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Biomedical subjects

K Kido

Publications and source records attributed to K Kido.

At least 91 records · Page 5Linked to original sources

Relationship of cellular calcium to salt sensitivity in patients with essential hypertension.

The significance of cellular calcium metabolism and systemic calcium balance in sodium chloride sensitivity was studied in 16 patients with essential hypertension and in 13 normotensive subjects. With changes in sodium chloride intake from 3 to 20 g/day, mean blood pressure, lymphocyte [Ca2+]i and the acute hypotensive response to nifedipine were increased in the hypertensive patients, but not in the normotensive subjects. Serum calcium concentration was decreased and urinary calcium excretion was increased in both groups. In the hypertensive patients, elevation of mean blood pressure was positively correlated with the increase in lymphocyte [Ca2+]i and with the enhancement of the hypotensive response to nifedipine, but it was not related to the change in serum or urinary calcium. These results suggest that enhancement of cellular-calcium-dependent vasoconstriction may lead to increased blood pressure following sodium chloride loading in patients with essential hypertension.

Calcium↗

Role of cellular calcium in salt sensitivity of patients with essential hypertension.

The mechanism by which excessive sodium chloride intake raises blood pressure has not been fully clarified. The present study was therefore undertaken in patients with essential hypertension to investigate the possible role of an intracellular calcium-dependent mechanism in salt sensitivity. The difference in mean blood pressure between a week of low sodium chloride diet (3 g/day) and a week of high sodium chloride diet (20 g/day) was studied in relation to the intracellular free calcium concentration in lymphocytes and an acute hypotensive response to a 10-mg sublingual dose of nifedipine in 12 inpatients. Sodium chloride loading induced significant increases in mean blood pressure (from 111 +/- 12 to 122 +/- 11 mm Hg; p less than 0.01), intracellular free calcium in lymphocytes (from 133 +/- 13 to 145 +/- 9 nmol/L; p less than 0.01), and the hypotensive response to nifedipine (from 19 +/- 6 to 31 +/- 10 mm Hg; p less than 0.01). In addition, serum total calcium concentration was decreased while urinary calcium excretion was increased. The elevation of mean blood pressure was closely and positively correlated with the increase in intracellular free calcium concentration (r = 0.71, p less than 0.05) and the increase in the hypotensive effect of nifedipine (r = 0.91, p less than 0.01) after sodium chloride loading. However, changes in these values had no relation to the change in serum concentration or urinary excretion of calcium. These data suggest that change in the cellular calcium-dependent vasoconstriction mechanism may be associated with salt sensitivity of patients with essential hypertension.

Adult↗

Intralymphocytic sodium and free calcium and plasma renin in essential hypertension.

Intracellular sodium, potassium, and free calcium concentrations were investigated in lymphocytes of 30 patients with essential hypertension and 30 normotensive controls. All subjects were placed on a diet containing 8 to 10 g of sodium chloride per day. Lymphocyte sodium concentration was higher in hypertensive patients than in normotensive controls (19.8 +/- 1.8 vs 18.4 +/- 1.8 mmol/kg wet weight; p less than 0.01), whereas lymphocyte potassium concentration was similar in both groups. Lymphocyte free calcium concentration was also higher in hypertensive patients than in normotensive controls (134.6 +/- 13.2 vs 120.2 +/- 16.4 nmol/L; p less than 0.01). There was a positive correlation between lymphocyte sodium and free calcium concentrations in normotensive controls, in hypertensive patients, and in the subjects combined (r = 0.59, p less than 0.01; r = 0.71, p less than 0.001; and r = 0.70, p less than 0.001, respectively). Lymphocyte potassium concentration was not related to lymphocyte sodium or free calcium concentration in each group. In patients with essential hypertension, intracellular sodium and free calcium concentrations were negatively correlated with plasma renin activity (r = -0.66, p less than 0.001; r = -0.60, p less than 0.001, plasma norepinephrine concentration. These results suggest that a considerable relationship exists between intracellular sodium and free calcium in lymphocytes and that, in essential hypertension, the alteration in cellular metabolism of sodium and calcium may be linked to the renin system but not to blood pressure, age, or adrenergic activity.

Adult↗

Intracellular sodium concentration in lymphocytes and erythrocytes of patients with essential hypertension.

In order to investigate the abnormalities in intracellular sodium concentration ([Na]i) in essential hypertension, [Na]i in lymphocytes and erythrocytes was determined in 37 outpatients with essential hypertension and 35 normotensive controls matched for sex and age. [Na]i in lymphocytes was higher in hypertensive patients than in normotensive controls, while no difference was observed in [Na]i in erythrocytes between the 2 groups. There was no significant correlation between [Na]i in lymphocytes and erythrocytes in either group. In hypertensive patients, plasma renin activity had a negative correlation with [Na]i in lymphocytes, but not with [Na]i in erythrocytes. These results suggest that the increase in [Na]i may be associated with essential hypertension with suppressed plasma renin activity and that lymphocytes are more suitable than erythrocytes for the analysis of [Na]i.

Erythrocytes↗

Intralymphocytic sodium and free calcium concentration in relation to salt sensitivity in patients with essential hypertension.

In order to clarify the relation between salt sensitivity and changes in intracellular sodium ([Na]i) and free calcium concentration ([Ca2+]i) after salt loading, [Na]i and [Ca2+]i were determined in lymphocytes of twenty patients with essential hypertension under a low salt diet (3 g/day) and a high salt diet (20 g/day) for seven days, respectively. They were classified as "salt-sensitive" (n = 10) or "nonsalt-sensitive" (n = 10) on the basis of the changes in blood pressure after salt loading. Both lymphocytic [Na]i and [Ca2+]i were significantly increased with salt loading in salt-sensitive patients (p less than 0.05 for both), while they were not affected by salt loading in nonsalt-sensitive patients. Lymphocytic [Ca2+]i showed a positive correlation with lymphocytic [Na]i under both low salt diet (r = 0.62, p less than 0.01) and high salt diet (r = 0.70, p less than 0.01) in all patients in both groups. In addition, a close and positive correlation was observed between the changes in lymphocytic [Na]i and those in lymphocytic [Ca2+]i after salt loading in all patients in both groups (r = 0.80, p less than 0.001). These results suggest that the increase in [Ca2+]i, possibly linked with the increase in [Na]i, may be involved in elevation of blood pressure in the salt-sensitive patients after salt loading.

Adult↗

[Approach to early diagnosis of acute mesenteric ischemia: evaluation in canine model].

The high mortality rate of patients with acute mesenteric ischemia may be mainly due to the difficulty of making an early diagnosis. Many clinical and experimental studies have been attempted to make an early diagnosis in the view of history, physical examination, laboratory data, X-rays and angiographies. This study was undertaken to estimate the diagnostic value of twenty one laboratory parameters and three clinical parameters measured after superior mesenteric artery occlusion (SMAO) in the mongrel dogs. Consequently, the valuable diagnostic indicators of SMAO that statistically had significant difference were serum CPK isoenzyme-BB, serum CPK isoenzyme-MB, serum inorganic phosphate, serum calcium and base excess of arterial blood gas analysis. In these indicators, serum CPK isoenzyme-BB, serum inorganic phosphate and serum calcium were especially valuable indicators of its early diagnosis, because they showed significant change in the early phase after SMAO. However, other indicators showed significant change within eighteen hours after SMAO. Therefore, if these indicators are able to be examined in a case of abdominal emergency, they are considered to play a valuable role in the diagnosis of acute mesenteric ischemia.

Acute Disease↗

[Experience with the familial occurrence of CIIP and review of the literature in Japan].

Recurrent intestinal obstruction for which no underlying cause can be found has been termed "chronic idiopathic intestinal pseudoobstruction (CIIP)" by Maldonado et al. Some clinical features of CIIP have been pointed out in literatures. More often than not, CIIP often shows hereditary occurrence. The authors have summed up twenty-one cases of CIIP reported till 1984 in Japan, In these cases, only one familial occurrence has been reported excluding our own. Our cases were a young woman and her father and they showed clinical features of CIIP and they might have hereditary factors.

Adolescent↗

Articulatory parameters for the perception of bilabials.

In order to investigate articulatory cues for the perception of bilabial consonants, a production model was set up whose control parameters were converted into acoustic parameters by which a terminal analogue speech synthesizer was driven to synthesize test sounds for the perception experiments. Experiments concerning discrimination between (b) and (w) and between (m) and (w) were then performed with these test sounds. Statistical testing of the results showed that discrimination among the bilabials in an intervocalic context entirely depended on the minimum value of lip opening and that, contrary to the facts hitherto known, it was independent of the rate of lip opening/closure. At the same time, the features [+ anterior, - coronal] and [+ nasal] turned out to be perceptually independent phonological attributes of bilabial and nasal consonants, respectively.

Cues↗

Analog computer simulation of maternal - fetal transfer of cefazolin.

Cefazolin concentration-time data after normal vaginal delivery were obtained for maternal serum, placenta, umbilical cord blood, and amniotic fluid. After normalizing of the data, concentration-time profiles were generated for each sampling compartment. A pharmacokinetic model for analog computer simulation was developed. Multiple dosing simulation suggests a higher accumulation of cefazolin in fetal than in maternal blood, and a slow accumulation in amniotic fluid, which acts as a depot or storage. The drug is transferred diaplacentally; paraplacental transfer seems to be absent for cefazolin.

Amniotic Fluid↗