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Biomedical subjects

K Kudo

Publications and source records attributed to K Kudo.

At least 325 records · Page 18Linked to original sources
PubMed1987

[Familial cardiomyopathy with different clinical features in individual members].

The mother and three children of a family whose parents were consanguineous, each had cardiomyopathy with various patterns of hypertrophy and dilatation. All members had asymmetrical septal hypertrophy (ASH), and three of them were characterized as hypertrophic cardiomyopathy (HCM). Another one had ventricular dilatation mimicking dilated cardiomyopathy (DCM). Case 1: The 57-year-old mother had a typical ASH pattern; her septal/posterior wall thickness ratio (IVST/LVPWT) was 2.5. Case 2: The 37-year-old daughter had basal septal hypertrophy. Case 3: The 32-year-old elder son had typical concentric hypertrophy. Case 4: The 30-year-old younger son had an episode of congestive heart failure, and showed DCM-like features with considerable dilatation and impaired wall motion of the left ventricle. The hypertrophic pattern in cardiomyopathies is thought to depend partially on the ages of the onset, or its evolution with aging.

Adult↗
PubMed1986

Isocholic acid formation from 7 alpha,12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid with human liver enzyme.

The formation of isocholic acid from 7 alpha, 12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid by human liver preparations was examined in vitro. Liver preparations were incubated with 7 alpha, 12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid at pH 7.4 in a phosphate buffer containing NADPH or NADH. The products formed were analyzed by gas chromatography and gas chromatography/mass spectrometry. Results showed that 7 alpha,12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid was reduced mainly to isocholic acid and to cholic acid in a smaller amount in the presence of NADPH, while it was reduced only to cholic acid in the presence of NADH. The reducing enzyme participating in the formation of isocholic acid was localized largely in the cytosol and had more specificity to the unconjugated form as substrate than to the conjugated forms. 3-Keto bile acid analogues, 3-keto-5 beta-cholanoic and 7 alpha-hydroxy-3-keto-5 beta-cholanoic acids were not reduced to the corresponding iso-bile acids by the cytosol in the same conditions used in the isocholic acid formation and the activity of the enzyme catalyzing the reduction of 7 alpha,12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid to isocholic acid was not inhibited by the addition of 3-keto-5 beta-cholanoic acid or 7 alpha-hydroxy-3-keto-5 beta-cholanoic acid to the reaction mixture. Furthermore, on column chromatography of Affi-Gel Blue, the peak of the enzyme catalyzing the reduction of 7 alpha,12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid to isocholic acid was clearly distinguished from that of the enzyme catalyzing the reduction of 3-keto-5 beta-cholanoic acid to isolithocholic acid and that of alcohol dehydrogenase. These results indicate that this enzyme catalyzing the reduction of 7 alpha,12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid to isocholic acid is different from the enzyme(s) catalyzing the reduction 3-keto-5 beta-cholanoic and 7 alpha-hydroxy-3-keto-5 beta-cholanoic acids to the corresponding iso-bile acids and from alcohol dehydrogenase, and has a stereospecific character for 7 alpha,12 alpha-dihydroxy-3-keto-5 beta-cholanoic acid.

Bile Acids and Salts↗
PubMed1986

Possible mechanism of generation of SEP far-field component in the brachial plexus in the cat.

By cutting the brachial plexus at a few levels on the side stimulated, it was verified that the first far-field component of SEPs with forepaw reference recording is generated in the brachial plexus in the cat. Incidentally, a reversal of the polarity of the earliest portion of the first component was observed with abduction of the upper arm to a high position on the side stimulated. X-ray photographs of the nerve course in such a high position disclosed that both the position and direction of the nerve course in the distal brachial plexus were changed substantially. On the other hand, bipolar derivations away from the bullfrog sciatic nerve volley revealed that a reversal of sign of the action potential could be observed by changing the direction and/or position of the nerve traveling impulse against two recording electrodes a long distance apart. These findings suggest that a reversal of polarity of the earliest portion of the first component in a high upper arm abducted position may be produced due to change in the direction and position of the nerve impulse against the two recording electrodes placed on the scalp and on the forepaw a along distance apart, that is, the forepaw electrode is neither the reference nor the indifferent, but is active to far-field components.

Action Potentials↗
PubMed1986

Prostaglandins and sodium balance during the reversal of chronic two-kidney, one clip hypertension in rats.

To determine the role of endogenous prostaglandins and sodium balance in the maintenance of high blood pressure in chronic two-kidney, one clip hypertension in rats, we studied the effect of indomethacin infusion on the reversal of hypertension by unclipping. Indomethacin was infused after control measurements, and blood pressure was monitored continuously in conscious rats. Parallel control experiments and sham operations were also performed. Inhibition of prostaglandin synthesis did not affect the postoperative course of blood pressure after the unclipping operation despite the marked decrease of urinary prostaglandin E excretion. The decrease of blood pressure after unclipping was significantly correlated with plasma renin activity prior to unclipping. Sodium balance was not significantly different between the experimental groups. These data indicate no major participation of prostaglandins in the reversal of chronic two-kidney, one clip hypertension, and suggest that the renin angiotensin system participates, at least in part, in the maintenance of high blood pressure in this model of hypertension.

Animals↗
PubMed1986

Urinary excretion of TXB2 after angiotensin converting enzyme inhibition in hypertensive patients.

Urinary excretion of thromboxane B2 (TXB2), a stable metabolite of thromboxane A2 (TXA2), was measured by radioimmunoassay in 7 essential hypertensive patients before and after a converting enzyme inhibitor, SQ 14225, administration. When a single oral dose of SQ 14225 (50mg) was given to 7 patients with essential hypertension, urinary excretion of TXB2 was increased significantly (from 58.9 +/- 18.1 to 116.1 +/- 20.7 pg/min, mean +/- SE, P less than 0.02) with simultaneous increase in plasma renin activity, urine volume, urinary sodium, urinary potassium and urinary excretion of PGE (from 58.8 +/- 12.8 to 135.1 +/- 30.0 pg/min, mean +/- SE, P less than 0.05). These results indicate that SQ 14225 stimulates vasoconstricting TXA2 production as well as vasodilating PGE production.

Adult↗
PubMed1986

Adenomatoid odontogenic tumor associated with calcifying epithelial odontogenic tumor.

A case of odontogenic tumor which contained areas diagnostic for both adenomatoid odontogenic tumor and calcifying epithelial odontogenic tumor arising in the upper left anterior region in a 17-year-old Japanese female is reported. The histopathological observation suggested that the lesion represented primarily adenomatoid odontogenic tumor in which multiple foci of calcifying epithelial odontogenic tumor had developed.

Adolescent↗
PubMed1986

Effects of sodium and angiotensin II on urinary active and inactive kallikrein in rats.

To assess possible relationships between sodium balance, angiotensin II (ANG II), and renal active and inactive kallikrein, we studied the effects of sodium loading with 1% NaCl and chronic ANG II infusion (900 micrograms/kg per day) on the urinary excretion of total and active kallikrein for 6 days in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Sodium loading produced a sustained increase in urinary total, active and inactive kallikrein excretion. Chronic infusion of ANG II induced a sustained increase in urinary total, active and inactive kallikrein excretion in rats on a regular diet. In rats loaded with sodium, however, ANG II did not induce any further changes in urinary kallikrein excretion. Thus, the present study suggests that both sodium loading and ANG II infusion might stimulate the synthesis of renal kallikrein. In addition, it is suggested that ANG II infusion might stimulate the synthesis of kallikrein, at least partly, via the same mechanism as sodium loading does.

Angiotensin II↗
PubMed1986

IgG1 antibodies to house dust mite (Dermatophagoides farinae) and late asthmatic response.

Thirteen asthmatic patients sensitive to mite were challenged by inhalation of an extract of mites (Dermatophagoides farinae). Seven showed dual bronchial reactions and 5 showed isolated immediate responses. No patient showed an isolated late reaction. Six of seven patients with dual reaction had higher IgG1 antibodies than the 5 patients with isolated immediate reaction when examined before the challenge. A similar result was obtained in terms of levels of immune complex. IgE, IgG4 and total IgG antibodies were not predictive for late reaction. These results suggest that there is a close correlation of the presence of high IgG1 antibodies with a propensity to develop late asthmatic responses. The meaning of this observation is discussed.

Adult↗
PubMed1986

Effect of atrial natriuretic factor on angiotensin II-induced hypertension in rats.

To assess the physiological role of atrial natriuretic factors in blood pressure regulation, we studied the effect of chronic infusion of a synthetic atrial natriuretic factor of 25 amino acid residues (Arg 102-Tyr 126) in rats with angiotensin II-induced hypertension. Rats were studied while on a normal sodium diet or during sodium loading with 1% NaCl solution used as drinking water. Systolic blood pressure decreased slightly during combined infusion of synthetic atrial natriuretic factor, 150 micrograms/kg/day, and angiotensin II, 900 micrograms/kg/day. This effect was sustained for 3 days in rats receiving a regular sodium intake (p less than 0.01) and during sodium loading (p less than 0.01). Administration of synthetic atrial natriuretic factor to rats made hypertensive by a 3-day infusion of angiotensin II reduced blood pressure slightly, but not to control levels, and this effect was sustained for the remaining 3 days of the experiment in both dietary groups. These results indicate that a nonhypotensive dose of synthetic atrial natriuretic factor can modulate the vasopressor effect of angiotensin II. Thus, the attenuating effect may be involved in blood pressure regulation independently of sodium metabolism, although its actual physiological importance remains undetermined.

Angiotensin II↗
PubMed1986

Atrial natriuretic factor and cyclic guanosine 3',5'-monophosphate in vascular smooth muscle.

To elucidate the molecular mechanism of the vascular action of atrial natriuretic factor (ANF), we investigated the effects of synthetic ANF and sodium nitroprusside on the levels of intracellular cyclic nucleotides and prostacyclin (measured as its stable metabolite 6-keto-prostaglandin F1 alpha) in cultured vascular smooth muscle cells from rat mesenteric artery and, in some experiments, from rat renal artery. Both ANF and sodium nitroprusside increased intracellular cyclic guanosine 3',5'-monophosphate (cGMP) levels in a dose-dependent manner but did not affect cyclic adenosine 3',5'-monophosphate levels or 6-keto-prostaglandin F1 alpha synthesis. The stimulatory effect of ANF and sodium nitroprusside on cGMP levels were additive. Neither the deprivation of extracellular Ca2+ nor calcium entry blockers affected ANF-stimulated cGMP levels. Preincubation of ANF or sodium nitroprusside with kallikrein attenuated only the effect of ANF on cGMP levels. The effect of kallikrein was abolished by serine protease inhibitors. In contrast, the oxidant methylene blue inhibited the effect of sodium nitroprusside on cGMP levels, but not that of ANF. The stimulatory effect of ANF on cGMP levels was greater in cells from renal artery than in those from mesenteric artery. These results in cultured vascular smooth muscle cells further support the hypothesis that cGMP mediates the vasorelaxant action of ANF.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Effects of acute water load, hypertonic saline infusion, and furosemide administration on atrial natriuretic peptide and vasopressin release in humans.

A new specific RIA for alpha-human atrial natriuretic hormone (alpha hANP) was used to determine whether changes in plasma volume elicited by acute water loading, hypertonic saline infusion, and furosemide administration caused changes in ANP release and resultant changes in renal and cardiovascular function in normal subjects. In addition, changes in plasma arginine vasopressin (AVP), PRA, and aldosterone concentrations were studied simultaneously. Mean plasma alpha hANP and AVP levels were 51.3 +/- 16.0 (+/- SE) and 3.1 +/- 0.6 pg/ml, respectively, in the basal state. Plasma alpha hANP rose to 77.8 +/- 27.6 in response to a 4.5% increase in plasma volume induced by water loading, increased further to 134.1 +/- 28.9 in response to a 23% volume increase induced by hypertonic saline, and fell to 70.2 +/- 15.8 pg/ml in response to a decrease in plasma volume after furosemide treatment (P less than 0.01-0.05). On the other hand, plasma AVP fell to 1.8 +/- 0.1 pg/ml after the water load, rose to 4.1 +/- 0.6 after hypertonic saline, and rose further to 5.8 +/- 0.8 pg/ml after furosemide (P less than 0.01-0.05). Water and hypertonic saline loading decreased PRA, but plasma aldosterone concentrations did not change; subsequent furosemide administration increased both (P less than 0.01-0.05). Arterial pressure and heart rate did not change significantly. Increases in urinary Na excretion and osmolar clearances were associated with a rise in plasma alpha hANP after water loading and hypertonic saline infusion (P less than 0.01-0.05), but changes in urine flow were mainly associated with alterations in AVP release. associated with alterations in AVP release.

Adult↗
PubMed1986

Antihypertensive effect of synthetic atrial natriuretic factor in vasopressin-infused rats.

To assess the pathophysiological role of atrial natriuretic factors in the regulation of blood pressure, we studied the effect of chronic infusion of a synthetic atrial natriuretic factor of 25 amino-acid residues on blood pressure and sodium-water excretion. Experimental subjects were rats with hypertension made by chronic infusion of vasopressin on regular intakes of sodium or on sodium loading with 1% NaCl as drinking water. When a subdepressor dose (150 micrograms/kg/day) of synthetic atrial natriuretic factor was delivered via an osmotic minipump into the jugular vein simultaneously with 7.2 U/kg/day of vasopressin infused intraperitoneally by another osmotic minipump, the expected elevation of systolic blood pressure was completely inhibited. This was not accompanied by any changes in urine volume and urinary sodium excretion. The antihypertensive effect was sustained throughout the experimental period lasting 3 days in rats on regular sodium intake (p less than 0.01) or on sodium loading with 1% NaCl as drinking water (p less than 0.01). These results indicate that a subdepressor dose of synthetic atrial natriuretic factor can modulate the vasopressor effect of vasopressin. Therefore it is suggested that an atrial natriuretic factor may be involved in the regulation of blood pressure via its antagonizing effect to vasopressin.

Animals↗
PubMed1986

Chronic effect of a synthetic atrial natriuretic factor on the development of hypertension in young spontaneously hypertensive rats.

The chronic effect of a synthetic atrial natriuretic factor (ANF) of 25 amino acid residues on the development of hypertension in the 6-week-old spontaneously hypertensive rat (SHR) was assessed. The SHR, on regular diets or given 1% NaCl solution for drinking, were continuously infused with ANF (150 micrograms/kg per day) or vehicle (physiological saline) as controls for up to 14 days. The ANF attenuated transiently the development of hypertension in the sodium-loaded SHR, but the blood pressure returned to control levels by day 5. In SHR on regular diets ANF did not affect the development of hypertension. In addition, ANF did not induce any significant changes in urine volume, fluid intake, urinary sodium and potassium excretion, heart rate, heart weight or haematocrit in young SHR on either normal or increased sodium intake when compared with those in vehicle-infused SHR. These results suggest that ANF may exert some role via a vascular effect at the early stage of development of hypertension in young sodium-loaded SHR.

Animals↗