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Biomedical subjects

Y Oiso

Publications and source records attributed to Y Oiso.

At least 145 records · Page 8Linked to original sources
PubMed1992

Regulation of proliferation by vasopressin in aortic smooth muscle cells: function of protein kinase C.

AIM: To investigate the effect of arginine vasopressin-stimulated prostaglandin synthesis and the activation of protein kinase C on DNA synthesis in rat aortic smooth muscle cells. METHODS: The effects of arginine vasopressin on the release of arachidonic acid and the synthesis of prostaglandin (PG) E2 and prostacyclin (PGI2) were determined. The effects of 12-o-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C-activating phorbol ester, and of 1-oleoyl-2-acetylglycerol, a specific activator of protein kinase C, were evaluated in cultured rat aortic smooth muscle cells. The effects of arginine vasopressin and prostaglandins on the progression from the late G1 to the S phase of the cell cycle were evaluated by measuring the DNA synthesis, and the effects of TPA on them were evaluated. RESULTS: Arginine vasopressin dose-dependently stimulated arachidonic acid release. TPA and 1-oleoyl-2-acetylglycerol dose-dependently increased the vasopressin-induced arachidonic acid release. Vasopressin stimulated the synthesis of both PGE2 and PGI2. TPA increased the vasopressin-stimulated prostaglandin synthesis as well as the arachidonic acid release. Vasopressin, added at the G0/G1 phase of the cell cycle, stimulated DNA synthesis of aortic smooth muscle cells. Exogenous PGE2 and PGI2 inhibited the DNA synthesis and showed maximum inhibition when added at the late G1 phase. TPA alone, added at the late G1 phase, reduced the DNA synthesis stimulated by vasopressin at the G0/G1 phase to about 45%, but vasopressin alone, added at the late G1 phase, had little effect. However, with TPA pretreatment, vasopressin significantly suppressed the DNA synthesis by about 70%. Staurosporine, a protein kinase C inhibitor, reduced the suppression by TPA alone or by vasopressin with TPA pretreatment almost to the control level. Indomethacin, a cyclo-oxygenase inhibitor, reduced the suppression by vasopressin with TPA pretreatment almost to the level of TPA alone. CONCLUSIONS: These results suggest that arginine vasopressin has a suppressive effect on DNA synthesis in rat aortic smooth muscle cells by inhibiting progression from the late G1 into the S phase of the cell cycle through the synthesis of PGE2 and PGI2, and that protein kinase C acts as an amplifier of this mechanism.

Animals↗
PubMed1991

Centrally administered galanin inhibits osmotically stimulated arginine vasopressin release in conscious rats.

The effect of centrally administered galanin on arginine vasopressin (AVP) release was investigated in conscious rats. Intracerebroventricular injection of porcine galanin suppressed hypertonic saline-induced increase in plasma AVP in a dose-dependent manner (12.5-100 pmol/rat) at 10 min after the injection. Pretreatment with subcutaneous injection of naloxone (1 mg/100 g b.wt.) partially blocked the galanin-induced effect on plasma AVP. These results suggest that central galanin inhibits osmotically stimulated AVP release and endogenous opioids are, at least in part, involved in the mechanism.

Animals↗
PubMed1991

Molecular cloning and primary structure of rat thyroxine-binding globulin.

Rat thyroxine-binding globulin (TBG) cDNAs were isolated from a rat liver cDNA library by using a human TBG cDNA as a probe. From two overlapping cDNA inserts, an aligned cDNA sequence of 1714 nucleotides was obtained. There was 70% homology with human TBG cDNA over the span of 1526 nucleotides. In order to confirm that the cloned cDNA encodes rat TBG and to localize the NH2-terminal amino acid of the mature molecule, the protein was purified by affinity chromatography and subjected to direct protein microsequencing. The NH2-terminal amino acid sequence was identical with that deduced from the nucleotide sequence. The rat TBG cDNA sequenced consisted of a truncated leader sequence (35 nucleotides), the complete sequence encoding the mature protein (1194 nucleotides) and the 3'-untranslated region (485 nucleotides), containing two polyadenylation signals. It was deduced that rat TBG consists of 398 amino acids (Mr = 44,607), three NH2-terminal residues more than human TBG, with which it shares 76% homology in primary structure. Of the six potential N-glycosylation sites, four are located in conserved positions compared to human TBG. Northern blot analysis of rat liver revealed an approximately 1.8-kilobase TBG mRNA. Its amount increased markedly following thyroidectomy and decreased with thyroxine treatment in a dose-dependent manner.

Amino Acid Sequence↗
PubMed1991

Aggravation of subclinical diabetes insipidus during pregnancy.

BACKGROUND: Transient polyuria and polydipsia during pregnancy are rare, and their cause is not entirely clear. Possible explanations include the exacerbation of preexisting abnormalities in the secretion or action of vasopressin and abnormally large increases in plasma vasopressinase activity. METHODS: We studied two women in whom overt polyuria and polydipsia developed during the third trimester of pregnancy and disappeared after delivery. The secretion and action of vasopressin were studied both when the women had polyuria and polydipsia and later, when their water intake and urine volume were normal. RESULTS: One patient had partial nephrogenic diabetes insipidus. She had little increase in urine osmolality in response to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopressin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulated plasma vasopressin concentrations were high (16.5 to 203.4 pmol per liter) before and during hypertonic-saline infusion 30 months post partum. The other patient had partial neurogenic diabetes insipidus. She had subnormal basal plasma vasopressin concentrations, a subnormal increase in the plasma vasopressin level and a subnormal decrease in urine flow in response to the administration of vasopressin, and a normal response to desmopressin. After pregnancy, when her urine volume was normal, she had no increase in plasma vasopressin in response to hypertonic-saline infusion, but she had a normal rise in the plasma vasopressin level and a normal renal response to vasopressin administration. CONCLUSIONS: Pregnancy may unmask subclinical forms of both nephrogenic and neurogenic diabetes insipidus. This exacerbation may result from both increased vasopressinase activity and diminished renal responsiveness to vasopressin.

Adult↗
PubMed1991

Effects of hypergravity on proliferation and differentiation of osteoblast-like cells.

We investigated the effects of hypergravity on DNA synthesis and alkaline phosphatase (ALP) activity in cloned osteoblast-like cells, MC3T3-E1. Hypergravity (5 x g) stimulated DNA synthesis in these cells in a time-dependent manner and increased it approximately up to 150% of that of the control (1 x g). 12-O-Tetra-decanoylphorbol-13-acetate (TPA), a protein kinase C activator, and insulin-like growth factor I (IGF-I) enhanced DNA synthesis additively with hypergravity (5 x g). An increase in ALP activity induced by 10% fetal calf serum (FCS) was suppressed by hypergravity (2 x g, 5 x g). Five x g completely suppressed the increase in ALP activity. TPA and hypergravity (2 x g) suppressed the increase in ALP activity induced by FCS additively. Hypergravity (5 x g) showed no significant effect on cAMP nor cGMP production in these cells, but increased prostaglandin E2 (PGE2) production. Exogenous PGE2 stimulated DNA synthesis in these cells but had little effect on 10% FCS-induced ALP activity. These results suggest that hypergravity stimulates proliferation but suppresses differentiation of osteoblast-like cells through a pathway independent of the activation of protein kinase C and the production of cyclic nucleotides, and that hypergravity and IGF-I stimulate proliferation of these cells through an independent signal transduction pathway. Moreover, our data strongly suggest that PGE2 mediates the signalling of hypergravity on the proliferation of osteoblast-like cells.

Alkaline Phosphatase↗
PubMed1991

Possible involvement of endogenous opioid peptides in the inhibition of arginine vasopressin release by gamma-aminobutyric acid in conscious rats.

We examined the effects of gamma-aminobutyric acid (GABA) and naloxone, a potent opioid antagonist, on arginine vasopressin (AVP) secretion in conscious rats in order to study the relationship of GABA and endogenous opioid peptides in the regulation of AVP secretion. Intracerebroventricular administration of GABA caused a time- and dose-dependent decrease in the plasma concentration of AVP that was elevated by hypertonic saline injection, whereas it did not affect the basal AVP. Pretreatment with naloxone (10 mg/kg) significantly attenuated the inhibitory effect of GABA (100 micrograms) on AVP release. These results suggest that GABA produces an inhibition of AVP release stimulated by hypertonic saline, and that this inhibitory effect may be mediated at least in part by the endogenous opioid systems.

Animals↗
PubMed1991

A single base substitution in the coding region for neurophysin II associated with familial central diabetes insipidus.

To elucidate the molecular mechanism of familial central diabetes insipidus (FDI), we sequenced the arginine vasopressin-neurophysin II (AVP-NPII) gene in 2 patients belonging to a pedigree that is consistent with an autosomal dominant mode of inheritance. 10 patients with idiopathic central diabetes insipidus (IDI) and 5 normals were also studied. The AVP-NPII gene, locating on chromosome 20, consists of three exons that encode putative signal peptide, AVP, NPII, and glycoprotein. Using polymerase chain reaction, fragments including the promoter region and all coding regions were amplified from genomic DNA and subjected to direct sequencing. Sequences of 10 patients with IDI were identical with those of normals, while in 2 patients with FDI, a single base substitution was detected in one of two alleles of the AVP-NPII gene, indicating they were heterozygotes for this mutation. It was a G----A transition at nucleotide position 1859 in the second exon, resulting in a substitution of Gly for Ser at amino acid position 57 in the NPII moiety. It was speculated that the mutated AVP-NPII precursor or the mutated NPII molecule, through their conformational changes, might be responsible for AVP deficiency.

Arginine Vasopressin↗
PubMed1991

Nucleotide deletion resulting in frameshift as a possible cause of complete thyroxine-binding globulin deficiency in six Japanese families.

Complete T4-binding globulin deficiency (TBG-CD) is inherited in an X-linked fashion. A nucleotide substitution has been shown to cause this hereditary condition in caucasians of French Canadian origin. Heterogeneity in molecular mechanisms for TBG-CD has also been reported. Genomic DNA from a Japanese male exhibiting TBG-CD was subjected to polymerase chain reaction, and the generated DNA fragments were sequenced. A single nucleotide deletion was found in the first base of the codon for amino acid 352 of the common-type TBG molecule. This mutation causes a frameshift in translation and premature termination. Compared with common-type TBG, the mutated polypeptide results in 1) 22 different amino acids on its carboxy-terminus, 2) a 22-amino acid truncation, and 3) the absence of a potential N-linked glycosylation site. These alterations may lead to profound changes in the secondary and tertiary structures of the molecule. To ascertain the presence of this nucleotide deletion in the genomic DNA of affected subjects, a mutated primer was designed which together with the nucleotide deletion produced a new endonuclease restriction site in the polymerase chain reaction fragment. Results revealed the presence of the mutation in genomic DNA of the subject, and his mother was shown to have both mutant and normal alleles. The same mutation was also detected in five other unrelated families carrying TBG-CD. This mutation may be frequent in Japanese subjects with TBG-CD.

Amino Acid Sequence↗
PubMed1991

Prolactin secretion in patients with idiopathic diabetes insipidus.

It has been demonstrated that hyperprolactinemia is sometimes present even in patients with idiopathic diabetes insipidus (DI). In this study, we examined the responses of serum prolactin (PRL) to hypertonic saline infusion and TRH injection in 11 patients with idiopathic DI diagnosed by clinical examinations. Serum sodium in these patients (147.5 +/- 3.2 mEq/L) was significantly higher at baseline than in normal subjects (139.7 +/- 2.4 mEq/L). The plasma arginine vasopressin (AVP) level was significantly lower in DI (0.42 +/- 0.24 pg/ml) at baseline than in normal subjects (2.53 +/- 1.03 pg/ml). However, the serum PRL level in both groups did not differ significantly except in one patient with idiopathic DI (35.6 ng/ml). There was no significant correlation between the basal serum sodium and basal serum PRL in either group. After an infusion of hypertonic saline, the serum sodium level gradually increased to 155.6 +/- 3.4 mEq/L in DI and to 146.5 +/- 4.3 mEq/L in the normal subjects. However, this increase did not affect PRL secretion in either group. PRL response to TRH was essentially normal in all patients with idiopathic DI. These results indicate that the secretion of PRL is not generally affected by chronic mild hypernatremic hypovolemia in the patients with idiopathic DI.

Adolescent↗
PubMed1991

Possible coupling of prostaglandin E2 receptor with pertussis toxin-sensitive guanine nucleotide-binding protein in osteoblast-like cells.

In cloned osteoblast-like cells, MC3T3-E1, prostaglandin E2 (PGE2) stimulated the formation of inositol phosphates in a dose-dependent manner in the range between 10 nM and 10 microM. Pertussis toxin inhibited the effect of PGE2 dose-dependently in the range between 1 ng/ml and 1 micrograms/ml. In the cell membranes, pertussis toxin catalyzed ADP-ribosylation of a protein with an Mr of about 40,000. Pretreatment of membranes with 10 microM PGE2 in the presence of 2.5 mM MgCl2 and 100 microM GTP markedly attenuated this pertussis toxin-catalyzed ADP-ribosylation of the protein in a time-dependent manner. G12 was detected in these cells by immunoblotting with purified anti-G12 alpha antibodies. The results indicate the possible coupling of PGE2 signalling with pertussis toxin-sensitive GTP-binding protein, which is probably G12, in osteoblast-like cells.

Cells, Cultured↗
PubMed1991

[Clinical assessment of posterior pituitary function by measurement of unextracted random urine].

To evaluate posterior pituitary function without any provocative examination, vasopressin (AVP) concentrations of random urine were measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). No apparent interference for the AVP measurement in unextracted urine was seen after appropriate dilution of urine sample. Urinary AVP did not degenerate at least for 24 hr at room temperature. AVP concentration of random urine was significantly correlated with AVP excretion in 24hr-urine in normal subjects. In 25 patients with neurogenic diabetes insipidus diagnosed by hypertonic saline infusion test, the AVP concentration in random urine was less than 13 pg/mg Cr. In approximately 1% of the normal subjects the urinary AVP level was below this range. Therefore, more intensive examinations should be planned to rule out the failure of AVP secretion in the case of such low AVP level in random urine. We also investigated the physiological changes in AVP secretion in 815 children and 352 pregnant women by measurement of urinary AVP. Even a large number of samples could be measured using this simple procedure.

Adolescent↗
PubMed1990

Involvement of pertussis toxin-sensitive GTP-binding protein in prostaglandin F2 alpha- induced phosphoinositide hydrolysis in osteoblast-like cells.

Prostaglandin F2 alpha (PGF2 alpha) stimulated the formation of inositol phosphates in a dose-dependent manner in cloned osteoblast-like MC3T3-E1 cells. This reaction was markedly inhibited dose-dependently by pertussis toxin. In the cell membranes, pertussis toxin-catalyzed ADP-ribosylation of a 40-kDa protein was significantly attenuated by pretreatment of PGF2 alpha. These results suggest that pertussis toxin-sensitive GTP-binding protein is involved in the coupling of PGF2 alpha receptor to phospholipase C in these cells.

Animals↗
PubMed1990

Plasma osmolality and exocrine pancreatic secretion.

To confirm the influence of plasma osmolality on exocrine pancreatic secretion, hypertonic saline (4% saline) was given intravenously to dogs with gastric and pancreatic fistulae. Intravenous administration of hypertonic saline caused a reduction of pancreatic juice flow and bicarbonate output, but did not alter protein output stimulated by secretin and cerulein. The changes of pancreatic juice flow(X) exhibited negative correlations with the changes in plasma osmolality(Y) (Y = -2.2X + 6.4, r = -0.74, p less than 0.01). Plasma osmolality and plasma vasopressin level were measured simultaneously. Plasma osmolality was elevated from 292 to 315 mOsm/kg with concurrent increase of plasma vasopressin level from 2.4 to 19.6 pg/mL. On the other hand, exogenous administration of vasopressin inhibited pancreatic juice flow and bicarbonate output dose-dependently. In conclusion, elevation of plasma osmolality decreased exocrine pancreatic secretion stimulated by secretin and cerulein, and vasopressin may play an important role in its mechanism.

Animals↗
PubMed1990

Osmoregulation of plasma vasopressin in myxedema.

We studied osmoregulation of plasma vasopressin (AVP) in eight patients with untreated myxedema due to primary hypothyroidism. All patients had severe thyroid hormone deficiency due to chronic thyroiditis and had been receiving no medication at the time of this study. AVP release was defined by 5% hypertonic saline infusion test in all patients, and urinary diluting capacity was estimated by the iv water-loading tests in five patients. Plasma AVP was measured by sensitive and specific RIA. The mean basal plasma AVP level in the patients (0.5 +/- 0.1 pmol/L) was significantly lower (P less than 0.01) than that in normal adults (2.5 +/- 0.5 pmol/L). During hypertonic saline infusion, the rise in plasma AVP was normal or subnormal in all patients. In two patients who showed mild to moderate hyponatremia in the basal state and mild urinary diluting defect during water loading, plasma AVP was appropriately suppressed in each case. These results indicate that inappropriate elevation of plasma AVP is not common in myxedema, and that impaired water excretion is due mainly to AVP-independent mechanisms.

Adult↗
PubMed1990

Effect of metyrapone pretreatment on adrenocorticotropin secretion induced by corticotropin-releasing hormone in normal subjects and patients with Cushing's disease.

To examine the influence of endogenous cortisol on the ACTH response to CRH, we compared ACTH secretion during CRH tests before and after metyrapone administration in 9 normal subjects and 12 patients with Cushing's disease. The administration of 4.5 g metyrapone (750 mg, orally, every 4 h) resulted in a decrease in basal (pre-CRH) plasma cortisol levels and an increase in basal plasma ACTH levels in both normal subjects and Cushing's patients. The pretreatment with metyrapone significantly blunted the increase in plasma cortisol levels and markedly enhanced ACTH secretion after iv injection of 100 micrograms human CRH. The peak ACTH levels during CRH test before and after metyrapone administration were 8 +/- 1 and 58 +/- 8 pmol/L, respectively, in normal subjects (P less than 0.01) and 26 +/- 5 and 50 +/- 11 pmol/L, respectively, in Cushing's patients (P less than 0.05). Although the basal and peak ACTH levels as well as delta ACTH (peak ACTH - basal ACTH) during the CRH test before metyrapone administration were significantly higher in Cushing's disease patients than in normal subjects (P less than 0.01), no such difference was observed between the 2 groups after metyrapone administration. The results clearly indicate that the endogenous cortisol levels greatly influence the ACTH response to CRH, and that the CRH test as commonly performed does not allow a correct evaluation of potential responsiveness of normal pituitaries and Cushing's adenomas to CRH.

Adolescent↗
PubMed1989

Ca2+ influx stimulated by vasopressin is mediated by phosphoinositide hydrolysis in rat smooth muscle cells.

The mechanism of Ca2+ influx stimulated by arginine vasopressin (AVP) was studied in cultured rat smooth muscle cells. AVP stimulated 45Ca2+ influx even in the presence of nifedipine, a Ca2+ antagonist that inhibits voltage-dependent Ca2+ channel. NaF, a GTP-binding protein activator, mimicked the AVP-stimulated 45Ca2+ influx. The 45Ca2+ influx stimulated by a combination of AVP and NaF was not additive. The affinity of AVP receptor was decreased by guanosine 5'-O-(3-thiotriphosphate). Pertussis toxin failed to affect the AVP-stimulated 45Ca2+ influx. AVP did not stimulate cAMP production, but increased inositol trisphosphate generation. Both AVP-stimulated 45Ca2+ influx and inositol trisphosphate generation were inhibited by neomycin, a phospholipase C inhibitor, in a dose-dependent manner, and the patterns of both inhibitions were similar. These results suggest that, in rat smooth muscle cells, AVP-stimulated Ca2+ influx is mediated exclusively through phosphoinositide hydrolysis.

Animals↗
PubMed1989

[Radioimmunoassay of vasopressin in unextracted random urine; clinical application for screening of central diabetes insipidus].

The concentration of unextracted urinary arginine vasopressin (UAVP) was directly measured by high-sensitive radioimmunoassay (AVP-RIA Kit, Mitsubishi Petrochemical Co., Ltd.). Urine was diluted to eliminate interference of nonspecific substance without prior extraction. When urine aliquots were diluted in 4 to 32 fold in assay buffer, the relationship between UAVP concentration and dilution ratio corresponded exactly in a linear regression line. The elution pattern on Sephadex G-25 of UAVP immunoreactivity was identical with that of synthesized AVP. The AVP concentration in unextracted urine was not significantly different from that of extracted urine by Sep-Pak C18 column (Water Associates, Milford MA). The mean recovery of added AVP to urine specimens was 101.1 +/- 9.8% (mean +/- SD). The immunoreactivity of UAVP was not modified by either albuminuria (50 and 100 mg/dl) or glycosuria (1000 g/dl). Mean coefficients of variance between-assay and within-assay were 8.3% and 6.6% respectively. In normal subjects (n = 28), significant correlation was observed between UAVP concentration and simultaneously measured plasma AVP (r = 0.701, p less than 0.001). Moreover, AVP concentration in random urine was significantly correlated with AVP excretion in 24 hr-urine (r = 0.703, p less than 0.05, n = 9), and this suggested that random UAVP concentration may indicate daily UAVP secretion. In normal subjects, AVP concentration in random urine was widely scattered from 9.2 to 470.6 pg/mg Cr (89.5 +/- 76.4 pg/mg Cr, n = 211). In patients with diabetes insipidus (DI), UAVP concentration (1.6 to 13.0 pg/mg Cr, 6.94 +/- 2.77 pg/mg Cr, n = 25) was significantly lower (p less than 0.001) than that of normal subjects. UAVP concentration in a patient with primary polydipsia (43.2 pg/mg Cr) was not similar to that of ID but to that of normal subjects. UAVP concentration in 2 patients with SIADH was not more than that of normal subjects, indicating that random UAVP concentration is not suitable for detecting inappropriate AVP secretion. In this study, it is suggested that patients of random UAVP concentration below 13.0 pg/mg Cr should be recommended other intensive examination to diagnose DI, even though 2 normal subjects (0.9%) were incorrectly estimated as DI. In conclusion, radioimmunoassay of AVP in unextracted random urine is easy to sample and assay, and useful in screening polyuric patients.

Diabetes Insipidus↗