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R Ozono

Publications and source records attributed to R Ozono.

45 records · Page 3Linked to original sources

Na(+)-Ca2+ exchange modulates Ca2+ handling of human platelets by altering intracellular Ca2+ store size.

OBJECTIVE: In order to elucidate the role of Na(+)-Ca2+ exchange in regulating cytosolic free Ca2+ concentration in human platelets, we investigated the relationship between cytosolic free Na+ and Ca2+ concentrations in human platelets. METHODS: Sodium-binding benzofuran isophthalate and fura-2 were used to monitor cytosolic free Na+ and Ca2+ concentrations, respectively. RESULTS: Ouabain at a concentration of 100 mumol/l induced an increase in cytosolic free Na+ concentration within 5 min, followed by increases in resting cytosolic free Ca2+ concentration and intracellular Ca2+ store. These three parameters were increased in a time-dependent manner significantly above the timed control over a period of 60 min. Pre-incubation of platelets with 100 mumol/l ouabain for 30 min significantly enhanced the cytosolic free Ca2+ response to thrombin and arginine vasopressin in the absence of extracellular Ca2+. The decrease from peak cytosolic free Ca2+ concentration in response to ionomycin in the absence of extracellular Ca2+ was significantly slower in low-Na+ buffer than in standard buffer. In addition, 5 mumol/ionomycin increased the cytosolic free Na+ concentration markedly in the presence of 0.1 mmol/l extracellular Ca2+, but the rise in cytosolic free Na+ concentration was suppressed by 2 mmol/l Ni2+ (NiCl2) or by removal of extracellular Ca2+. CONCLUSIONS: These results suggest that Na(+)-Ca2+ exchange is important in extruding Ca2+ from the cytosol in human platelets, and inhibition of this exchange leads to the accumulation of intracellular Ca2+ store, which may be responsible for the enhanced responsiveness of cytosolic free Ca2+ to agonists.

Blood Platelets↗

Primary aldosteronism with ipsilateral adrenal cyst: report of a case.

Adrenal cysts are rare; most lack endocrinologic activity and do not produce clinical symptoms. The present case is the first to be reported with both an adrenal cyst and a functioning adenoma present ipsilaterally. This 39-year-old male with hypertension was diagnosed as having primary aldosteronism as reflected by hypokalemia and an excess plasma aldosterone concentration (PAC). However, examination by computed tomography revealed a grossly enlarged left adrenal gland with a cyst-like lesion. The right adrenal appeared normal. At surgery, an adenoma and a cyst were found to coexist in the left adrenal cortex. The cyst fluid contained three times the amount of aldosterone present in plasma, less than in previous reports, and was considered to lack endocrinologic activity. Following a left adrenectomy, the patient's blood pressure, serum potassium concentration, and PAC all normalized without the need for medical treatment.

Adenoma↗

Erythrocyte sodium cannot predict hypotensive effects of calcium channel blockers.

Antihypertensive efficacy of the calcium channel blocker, nilvadipine, was investigated in 21 patients with essential hypertension in relation to the intracellular sodium concentration ([Na]i) in erythrocytes and clinical variables, such as age, body weight, pretreatment blood pressure and plasma renin activity. Dihydropyridine nilvadipine reduced mean blood pressure from 120 +/- 6 to 106 +/- 8 mmHg (p < 0.01). The hypotensive effect of nilvadipine was positively correlated with age (r = 0.67, p < 0.01) and inversely correlated with plasma renin activity (r = -0.62, p < 0.01), but was not correlated with erythrocyte [Na]i or any other indices. Erythrocyte [Na]i was decreased with nilvadipine treatment (8.27 +/- 1.69 to 7.97 +/- 1.49 mM, p < 0.01). However, no link was found between the change in [Na]i and the hypotensive effect of the drug. In conclusion, the antihypertensive efficacy of nilvadipine was predictable by age and renin status, but not by erythrocyte [Na]i. A significant role of reduction of [Na]i in the hypotensive effect of the calcium channel blockers was not detected.

Age Factors↗

Familial influence upon NaCl sensitivity in patients with essential hypertension.

OBJECTIVE: The role of genetic factors in the pathogenesis of essential hypertension has not been fully clarified. In order to characterize the relation between NaCl sensitivity and genetic features of hypertension, the responses to dietary Na manipulations were examined in essential hypertensive patients with and without a family history of hypertension. METHODS: Fifteen essential hypertensive patients, both of whose parents were hypertensive, were compared with 25 hypertensive patients in whom a family history of hypertension was known to be absent in first- and second-degree relatives. There were no differences in gender distribution, age, blood pressure or duration of hypertension between the two groups. Subjects were studied as inpatients on a daily diet of 170 mmol NaCl for 1 week, followed by 1 week on a low-NaCl diet (50 mmol/day) and then by 1 week on a high-NaCl diet (340 mmol/day). RESULTS: Plasma renin activity on a low-NaCl diet was lower, and the erythrocyte Na+ concentration on both diets higher, in hypertensive patients with than in those without a family history. The elevations in mean blood pressure and in erythrocyte Na+ concentration with a high-NaCl diet were greater in patients with a family history. A significant correlation between the change in mean blood pressure and the change in erythrocyte Na+ concentration was found in patients with a positive family history, but not in those with a negative family history. CONCLUSIONS: Essential hypertensive patients with an apparent hereditary component of hypertension can be characterized as the low-renin and Na-sensitive subgroup with intracellular Na+ accumulation. Genetic features may underlie, at least in part, the heterogeneity of essential hypertension.

Blood Pressure↗

[A case report of two mitral valve aneurysms with one perforation after two attacks of infective endocarditis].

Aneurysms of the mitral valve complicating infective endocarditis (IE) are uncommon. The patient was a 57-year-old man who was admitted to our hospital for a precise examination of heart failure. One year before, the first two-dimensional echocardiography showed an aneurysm of the anterior mitral leaflet possibly due to a previous attack of IE. Doppler color flow mapping detected a regurgitant jet from the mitral valve aneurysm into the left atrium during systole, which suggested perforation of the aneurysm, and an aortic regurgitant jet flowing against the anterior mitral leaflet. Because the patient's family refused cardiac catheter examination and surgery, we treated him in the out-patient clinic. A few weeks before his admission, he had discontinued taking diuretics because of uncomfortable urinary frequency. He gradually developed the symptoms of heart failure and entered our hospital. IE was suspected because of leucocytosis and slight fever. Two-dimensional echocardiography revealed a new aneurysm of the anterior mitral leaflet without perforation, located in the distal part of the old aneurysm. This time, his family consented to the surgical treatment. Aortic and mitral valve replacement was successfully performed. It was pathologically confirmed that the two mitral aneurysms had been caused by IE.

Aortic Valve↗

Role of intracellular cation abnormalities in development of left ventricular hypertrophy.

To elucidate factors determining the development of left ventricular hypertrophy, we performed measurements of intraerythrocyte sodium and intraplatelet calcium concentrations, measurements of plasma and urinary catecholamine levels and plasma renin activity, calculation of left ventricular mass using echocardiography, and 24-h ambulatory blood pressure (BP) monitoring. The results indicate that abnormalities of sodium and calcium mobilization may play an important role in the adaptation of left ventricular muscle to a persistent increase in BP.

Adult↗

[Clinicopathologic study of acute coronary occlusion in percutaneous transluminal coronary angioplasty].

ACO occurred within 40 min (mean 15.7 min) after PTCA in 22 patients and more than 12 hours in 2. The group with ACO had a significantly higher incidence of female (46% vs 23%), acute myocardial infarction (63% vs 35%), eccentric lesions (73% vs 28%), tortuous lesions (30% vs 4%) and coronary dissection or intraluminal haziness (89% vs 34%). Luminal narrowing before and after PTCA was significantly higher in ACO group than in control group (93% and 56% vs 87% and 23%). Repeat PTCA was performed in 17 patients and was successful in 13. Coronary bypass surgery was performed in 4 patients. Intracoronary urokinase was ineffective to ACO. In 3 autopsy cases dying 5, 14 and 17 days after PTCA, large extent of intimal tears and thrombus in the space of tears and the lumens were observed. These results suggest that coronary dissection chiefly contributes to ACO and coronary thrombosis is superimposed for a secondary event in most of cases with ACO.

Adult↗

Combination of nifedipine and carteolol compared to nifedipine alone in diurnal blood pressure variation and exercise blood pressure in patients with essential hypertension.

A combination of nifedipine (40 mg twice daily) plus carteolol (10 mg twice daily) was compared with nifedipine monotherapy in ten patients with essential hypertension. Ambulatory blood pressure (BP) monitoring over 24 hours and treadmill exercise testing were performed before treatment with nifedipine (but after the placebo period), after four weeks of nifedipine treatment, and after four weeks of nifedipine+carteolol combination therapy. At the end of nifedipine monotherapy, 24-hour average ambulatory BP, minimum ambulatory BP during sleep, maximum ambulatory BP, and casual BP all decreased significantly (P less than 0.01). However, the standard deviation (SD) of the ambulatory BP was not affected. The change in systolic BP response to treadmill exercise increased. After a four-week period of nifedipine+carteolol combination therapy, average ambulatory BP and maximum ambulatory BP were further decreased (P less than 0.01). The SD of the ambulatory BP and the change in BP response to exercise were significantly decreased (P less than 0.01), but the minimum ambulatory BP was not affected. These findings suggest that nifedipine and carteolol differ in their influence on diurnal BP variation and on exercise-induced BP elevation. Carteolol may mainly attenuate stress-induced BP elevation and have little influence on nocturnal BP decline. In contrast, nifedipine may affect the BP profile uniformly over the entire day. Nifedipine+carteolol combination therapy may be superior to nifedipine monotherapy because carteolol has a minimal effect on nocturnal BP and decreases stress-induced BP elevation.

Blood Pressure↗