Search PubMed⌕ Search

Biomedical subjects

Y Kuribayashi

Publications and source records attributed to Y Kuribayashi.

At least 37 records · Page 2Linked to original sources
PubMed1994

Hypertension induced by a nonpressor dose of angiotensin II in kininogen-deficient rats.

Brown Norway Katholiek rats with very low levels of plasma kininogens excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats (132 +/- 2 mmHg, n = 7) was not different from that of normal rats. Angiotensin II (Ang II) (20 micrograms/d SC) from 7 weeks of age for 2 weeks with a micro-osmotic pump caused significant increases in blood pressure (181 +/- 5 mm Hg, n = 7, 9 weeks old) in the deficient rats, although the same treatment induced no blood pressure increase in the normal rats. Also during this period, the deficient rats had significantly higher heart rates, tended to excrete less urinary sodium, and showed significantly higher sodium levels in serum, erythrocytes, and cerebrospinal fluid compared with the normal rats. Ang II increased urinary excretion of aldosterone in both deficient and normal rats (P < .05). Spironolactone treatment (50 mg/kg per day) for 7 days in deficient rats restored blood pressure and heart rate to normal levels and significantly reduced sodium levels in erythrocytes and cerebrospinal fluid. Subcutaneous infusion of bovine low-molecular-weight kininogen with an osmotic pump in Ang II-treated deficient rats induced significant reductions in blood pressure, heart rate, and erythrocyte sodium levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 in Ang II-treated normal rats induced a hypertensive response in parallel with significant increases in heart rate and erythrocyte sodium level. These results suggest that the lack of kinin generation observed in the kininogen-deficient rats may cause the hypertensive response during the administration of a nonpressor dose of Ang II mainly through sodium retention probably caused by aldosterone release.

Aldosterone↗
PubMed1994

Diuretic and natriuretic effect of ebelactone B in anesthetized rats by inhibition of a urinary carboxypeptidase Y-like kininase.

Ebelactone B (EB) (10(-7)-10(-5) M) inhibited dose-dependently carboxypeptidase (CP) Y-like exopeptidase, one of the major kininases separated from rat urine, whereas it inhibited neither CPA, CPB or neutral endopeptidase (NEP). Degradation of bradykinin (BK) to BK-(1-8) in rat urine was completely inhibited by EB (10(-5) M) with the increased generation of BK-(1-7). Intraduodenal administration of EB (3 mg/kg) to anesthetized rats caused marked diuresis (by 110%) and natriuresis (130%), in parallel with the increase in urinary kinin levels (110%). Intravenous infusion of a BK antagonist, Hoe140 (3 mg/kg/hr), strongly blocked both EB-induced diuresis and natriuresis. EB may be a novel type of diuretic and natriuretic agent that acts by increasing urinary kinin levels.

Amino Acid Sequence↗
PubMed1994

Effects of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1- benzopyran-6yl-hydrogen phosphate] potassium salt on cerebral energy state and consciousness recovery following transient forebrain ischemia in gerbils.

Effect of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H -1- benzopyran-6yl-hydrogen phosphate] potassium salt (EPC-K1, CAS 127061-56-7), a diester of alpha-tocopherol and ascorbic acid, on transient cerebral ischemia was studied in Mongolian gerbils. Cerebral energy metabolism and intracellular pH (pHi) were estimated employing in vivo 31P nuclear magnetic resonance (NMR) spectroscopy. Intraperitoneal injection of EPC-K1 (5 or 10 mg/kg) prior to ischemia significantly ameliorated pHi reduction in a dose dependent manner during ischemia. After reperfusion, energy and pHi recoveries were significantly faster in the EPC-K1 groups than in the control group. EPC-K1 (10 mg/kg) significantly reduced the extent of cerebral edema. Moreover, administration of EPC-K1 immediately after reperfusion significantly shortened the consciousness recovery in a dose dependent manner. The results suggest that EPC-K1 may exert protective effects on ischemic brain and may have therapeutic value in ischemic stroke.

Animals↗
PubMed1993

Poststatin, a novel inhibitor of bradykinin-degrading enzymes in rat urine.

Incubation of bradykinin with rat urine resulted in the successive degradation of bradykinin to bradykinin-(1-8), bradykinin-(1-7) and bradykinin-(1-6). In contrast, in rat plasma, bradykinin was degraded via either bradykinin-(1-8) or bradykinin-(1-7) to bradykinin-(1-5). Phosphoramidon (1 mM) partially inhibited the degradation of bradykinin by rat urine, as well as the conversion of bradykinin-(1-7) to bradykinin-(1-6). D,L-2-Mercaptomethyl-3-guanidinoethylthiopropanoic acid (1 mM) and captopril (1 mM) did not have a significant effect on any of the degradation steps in rat urine. In contrast, all of the degradation steps in urine, namely, from bradykinin to bradykinin-(1-8), from bradykinin-(1-8) to bradykinin-(1-7) and from bradykinin-(1-7) to bradykinin-(1-6), were markedly inhibited by poststatin (1 mM), even though this compound was reported originally to be a novel inhibitor of post-proline cleaving enzyme. Poststatin (1 mM) did not inhibit the degradation of bradykinin in rat plasma. These results indicate that poststatin is an effective inhibitor of kinin-degrading enzyme in rat urine.

Amino Acid Sequence↗
PubMed1993

High sensitivity to salt in kininogen-deficient brown Norway Katholiek rats.

Brown Norway Katholiek rats, which have very low levels of plasma kininogens, excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats fed low (0.3%) NaCl diets (131 +/- 4 mm Hg, n = 12) was not different from that in normal rats. Two percent NaCl diets given from 7 weeks of age for 4 weeks caused rapid increases in blood pressure (167 +/- 4 mm Hg, n = 12, 9 weeks old) in deficient rats, although the same diets induced no blood pressure increase in normal rats. Urinary excretion of active kallikrein and prokallikrein remained constant in both rat groups throughout NaCl loading. During this period, the deficient rats secreted less urine (9 weeks old, P < .05) and less urinary sodium (11 weeks old, P < .05). Serum levels of sodium in deficient rats were higher (P < .05) than in normal rats at 9 weeks of age. Intracellular concentrations of sodium in the erythrocytes of deficient rats were higher (P < .05) than in normal rats throughout NaCl loading. Subcutaneous infusion of bovine low molecular weight kininogen with an osmotic pump in NaCl-loaded deficient rats induced a reduction (P < .01) in blood pressure and increases (P < .05) in urine volume and urinary sodium and kinin levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 or of aprotinin in NaCl-loaded normal rats induced a hypertensive response. This antagonist treatment reduced urine volume and urinary sodium. These results indicate that the lack of kinin generation observed in the kininogen-deficient rats was related through sodium retention to the hypertensive response to NaCl loading.

Aging↗
PubMed1992

[A case of significant, non-neoplastic, ovarian hypertestosteronism].

A 24-year-old female with significant ovarian hypertestosteronism, who responded well both to gonadotropin releasing hormone (GnRH) agonist and cyclic administration of estrogen and gestagens in terms of suppressing circulating testosterone levels is reported. The patient's menstrual periods had been regular since menarche at the age of 12 until she became amenorrheic at the age of 20. She visited our facility in November 1988 after receiving three cycles of estrogen and gestagen replacement therapy from a previous physician which caused withdrawal bleeding. Clomiphen citrate reportedly failed to induce apparent ovulation. On her first visit with us, she was 160 cm tall weighing 47 kg with apparent hoarseness but not with hirsutism. Pelvic examination revealed significant clitoromegaly but otherwise normal external and internal genitalia. Laparoscopic examination disclosed that her uterus appeared to be normal with bilateral ovaries relatively small (4 x 4 x 3 cm) without tumorous or polycystic appearance. Histological examination of her ovaries obtained at laparoscopy showed several primary follicles with mild infiltration of the stromal cells. No thickened tunica albuginea or cystic formation were observed. These findings did not support either polycystic ovary or hyperthecosis. Serum testosterone (T) levels were extremely high (7.1 ng/ml), while serum androstenedione levels were only slightly above normal range (3.1 ng/ml). Urine 17-KS excretion was slightly increased (6.1 mg/day), while 17-OHCS output was within normal range (4.0 mg/day). Basal serum LH and FSH levels were within normal range and LH pulse frequency was reduced to 1 in 4 hours. Administration of dexamethasone 1 mg/day for 2 days did not suppress circulating T and free T levels but lowered serum cortisol concentration and urine excretion of 17-OHCS. Blood glucose and insulin levels were within normal limits and their responses to oral glucose administration were normal. Abdominal and pelvic ultrasonography and computed tomography as well as adrenal scintigraphy did not reveal any tumorous lesions in bilateral adrenals and ovaries. Administration of GnRH agonist, Buserelin 900 micrograms/day, suppressed circulating T concentrations to 0.7 ng/ml in 8 days, while it had no significant effects on DHEA and DHEA-S levels. After 16 weeks of Buserelin administration, ovulation was successfully induced by hMG administration. Cyclic estrogen and gestagen replacement therapy by Kaufmann's schedule for 2 cycles also suppressed serum T levels to normal, female range. Thus, the present case represents non-neoplastic, non-PCO, ovarian hypertestosteronism which responded well both to GnRH agonist and estrogen and gestagen replacement therapy in terms of lowering circulating T levels.

Adult↗
PubMed1992

In vitro studies on the influence of L-ascorbic acid 2-[3,4-dihydro- 2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6yl-hy drogen phosphate] potassium salt on lipid peroxidation and phospholipase A2 activity.

The effects of L-ascorbic acid 2-[3,4-dihydro-2,5,7,8-tetramethyl-2- (4,8,12-trimethyltridecyl)-2H-1-benzopyran-6yl-hydrogen phosphate] potassium salt (EPC-K1, CAS 127061-56-7), a new compound for ischemia-reperfusion injuries, on lipid peroxidation and phospholipase A2 activity were studied in vitro using rat brain homogenates and human plasma. EPC-K1 inhibited phospholipase A2 activity in human plasma in a concentration-dependent manner (IC50 = 7.3 x 10(-4) mol/l), whereas a mixture of alpha-tocopherol and ascorbic acid did not exhibit this effect. In rat brain homogenates, EPC-K1 also inhibited lipid peroxidation in a concentration-dependent manner (IC50 = 2.3 x 10(-6) mol/l). alpha-Tocopherol was less active than EPC-K1. These properties of EPC-K1 suggest that EPC-K1 may prove useful in the treatment of ischemia-reperfusion injuries.

Animals↗
PubMed1988

[The development of a new operating hysteroscopic fiberscope and its clinical application].

A new operating hysteroscopic fiberscope consisting of soft and rigid parts (4.8mm outer diameter) was developed with the support of Fuji Photo Optical Company. The working part of the scope can be divided into three sections: A flexible soft front section, a rotary rigid middle section and a flexible self retained semirigid rear section. With these functional parts the intrauterine target can be approached directly to perform the following operations. 1. Directed intrauterine biopsy. Thirty-five patients diagnosed as having endometrial polyp (13), submucous myoma (8), endometrial hyperplasia (4), endocervical polyp (3), endometrial carcinoma (2) and others (5) underwent direct biopsy with hysteroscopic control. No cervical dilatation or anesthesia was necessary. 2. Transcervical recanalization. In six cases of proximal tubal occlusion, a ureteral catheter or a percutaneous coronary balloon angiocatheter was introduced into the tubal ostium of the obstructed side to resolve the occlusion successfully with concomitant laparoscopy. 3. Hysteroscopic chorionic villus sampling. Chorionic villus sampling was performed with a ureteral catheter under direct hysteroscopic control and ultrasound guidance in eighteen pregnant women at from seven to fourteen gestational weeks. In fifteen cases, the samplings were performed satisfactory. 4. Removal of a lost IUD. Three cases of lost IUD underwent hysteroscopic removal without difficulty. Our results have proved that this scope is a very useful tool for intrauterine operations.

Adult↗
PubMed1987

In vivo measurements of intra- and extracellular Na+ and water in the brain and muscle by nuclear magnetic resonance spectroscopy with shift reagent.

The introduction of new paramagnetic shift reagents in the nuclear magnetic resonance (NMR) method has made it possible to distinguish intra- and extracellular ions in tissues or organs in vitro. We measured the intra- and extracellular 23Na and 1H in vivo in the gerbil brain and skeletal muscle by NMR spectroscopy employing the shift reagent, dysprosium triethylenetetraminehexaacetate (Dy[TTHA]3-). Without Dy(TTHA)3-, the 23Na and 1H signals were seen only as single peaks, but gradual intravenous infusion of Dy(TTHA)3- separated these signals into two peaks, respectively. The unshifted peaks reflected the intracellular 23Na and 1H signals, while the shifted peaks reflected the extracellular signals. In the brain spectra, an additional small peak, which represented intravascular signals, was detected and its intensity increased after injection of papaverine hydrochloride. The present method is advantageous over the microelectrode technique because of its nondestructiveness and its capability for obtaining intra- and extracellular volume information from measurements of the 1H spectra, the peaks of which reflect the intra- and extracellular water amounts. The intracellular Na+ increase associating with increased cellular volume after ouabain in the muscle was clearly visualized by this method. The technique is clearly of use for physiological and pathophysiological studies of organs.

Aging↗
PubMed1985

Activation of urinary inactive kallikrein by an extract from the rat kidney cortex.

Activation of purified urinary inactive kallikrein by an extract from the rat kidney cortex was investigated. The extract produced a dose-dependent activation of the inactive kallikrein and the optimum pH for this activation was 5.0. Marked depression of the activation was observed when the extract was pre-incubated with E-64, p-CMB and iodoacetate, but not with DFP, PMSF or pepstatin A. The molecular weight of the inactive kallikrein (Mr 44,000) was reduced to 38,000 by treatment with the extract, this molecular weight value being identical with that of urinary active kallikrein. These results indicate that the rat kidney cortex contains a protease catalyzing conversion of urinary inactive kallikrein into its active form, and that the protease has properties compatible with those of a thiol protease, but not of trypsin which has been used as a tool for the activation of urinary inactive kallikrein. The thiol protease is probably one of regulators of the kallikrein-kinin system in the kidney.

Animals↗