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Biomedical subjects

Y Takamitsu

Publications and source records attributed to Y Takamitsu.

At least 55 records · Page 3Linked to original sources
PubMed1991

Total and split renal function assessed by ultrasound Doppler techniques.

We evaluated total and split renal functions from the pattern for renal arterial blood flow detected by ultrasound Doppler in healthy subjects and patients with varying degrees of renal function and disorders other than renovascular hypertension or severe aortic valvular disease. A renal-time pulsed ultrasonic echo-Doppler device at 2.5 MHz was used with a translumbar approach. The ratio of peak diastolic (D) to systolic (S) velocity correlated well with both p-aminohippurate clearance and creatinine clearance. Acceleration time was correlated with the clearance of neither compound. To evaluate the clinical usefulness of ultrasound Doppler in the assessment of split renal function, we compared the D/S ratio with the renal function obtained by radionuclide methods for individuals. The split renal glomerular filtration rate, calculated by a method which makes use of the early renal uptake of 99mTc-diethylenetriam-inepentaacetic acid, correlated well with the D/S ratio. These results indicate that the ultrasonic measurement of renal arterial blood flow by the pulsed Doppler method should be useful for assessment of total and split renal functions.

Adolescent↗
PubMed1991

[Effect of azosemide and furosemide on body fluid distribution and vasoactive hormones].

We examined the diuretic action of orally administered azosemide (AZ: 60 mg) and furosemide (FM: 40 mg) and their effects on body fluid distribution and circulatory vasoactive hormones in normal male volunteers. Urine volume and urinary sodium excretion were increased, peaking during 0 to 2 hours in FM and 2 to 4 hours in AZ in response to administration of both diuretics. The cumulative urine volume and urinary sodium excretion for 8 hours showed no significant difference between AZ and FM. Total body water (TBW) was measured by the dynamic distribution of deuterium oxide and a percentage change in circulating plasma volume (ICG ratio) was determined by using indocyanine green. The decrease in TBW and ICG ratio was detected in proportion to the increase in urine volume after administration of AZ and FM. Plasma renin activity (PRA) and plasma concentration of aldosterone (PAC), angiotensin II (ANG II) and arginine vasopressin (AVP) were elevated in response to the reduction in ICG ratio by both diuretics. The responses of PRA, PAC and ANG II to AZ were delayed about 2 hours as compared with those of FM. The increase in AVP with FM was significantly greater than that with AZ detected 2 hours after administration. The elevation of AVP in AZ was delayed and blunted compared with FM. These data indicate that the difference in diuretic property of AZ and FM may induce different stimulation to the secretion of vasoactive hormones through the changes in body fluid distribution and these hormones might modify the anti-edematic effect of AZ and FM.

Administration, Oral↗
PubMed1990

[Evaluation of the changes in intracranial water, sodium, phosphorus metabolites and intracellular cerebral pH in rats with acute dilutional hyponatremia].

Although most prominent among the clinical manifestations associated with hyponatremia are central nervous system (CNS) symptoms, the alterations in brain function remain poorly understood. In the present study, the alterations in intracellular cerebral pH and intracranial water, sodium and phosphorus metabolites content in rats with acute dilutional hyponatremia were examined by using an in vivo nuclear magnetic resonance (NMR) technique which noninvasively provides continuous informations on intracellular phenomena. Acute dilutional hyponatremia was induced on anesthetized male Sprague-Dawley rats by intraperitoneal injection of distilled water with an initial dose of 10 ml/100 g bw, followed by an additional dose of 5 ml/100 g bw 40 min later. Arterial blood sampling and NMR measurements were made before and every 60 min after the initial injection of distilled water. The treatment with distilled water resulted in dramatic falls in serum Na, Cl and osmolality at 60 min after water loading (Na; from 143.4 +/- 2.6 to 112.3 +/- 1.3 mmol/l, Cl; from 101.02 +/- 2.2 to 78.4 +/- 5.4 mmol/l, Osm; from 306.3 +/- 5.8 to 247.3 +/- 7.3 mOsm/kg H20). 1H-NMR imaging showed the accumulation of brain water as dilutional hyponatremia developed. Intracranial Na content measured by 23Na-NMR spectroscopy decreased significantly at 60 min after of water loading to about 70% of that observed under control condition. Since it has been demonstrated that solute extrusion from the brain with resultant reduction of brain swelling occurs within 60 min after the dilution, this result may be, at least in part, explained by this protective mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1990

[Hyponatremia in isolated deficiency of adrenocorticotropic hormone: role of a decrease in aldosterone secretion independent of antidiuretic hormone excess].

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.

Adrenocorticotropic Hormone↗
PubMed1990

[Angiotensin and prostaglandins in the pressure-natriuresis response in rats].

The possible roles of angiotensin and prostaglandins as humoral mediators of the pressure-natriuresis response were studied in anesthetized Sprague-Dawley rats. Neural and other hormonal influences on the kidney were held constant by denervating the kidney and by maintaining fixed high plasma levels of aldosterone, corticosterone, vasopressin and norepinephrine by continuous intravenous infusion. Acute elevation of arterial pressure by tightening the ligature placed around the abdominal aorta below the renal artery produced marked increases in urine flow and sodium excretion with no detectable changes in renal blood flow or glomerular filtration rate. In rats undergoing a saline diuresis, the pressure-natriuresis response was markedly inhibited by intravenous infusion of angiotensin II at a rate of 10 ng/kg/min. Blockade of prostaglandin synthesis with indomethacin also reduced the pressure-natriuresis response in the presence of low-dose (2 ng/kg/min) of angiotensin II, but indomethacin alone did not affect significantly. On the other hand, in rats with hydropenia indomethacin alone significantly inhibited the sodium excretory response to changes in arterial pressure. This indomethacin-induced inhibitory effect on the pressure-natriuresis response was completely attenuated in rats treated with captopril. These results indicate that angiotensin II is a powerful modulator of the pressure-natriuresis response. In addition, it has been suggested that prostaglandins are also capable of modulating the response only in the presence of the renin-angiotensin system. However, neither angiotensin nor prostaglandins appears to be essential for the basic pressure-natriuresis phenomenon since the pressure-natriuresis response can occur during blockade of both the renin-angiotensin and prostaglandin systems.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1988

Vascular response to carbon dioxide in areas with and without diaschisis in patients with small, deep hemispheric infarction.

The reactivity of cerebral blood vessels to changes in PaCO2 in areas of the cerebral cortex with or without diaschisis was investigated in 13 patients in a subacute or chronic stage after a small capsular infarct. A focal area of hypoperfusion (area of diaschisis) was detected in the ipsilateral sensorimotor cortex in each patient. Hyperventilation caused a significant reduction of regional cerebral blood flow in the area without diaschisis and only a tendency for regional cerebral blood flow to decrease in the area with diaschisis; CO2 inhalation induced a slight increase in regional cerebral blood flow in the area without diaschisis and a significant increase in regional cerebral blood flow in the area with diaschisis. Regional cerebral blood flow reactivity to hypocapnia was significantly less in the area with diaschisis than in the area without, whereas the hypercapnic response was more marked in the area with diaschisis than in the area without. Our results suggest that in the area with diaschisis, the arterioles may be abnormally vasoconstricted at rest such that they cannot constrict further in response to hypocapnia but can dilate more during hypercapnia than in the area without diaschisis. This excessive resting vasoconstriction may result from decreased tissue elaboration of CO2 due to local decrease of metabolic function.

Adult↗
PubMed1986

Effect of indomethacin on papillary solute concentration in the potassium-deficient rat.

Administration of indomethacin or meclofenamate to normal rats increases renal papillary solute concentration primarily by enhancing solute addition. A reduction in papillary solute concentration is characteristic of potassium deficiency. Of the multiple factors probably responsible for this reduction, several can be influenced by indomethacin or meclofenamate. The present study examined the effect of indomethacin on papillary solute concentration in the potassium-deficient rat. Indomethacin increased papillary solute concentration in normal but not potassium-deficient rats when studied in the conscious hydropenic state. Since indomethacin could increase papillary plasma flow in the potassium-deficient rat, potentially negating any enhancement of solute transport into the papilla, papillary plasma flow and papillary Cl concentration were determined in anesthetized surgically manipulated rats. Base-line papillary Cl concentrations were reduced in this setting. Indomethacin increased papillary plasma flow only in potassium-deficient rats but increased papillary Cl concentration equivalently in normal and potassium-deficient rats. The ability of indomethacin to increase papillary solute concentration in the potassium-deficient rat seemingly depends upon the experimental setting.

Animals↗
PubMed1985

Role of mesangial proliferation in angiotensin II and antidiuretic hormone induced changes in glomerular filtration rate.

The effects of administration of angiotensin II (ANG II) and antidiuretic hormone (ADH) on the glomerular filtration rate (GFR, measured as creatinine clearance) were examined in patients with mesangial proliferation. For this study, the patients whose conditions were similar to that of healthy subjects, except for asymptomatic urinary abnormalities and glomerular histological changes, were selected. Both ANG II and ADH administration significantly decreased GFR in the patients and the healthy subjects. Compared to the healthy subjects, a significantly greater drop in GFR was observed in the patients following ANG II infusion with or without SQ14225 administration, but not following ADH infusion. We conclude that mesangial proliferation may modulate an ANG II induced drop in GFR.

Adult↗
PubMed1985

[Effect of calcium antagonist (diltiazem) on left ventricular diastolic properties in essential hypertension: a pulsed Doppler echocardiographic study].

To evaluate the acute effect of diltiazem on left ventricular diastolic properties, we measured transmitral flow in 15 patients with essential hypertension using pulsed Doppler techniques. Before administering diltiazem, the peak velocity (R) and the deceleration rate of rapid inflow decreased significantly as compared with healthy subjects, but the peak velocity during atrial contraction (A) and the A/R increased significantly. Immediately after the intravenous administration of 10 mg diltiazem, blood pressure decreased from 157 +/- 22/96 +/- 12 mmHg to 135 +/- 19/82 +/- 11 mmHg (p less than 0.001) and the heart rate increased from 69 +/- 10/min to 74 +/- 10/min (p less than 0.05). However, 30 minutes after the injection, these returned to control values. The peak velocity and deceleration rate of rapid inflow were 52 +/- 9 cm/sec and 227 +/- 65 cm/sec2, respectively, before administering diltiazem, and five minutes after injection, these parameters increased to 63 +/- 13 cm/sec (p less than 0.001) and 292 +/- 82 cm/sec2 (p less than 0.001), respectively. Thirty minutes later, these values leveled off at 58 +/- 12 cm/sec (p less than 0.01) and 257 +/- 76 cm/sec2 (p less than 0.05), respectively. The peak velocity during atrial contraction was 67 +/- 12 cm/sec before administration, and this did not change significantly after injecting diltiazem. Significant increases in peak velocity and deceleration rate of rapid inflow and decreases in the A/R continued after the blood pressure and heart rate returned to control values. It was therefore concluded that diltiazem improves impaired early diastolic left ventricular filling in essential hypertension.

Adult↗
PubMed1984

Indomethacin blunts the orthostatic increase in plasma aldosterone in glomerulonephritis.

To determine factors mediating the aldosterone secretory response to orthostasis, we examined the effect of angiotensin-converting enzyme inhibition (CEI) on orthostasis in eight normal subjects and 10 normotensive patients with primary glomerulonephritis ingesting a normal sodium intake. On standing with CEI, the mean plasma aldosterone concentration (PAC) did not change [68.6 +/- 3.9 (+/- SE) and 63.4 +/- 6.9 pg/ml] in normal subjects, while PAC rose significantly from 72.3 +/- 7.5 to 129.5 +/- 13.2 pg/ml (P less than 0.001) in the glomerulonephritis patients without a concurrent rise in plasma angiotensin II, serum potassium, plasma ACTH, or mean blood pressure. There was a good correlation (r = -0.7064; P less than 0.03) between the changes in PAC and the changes in fractional sodium excretion in the patients. Pretreatment with indomethacin blunted the rise in PAC from 159.0 +/- 21.5 to 63.3 +/- 10.2 pg/ml upon standing with CEI, without a concurrent change in circulating 6-keto prostaglandin F1 alpha (from 57.7 +/- 9.5 to 56.0 +/- 11.1 pg/ml) in 4 patients. These results suggest that the aldosterone secretory response to orthostasis in patients with glomerulonephritis is dependent on factors blunted by pretreatment with indomethacin in addition to angiotensin II.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Influence of mesangial proliferation on posturally induced change in glomerular filtration rate.

The effect of the change from supine to upright position on GFR (measured by creatinine clearance) was studied in nonazotemic patients with biopsy-proven primary glomerulonephritis. Compared to healthy subjects, the fall in GFR following the postural change was significantly larger in patients with mesangial proliferation (MP) and with both MP and thickening of glomerular capillary wall (GCW), while similar in those with thickening of GCW alone, suggesting that MP, but not thickening of GCW, augments posturally induced fall in GFR. The augmented fall in GFR in patients with MP was accompanied by larger fall in GFR per unit increase in plasma renin activity than in healthy subjects, and was eliminated by angiotensin-converting enzyme inhibition. We conclude that MP augments posturally induced fall in GFR through affecting glomerular reactivity to angiotensin II.

Adolescent↗
PubMed1980

Interaction of calcium and microtubules in the action of cyclic AMP on the toad urinary bladder.

Involvement of microtubules in the cellular action of vasopressin was studied by physiological and biochemical procedures. The inhibitory effect of 10(-4) M colchicine on the hydro-osmotic response of the toad bladder to 2 mM cyclic AMP was completely blocked by an increase in the concentration of calcium in the serosal bathing medium from 1 to 8 mM. Most of the colchicine-binding activity of extracts of the bladder epithelial cells was recovered by DEAE-Sephadex chromatography in a procedure similar to that used to isolate tubulin of bovine brain. Sodium dodecyl sulfate urea and urea gel electrophoresis of the DEAE-Sephadex fraction from the bladder epithelial cells yielded bands that corresponded to those of bovine brain tubulin. When 8 mM CaCl2 was present in an incubation mixture, the binding of colchicine to tubulin from the bladder epithelial cells and bovine brain was significantly inhibited. However, 1 mM CaCl2 did not affect the binding of colchicine to tubulin. Although the present study supports the concept that microtubules and calcium play an important role in the cellular action of vasopressin on the toad urinary bladder, the mechanism by which calcium blocks the inhibitory effect of colchicine on the hydro-osmotic response to cyclic AMP could not be elucidated.

Animals↗