadecyl-2-0-acetyl-sn-glycero-3-phosphorylcholine (HAGPC), a component of semisynthetic antihypertensive polar renomedullary lipid (APRL) reported by Muirhead et al. in chemically treated rabbit renomedullary lipid had a strong hypotensive action, a cardiosuppressing action and an apparent anti-norepinephrine action. 3-(N-n-octadecylcarbamoyloxy)-2-methoxypropyl-2-thiazolio ethyl phosphate significantly inhibited the hypotensive action of HAGPC, whereas the hypotensive activities of prostaglandin I2, prostaglandin E2, bradykinin, histamine and acetylcholine were not affected by this drug. The blood pressure of rats with established hypertension produced by clipping one renal artery and contralateral nephrectomy normally decreases rapidly after unclipping the renal artery, but the initial rapid decrease was significantly inhibited by an intravenous infusion of 3-(N-n-octadecylcarbamoyloxy)-2-methoxypropyl-2-thiazolio ethyl phosphate. This shows that endogenous 1-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine participates in the rapid decrease of blood pressure after unclipping the renal artery in one-kidney, one clip hypertensive rats.
Acetylcholine↗