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Biomedical subjects

M Naruse

Publications and source records attributed to M Naruse.

At least 109 records · Page 6Linked to original sources
PubMed1996

A novel endogenous mouse mammary tumor virus locus in Asian wild mice and its evolutionary divergency.

The divergency of endogenous mouse mammary tumor virus (MMTV) in European mouse strains indicates acquisition of exogenous MMTV into their genomes during evolution. In the present study, we selected two strains of Asian wild mice, Cas-Hmi (Mus musculus castaneus) and Sub-Kjr (M. m. subspecies) to investigate a possible divergency of endogenous MMTVs among Asian mouse strains. Southern blot analysis and polymerase chain reaction (PCR) demonstrated that Cas-Hmi and Sub-Kjr have the full structure of integrated endogenous MMTVs, suggesting that these mice were diverged during evolution after MMTV endemics.

Animals↗
PubMed1996

A very small juxtaglomerular cell tumor preoperatively identified by magnetic resonance imaging.

We describe a 31-year-old man. Although the plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were elevated, computed tomography and rapid sequence pyelography disclosed no abnormality. However, based on the findings of the small tumor (8 x 8 mm) in the kidney visualized by magnetic resonance imaging (MRI) and excessive PRA in the right renal vein, tumor resection was performed. The positive immunohistochemical staining of renin and the visualization of renin mRNA by in situ hybridization provided evidence supporting the diagnosis of juxtaglomerular cell tumor. Blood pressure, PRA, and PAC were normalized after the surgery. The observations suggest that MRI is a powerful diagnostic procedure in small juxtaglomerular cell tumor.

Adenocarcinoma↗
PubMed1996

Functional characterization of vasopressin V1 and V2 receptors in the rabbit renal cortical collecting duct.

Recently we clarified the mechanism in which arginine-vasopressin (AVP) applied from the luminal side inhibits the basolateral Cl- conductance, which is stimulated by basolateral AVP. However, to prove that these vasopressin phenomena are expressed via receptor mediated actions, we examined the effect of specific V1 and V2 receptor antagonists, OPC-21268 and OPC-31260, respectively, on the electrical response to vasopressin in the rabbit CCD perfused in vitro. In the presence of the V2-antagonist, basolateral AVP caused only the activation of luminal Na+ conductance, indicating a V1 action. In the presence of the V1 antagonist, basolateral AVP caused the same biphasic responses in electrical parameters as cyclic AMP, representing a pure V2 action. On the other hand, a rise in cell Ca2+ in response to AVP was completely abolished in the presence of the V1-antagonist, but not by the V2-antagonist in the bath. These data confirm our earlier findings that rabbit CCD possesses both V1 and V2 receptors in the basolateral membrane. We conclude that electrical responses to AVP in the rabbit CCD are a complex of V1 and V2 receptor-mediated actions.

Animals↗
PubMed1996

[Pseudohypoaldosteronism].

Mineralocorticoid resistance results from inability of aldosterone to exert its effect on its target tissues. The syndrome is associated with salt loss, hypotension and hyperkalemic acidosis. We have cloned and sequenced the cDNA of the mineralocorticoid receptor of five sporadic cases with this syndrome but have found no mutations of pathophysiological significance, which would explain the resistance of these patients to aldosterone. In all of these patients, we also examined 0.9 kb of the 5' regulatory region and the first untranslated exon of the mineralocorticoid receptor gene, without detecting any abnormalities. We are now studying the subunits of the amiloride-sensitive sodium channel (ENaC), which are in the postreceptor pathway of aldosterone action, in this disease.

Aldosterone↗
PubMed1996

[Carcinoid tumor].

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Carcinoid Tumor↗
PubMed1995

Differential gene expression of vascular natriuretic peptide receptor subtype in artery and vein.

Although the vasorelaxation by natriuretic peptide (NP) is much less potent in the vein than in the artery, mechanism underlying the phenomenon remains unknown. Since NP receptor consists of three subtypes with different functions, we determined the mRNA level of each NP receptor subtype in the artery and vein by ribonuclease protection assay. In the aorta, NP-A receptor related to the biological action of NP was the predominant form. By contrast, NP-C receptor related mainly to the clearance of NP was the predominant form in the inferior vena cava: NP-C mRNA level was about two fold higher than in the aorta, while both NP-A and NP-B receptor mRNA levels were about half of that in the aorta. These results provide the molecular basis for the different biological response to NP in the artery and vein. Differential gene expression of NP receptor subtype could be an important determinant of the biological actions of NP.

Animals↗
PubMed1995

Alterations of angiotensin II receptor contents in hypertrophied hearts.

Tsukuba hypertensive mice, which carry the human genes for renin and angiotensinogen, show cardiac hypertrophy as well as hypertension due to activation of the renin-angiotensin system (RAS). Here, we compared the cardiac angiotensin II (Ang II) receptor contents in these and normotensive control mice by means of ligand binding studies and competitive reverse transcription-polymerase chain reaction analyses. The content of the Ang II receptor type 1 (AT1) was significantly higher at both the protein (2.5-fold; p < 0.01) and mRNA (1.4-fold; p < 0.05) levels in the hypertensive mice than that in control mice. Almost identical levels of the Ang II receptor type 2 (AT2) expression were identified at the mRNA levels in the two types of mice, although the levels were less than 20% of those of AT1 mRNA in control mice. These results suggest that AT1 in the heart is upregulated in response to Ang II-induced hypertrophic change and that, in particular, the upregulation of AT1 in particular contributes to the development and/or maintenance of cardiac hypertrophy in conjunction with the increase in Ang II production, because AT1 is responsible for cardiac hypertrophy related to the RAS.

Animals↗
PubMed1995

Characterization of angiotensin II receptor type 2 during differentiation and apoptosis of rat ovarian cultured granulosa cells.

We examined the change in the content of angiotensin II (AII) receptor type 2 (AT2) during differentiation and apoptosis of rat ovarian granulosa cells in culture. The AT2 content was not changed by follicle stimulating hormone (FSH), a differentiation factor of granulosa cells, but was markedly increased in FSH-free media. The cells cultured without FSH underwent internucleosomal DNA fragmentation characteristic of apoptosis, which occurs during follicle atresia. AII augmented the increase in the AT2 content in the absence of FSH. This AII-induced augmentation was suppressed by the AT2-selective antagonist PD123319 but not by Dup753, an antagonist specific for type 1 receptor, suggesting that AII up-regulates the AT2 expression via AT2 itself. These data strongly support the hypothesis that AT2 might modulate the onset and progression of follicle atresia involving apoptosis of granulosa cells.

Angiotensin II↗
PubMed1995

In vivo transfection of genes for renin and angiotensinogen into the glomerular cells induced phenotypic change of the mesangial cells and glomerular sclerosis.

Locally activated renin angiotensin system plays an important role in the progression of the glomerular diseases. In order to understand the local effect of overexpressed angiotensin II in the glomerulus in situ, we introduced human genes for renin and angiotensinogen into the rat kidney by hemagglutinating virus of Japan-liposome procedure. Three days after transfection human renin was detected in the glomeruli by immunohistochemistry. Seven days after transfection, extracellular matrix was expanded in the glomeruli and alpha-smooth muscle actin was expressed in the mesangial cells. These results suggest that locally activated renin angiotensin system induces glomerular sclerosis and a phenotypic change in mesangial cells.

Actins↗
PubMed1995

Insulin resistance is associated with high plasma ouabain-like immunoreactivity concentration in NIDDM.

The aim of the present study was to elucidate the pathophysiologic significance of circulating ouabain as a link between insulin resistance (IR) and hypertension (HT) in NIDDM. Euglycaemic (4.5 mmol/l) hyperinsulinaemic (360-580 pmol/l) clamping was performed using an artificial endocrine pancreas. Plasma ouabain-like immunoreactivity (OLI) was determined by radioimmunoassay using a highly specific antibody to ouabain. HT was defined as systolic blood pressure > 140 mm Hg and/or diastolic > 90 mm Hg or being treated with antihypertensive agents. The values (mean +/- SEM) of glucose infusion rate (GIR) and plasma OLI were compared among the four groups classified using IR and HT as factors. Group I (IR-/HT-, n = 15): GIR 7.20 +/- 0.36 mg.kg-1.min-1, OLI 130.8 +/- 20.9 pmol/l, which was not different from that in eight normal control subjects (7.69 +/- 0.40 mg.kg-1.min-1 and 142.6 +/- 32.3 pmol/l, respectively); Group II (IR-/HT+, n = 13): 5.89 +/- 0.36 mg.kg-1.min-1, 172.5 +/- 35.0 pmol/l; Group III (IR+/HT-, n = 14) 1.91 +/- 0.28 mg.kg-1.min-1, 576.6 +/- 161.5 pmol/l (p < 0.01 vs Group I and II); Group IV (IR+/HT+, n = 15) 1.79 +/- 0.22 mg.kg-1.min-1, 703.1 +/- 170.1 pmol/l (p < 0.01 vs Group I and II), respectively. Six of 57 NIDDM patients studied exhibited very high (> 1500 pmol/l) plasma OLI concentrations, showed marked insulin resistance and were all hypertensive. When analysed as a whole, plasma OLI was negatively correlated with GIR (p < 0.001), but was not correlated with arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Chlordiazepoxide attenuates stress-induced activation of neurons, corticotropin-releasing factor (CRF) gene transcription and CRF biosynthesis in the paraventricular nucleus (PVN).

Corticotropin-releasing factor (CRF) plays a role in coordinating endocrine, autonomic, and behavioral responses to stressful stimuli. Benzodiazepines exert many effects which oppose those of CRF, including anxiolysis and suppression of the pituitary-adrenal axis. In the present study, we employed in situ analysis of CRF heteronucleous RNA (hnRNA) and c-fos mRNA to assess stimulus-induced CRF gene transcription rate following stress and its modulation by chlordiazepoxide (CDP). Male albino rats were exposed to restraint stress for 30 min and sacrificed 30 and 120 min after the onset of stress. Either CDP or vehicle was given intraperitoneally 60 min before stress. To determine plasma ACTH levels by immunoradiometric assay, another group of rats was decapitated 10 min after the onset of restraint stress. Restraint stress induced rapidly and significantly c-fos mRNA and CRF hnRNA expression in the PVN at the 30 min time point. Increases in both RNA copies were significantly inhibited by administration of CDP at doses of 5 and 10 mg/kg. CRF mRNA concentrations were increased significantly in the PVN 120 min after stress and again, CDP attenuated significantly these increases in the PVN. The plasma ACTH increase in response to stress was inhibited significantly by CDP administration at every dose tested. CDP did not change CRF mRNA levels in the non-stressed animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Gene expression of vascular natriuretic peptide receptor in the aorta of hypertensive rats.

1. To elucidate the pathophysiologic role of vascular natriuretic peptide (NP) receptor in hypertension, we determined NP-A and NP-B receptor mRNA levels by means of ribonuclease protection assay in aorta of three types of hypertensive rats. 2. The NP-A receptor mRNA level was higher in stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and deoxycorticosterone acetate-salt hypertensive rats than that in their respective control rats. On the contrary, the NP-A receptor mRNA level was lower in NG-nitro-L-arginine-methyl ester (L-NAME)-induced hypertensive rats compared with that in the control. 3. The NP-B receptor mRNA level did not show any significant change in all three hypertensive rats compared with their respective controls. 4. The present study suggests that high blood pressure is not the major factor regulating the NP receptor gene expression and also that the receptor subtype is independently regulated from each other.

Animals↗
PubMed1995

Electrophysiological study of luminal and basolateral vasopressin in rabbit cortical collecting duct.

To clarify the mechanism of action of arginine vasopressin (AVP) on ionic conductances, electrophysiological technique was applied to the rabbit cortical collecting duct (CCD) perfused in vitro. When AVP (100 pM) was added to the bath, transepithelial voltage (VT), transepithelial resistance (RT), and fractional resistance of the apical membrane (fRA) of the principal cell displayed biphasic responses: initial increase in lumen-negative VT (phase I) was associated with decreases in RT and fRA, whereas secondary decrease in VT (phase II) was associated with increases in RT and fRA. In phase I, depolarization of the luminal membrane was observed due to stimulation of Na+ conductance in the luminal membrane. In phase II, mixed responses of both hyperpolarization of the luminal membrane, due to late inhibition of Na+ conductance, and depolarization of the basolateral membrane, due to stimulation of Cl- conductance, were observed. 8-(4-Chlorophenylthio)-adenosine 3',5'-cyclic monophosphate, as a pure vascular AVP receptor 2 (V2) action, mimicked the actions of AVP. Addition of AVP (100 pM to 1 nM) in the lumen resulted in increases in lumen-negative VT and RT. Luminal AVP did not affect the electrical parameters in beta-intercalated cells. In principal cells, luminal AVP caused sustained increase in total membrane resistance (Ri), together with an initial depolarization of the luminal membrane followed by a late hyperpolarization of the basolateral membrane. Because the initial response was abolished in the presence of 2 mM Ba2+ in the lumen, an inhibition of luminal K+ conductance may be responsible for the initial phase of luminal AVP action. Late hyperpolarization of the basolateral membrane associated with an increase in membrane resistance was abolished in the absence of ambient Cl-. Under the condition where Cl- conductance of the basolateral membrane was stimulated by administration of cAMP in the bath, voltage deflections of the basolateral membrane on changing Cl- concentration in the bath from 120 to 12 mM decreased by 88% in the presence of luminal AVP. These observations are in accord with the view that the basolateral Cl- conductance was inhibited by luminal AVP in the later phase. These data indicate that AVP in the lumen inhibits basolateral Cl- conductance, which is stimulated by AVP in the bath.

Animals↗
PubMed1995

Stress-induced activation of neuronal activity and corticotropin-releasing factor gene expression in the paraventricular nucleus is modulated by glucocorticoids in rats.

Intronic in situ hybridization methodology provides a means of determining the rate of gene transcription under basal and stimulated conditions. In the present study, we have used intronic in situ hybridization to the corticotropin-releasing factor (CRF) gene to measure hypothalamic CRF gene transcription after stress as well as its modulation by glucocorticoids. Using this and conventional exonic in situ hybridization we examined the time course of changes in c-fos mRNA, and CRF heteronuclear RNA (hnRNA) and mRNA concentrations in the paraventricular nucleus (PVN) of male Wistar rats after restraint stress. In addition, we determined the effects of adrenalectomy and dexamethasone administration on c-fos and CRF gene expression in the PVN. Restraint stress induced a rapid induction (within 5 min) of c-fos mRNA and CRF hnRNA expression in the PVN. Both RNA concentrations peaked at 30 min then decreased and were undetectable 2 h after stress onset. In contrast, the concentration of CRF mRNA increased gradually and a significant elevation was first detected 60 min after the beginning of stress. Adrenalectomy augmented and dexamethasone pretreatment inhibited c-fos mRNA, CRF hnRNA, and mRNA induction after stress. The data suggest that stress-induced activation of neurons, CRF gene transcription, and CRF synthesis in the PVN are modulated by glucocorticoids.

Adrenalectomy↗