Search PubMed⌕ Search

Biomedical subjects

Z Ota

Publications and source records attributed to Z Ota.

At least 199 records · Page 11Linked to original sources
PubMed1988

Properties of [3H]bunazosin binding in rat kidney.

Properties of alpha 1-adrenoceptor binding in the renal cortex of rats were studied with [3H]bunazosin as the radiolabeled ligand. Both temperature and incubation time influenced bunazosin receptor binding. Subcellular distribution of [3H]-bunazosin binding revealed that the membrane fraction (30,000 x g pellet) had the largest proportion of total binding sites. Pretreatment of membrane preparation at 56 degrees C for 30 minutes greatly decreased the specific binding of [3H]-bunazosin, though there was no significant effect of the pretreatment at 24 degrees C and 37 degrees C for 30 minutes. Among various cations, some divalent ions such as Cu++ and Zn++ greatly decreased bunazosin binding, whereas monovalent ions had no effect on specific binding. Results of Scatchard analysis suggested that the rat renal cortex membrane has single binding sites with an apparent dissociation constant of 0.38 +/- 0.06 nmol/L, though the rat medulla membrane has no potent binding activity with bunazosin. The displacement study revealed that various adrenergic agents inhibit [3H]bunazosin binding in dose-dependent fashion; the rank order of potencies was bunazosin prazosin > phentolamine >> dl-norepinephrine > clonidine, yohimbine >> pindolol, propranolol. These findings reveal that bunazosin has specific receptor binding in the rat renal cortex, indicating that alpha 1-adrenoceptors exist in the rat renal cortex.

Adrenergic alpha-Antagonists↗
PubMed1987

Regional responses of rat brain muscarinic cholinergic receptors to immobilization stress.

The effect of immobilization stress (IM-stress) on the muscarinic cholinergic (m-Ch) receptor binding was determined in 8 brain regions using [3H]quinuclidinyl benzilate (QNB). IM-stress produced an increase in specific QNB binding in the septum, striatum, hippocampus and pons + medulla oblongata. Scatchard analysis revealed that IM-stress produced an increase in the affinity of m-Ch receptors in the septum, hippocampus and pons + medulla oblongata, but did not alter the maximum number of binding sites (Bmax). In the striatum, an increase in specific QNB binding was due to both the increase in Bmax and reduction of the dissociation constant (Kd). The present study suggests that IM-stress induces supersensitivity of postsynaptic m-Ch receptors probably due to a decrease in presynaptic cholinergic activities in the septum, striatum, hippocampus and pons + medulla oblongata. As the m-Ch receptors in the striatum and pons + medulla oblongata are affected by IM-stress, further studies of the m-Ch neural system must be performed under stressful situations in these regions as well as in the septum, hippocampus and cerebral cortex.

Animals↗
PubMed1987

Differential changes in atrial natriuretic peptide and vasopressin receptor bindings in kidney of spontaneously hypertensive rat.

To elucidate the role of atrial natriuretic peptide (ANP) and vasopressin (VP) in a hypertensive state, ANP and VP receptor bindings in spontaneously hypertensive rat (SHR) kidney were analyzed using the radiolabeled receptor assay (RRA) technique. Systolic blood pressure of SHR aged 12 weeks was statistically higher than that of age-matched Wistar Kyoto (WKY) rats. Maximum binding capacity (Bmax) of [125I]-ANP binding to the SHR kidney membrane preparations was statistically lower than that of WKY rats, but dissociation constant (Kd) was not significantly different. On the other hand, Bmax of [3H]-VP binding to the SHR kidney membrane preparations was statistically higher than that of WKY rats, but Kd were similar. Since the physiological action of ANP is natriuresis and VP is the most important antidiuretic hormone in mammalia, these opposite changes of ANP and VP receptor bindings in SHR kidney suggested that these peptides may play an important role in the pathophysiology of the hypertensive state, although it has not been confirmed as yet.

Animals↗
PubMed1987

Serum C3 and C4 levels and complement-dependent antibody-mediated cytotoxic activity of islet cell surface antibody in type 1 (insulin-dependent) diabetic children.

The role of complement in the pathogenesis of diabetes was studied in 31 Type 1 (insulin-dependent) diabetic children by assaying serum islet cell surface antibody, C3, C4 and serum complement-dependent antibody-mediated cytotoxicity. Nine of 21 islet cell surface antibody-positive children were within 5 months of disease onset and showed significantly lower serum C3 and C4 levels than either 1 year later or the remainder of the islet cell surface antibody-positive children at 6-12 months after disease onset. The overall trend of all islet cell surface antibody-positive diabetic children within 1 year of disease onset was toward increased serum C3 and C4 levels as the disease progressed. Serum C4 concentration and complement-dependent antibody-mediated cytotoxicity which showed an initial negative correlation were uncorrelated 1 year later. Four children who were initially strongly islet cell surface antibody-positive but negative 1 year later also exhibited significantly higher (p less than 0.05) mean serum C4 levels after 1 year. There was a significant decrease in complement-dependent antibody-mediated cytotoxicity when sera from the diabetic children were treated with either ethylene glycol tetra-acetic acid or ethylene diamine tetra-acetic acid. These data strongly suggest that complement-dependent antibody-mediated cytotoxicity induced by the classical complement pathway involving an islet cell surface antibody may play an important role in the pathogenesis of Type 1 diabetes.

Adolescent↗
PubMed1987

Atrial natriuretic peptide does not affect corticotropin-releasing factor-, arginine vasopressin- and angiotensin II-induced adrenocorticotropic hormone release in vivo or in vitro.

The effect of synthetic atrial natriuretic peptide (ANP) was examined on the in vivo and in vitro release of ACTH. Intravenous ANP (4 micrograms/kg body weight) administration did not affect the corticotropin releasing factor (CRF, 4 micrograms/kg body weight)-, arginine vasopressin (AVP, 2 micrograms/kg body weight)- and angiotensin II (A II, 4 micrograms/kg body weight)-induced ACTH release in unanesthetized freely moving rats. ANP did not inhibit the basal, CRF- and AVP-induced release of ACTH in pituitary cell cultures. ANP did not affect the CRF- and AVP-induced plasma corticosterone elevation, while it attenuated the AVP-induced corticosterone elevation. These results indicate that ANP does not affect the ACTH release at the pituitary level in vivo and in vitro.

Adrenocorticotropic Hormone↗
PubMed1987

A case of postganglionic cholinergic dysautonomia.

A 24 year old female presented with signs and symptoms of postganglionic cholinergic autonomic dysfunction manifested by impaired lachrymation and salivation, mydriasis of the pupil, decreased gastrointestinal motility, atony of the bladder, and sweating and taste disturbance. Clinical and pharmacological studies confirmed that the abnormalities were restricted mainly to the postganglionic cholinergic autonomic systems. The titre of serum complement was low, antinuclear antibodies revealed a diffuse pattern, and anti SS-A antibody was positive, suggesting that this disorder was caused by an immune mechanism.

Adult↗
PubMed1987

Fibrillar ultrastructure of the glomerular basement membrane of the rat kidney as revealed by digestive treatment.

Rat kidney glomerular basement membrane (GBM) was isolated and digested with alpha-amylase and elastase. Electron microscopy revealed a meshwork structure composed of fibrils 3 nm in width. They appeared to be type IV collagen fibrils. We succeeded in clarifying a significant ultrastructural aspect of the GBM which had been unclear until now. The findings are consistent with our previously proposed GBM molecular sieve theory.

Animals↗
PubMed1987

Dog erythrocyte rosette-forming lymphocyte: blockage by OKT11 monoclonal antibody.

Human peripheral blood mononuclear cells (PBM) were separated into sheep erythrocyte rosette-forming (Es+) and non Es+ cells by the Ficoll-Hypaque gradient sedimentation method. Thirty-eight percent of the Es+ cells formed rosettes with dog erythrocytes and were designated as Es+Ed+ cells. The remaining Es+ cells were designated as Es+Ed- cells. Only a few non Es+ cells formed rosettes with dog erythrocytes. Among Es+Ed+ cells, T4 antigen-positive cells were observed approximately 1.7 times as often as T8 antigen-positive cells, when measured by staining with OKT4 or OKT8 monoclonal antibody. Among Es+Ed- cells, however, T4 and T8 antigen-positive cells were observed in almost equal proportion. Preincubation of PBM with OKT11 monoclonal antibody, but not with OKT4 monoclonal antibody, inhibited the rosette formation with dog as well as sheep erythrocytes. These results indicated that Es+Ed+ cells were a subpopulation of T-cells in which a majority of the cells were T4 antigen-positive, and that the binding sites of dog erythrocytes on human T-cells was closely linked with that of sheep erythrocytes.

Animals↗
PubMed1987

In vitro macro- and micro-autoradiographic localization of atrial natriuretic peptide in the rat kidney.

We investigated the receptor localization of atrial natriuretic peptide (ANP) in the rat kidney, by in vitro macro- and micro-autoradiography (ARG) of [125I]-ANP using nonfixed frozen sections. First, we examined the optimum conditions for ARG with respect to the effects of polyethylenimine (PEI), thickness of section, incubation time and degradation of [125I]-ANP. Saturation experiments of [125I]-ANP using rat kidney sections revealed the presence of high affinity binding sites of [125I]-ANP in the renal cortex (Kd = 0.52 nM). Macro-autoradiograms showed that the dense grains representing specific binding sites of [125I]-ANP were distributed in the cortex in a punctate pattern. Using micro-autoradiography, the localization of the dense grains on the emulsion was compared with the staining pattern of the same section subjected to double staining. In the renal cortex, the dense grains were observed on the glomerulus, blood vessels and proximal tubules. Dense grains were also observed in the mesangium area of glomeruli, the inside wall of blood vessels (especially endothelium), and the inside wall of proximal tubules (possibly brush border). These results suggested that the physiological action of ANP in the kidney is mediated by its receptors. Also, ARG was useful for accurately detecting the action sites of ANP.

Animals↗
PubMed1987

Bilateral vocal cord paralysis due to laryngeal carcinoma in Parkinson's disease.

A laryngeal carcinoma presenting as severe dyspnea and stridor due to bilateral vocal cord paralysis was found in a 66-year-old man who had been suffering from Parkinson's disease (PD) for twenty years. Although laryngeal carcinoma is a common cause of bilateral vocal cord paralysis, patients with PD have been suspected to have a low cancer incidence, and this may be the first case report. Therapeutics have extended the survival of patients with PD, and the possibility of developing vocal cord paralysis. Thus, it is important for the physician to be aware that this condition may be caused by carcinoma even in PD cases.

Aged↗
PubMed1986

Starvation-induced changes in rat brain corticotropin-releasing factor (CRF) and pituitary-adrenocortical response.

Starvation-induced changes in CRF concentration in major brain regions and abnormalities in the pituitary-adrenal axis were examined in rats using rat CRF radioimmunoassay. The CRF concentrations in the hypothalamus and cerebellum were significantly reduced in the completely starved rats, while those in the midbrain, thalamus and neurointermediate lobe of the pituitary were significantly increased in the semi-starved or completely starved rats. No significant changes in the CRF concentrations were found in the pons, medulla oblongata and cerebral cortex. In the completely starved rats, the serum ACTH level was significantly reduced, whereas the serum corticosterone level was markedly elevated. These observations suggest that starvation may stimulate the CRF-ACTH-corticosterone system and that not only hypothalamic CRF but also extrahypothalamic CRF may be discretely related to feeding behavior or starvation. The reduced serum ACTH level in starved rats may be ascribed to the negative feedback effect of the elevated serum corticosterone.

Adrenocorticotropic Hormone↗
PubMed1986

Effect of immobilization stress on neuropeptides and their receptors in rat central nervous system.

The effect of immobilization stress (IM-stress) on the concentration and the receptor binding of substance P (SP), methionine-enkephalin (ME) and thyrotropin-releasing hormone (TRH) was determined in eight brain regions and the spinal cord. The concentration of SP was decreased in the septum, striatum and hippocampus, and SP receptor binding was decreased in the septum, amygdala + pyriform cortex and hypothalamus. Scatchard analysis indicated that the decrease in the SP binding is mainly due to the decrease in the number of receptors. The concentration of ME was not changed, but ME receptor binding was decreased in the septum. The concentration of TRH was decreased in the frontal cortex, septum, amygdala + pyriform cortex and pons + medulla oblongata, but increased in the spinal cord. TRH receptor binding was decreased in the septum, amygdala + pyriform cortex and hypothalamus. Scatchard analysis indicated that the decrease in TRH binding is due to the decrease in the number of receptors. These results show that IM-stress affects the neuropeptide receptor as well as neuropeptide concentration, and that the septum is a very important region under IM-stress.

Animals↗
PubMed1986

Brain corticotropin releasing factor in the spontaneously hypertensive rat.

Corticotropin releasing factor and vasopressin were measured in major brain regions including the neurohypophysis in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) during development of hypertension. The highest concentration of corticotropin releasing factor was found in the hypothalamus in both strains. Corticotropin releasing factor was decreased in most major brain regions of SHR. In the hypothalamus, corticotropin releasing factor was lower in 3- and 6-week-old SHR than in age-matched WKY (p less than 0.01), but was similar at 12 and 24 weeks of age. The content of corticotropin releasing factor did not differ in the neurohypophysis in 3-week-old rats but began to decrease at 6 weeks of age (p less than 0.01) and continued to decrease during the development of hypertension (p less than 0.01). Brain vasopressin concentration did not differ between SHR and WKY except in the hypothalamus. The level of hypothalamic vasopressin was consistently lower in SHR than in WKY (p less than 0.01). These peptides are thought to be associated with autonomic nervous regulation, and our results may further strengthen the possibility that the deficit of the peptides may be involved in the development of spontaneous hypertension.

Age Factors↗
PubMed1986

Adrenocorticotropin responses to corticotropin releasing factor and vasopressin in spontaneously hypertensive rats.

The effects of exogenous corticotropin releasing factor and arginine vasopressin were evaluated in 6- and 11-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Basal adrenocorticotropic hormone (ACTH) and vasopressin levels did not differ between SHR and WKY, but basal corticosterone level was higher in 6-week-old SHR (p less than 0.01). To block endogenous corticotropin releasing factor secretion and nonspecific systemic responses, both groups were pretreated with chlorpromazine, morphine, and sodium pentobarbital anesthesia before measurement of ACTH responses to corticotropin releasing factor and vasopressin infusion. Basal ACTH level was lower in anesthetized 6-week-old SHR than in age-matched WKY (p less than 0.01), but no difference was seen between 11-week-old WKY and SHR. The ACTH response to corticotropin releasing factor in 6-week-old WKY was significantly greater than that in age-matched SHR (p less than 0.01), whereas in 11-week-old SHR and WKY the response was similar. Compared with responses in WKY, SHR showed an increased ACTH response to high doses of vasopressin (0.25 micrograms/100 g body weight) at both ages (p less than 0.05). These results indicate that the ACTH response to corticotropin releasing factor is blunted in the early stages of hypertension in SHR but later recovers. These abnormal responses to corticotropin releasing factor and vasopressin may be related to the development of spontaneous hypertension.

Adrenocorticotropic Hormone↗
PubMed1986

Effect of clonidine on insulin secretion: a case report.

We have recently seen a case of non-insulin-dependent diabetes mellitus with hypertension in which chronic treatment with oral clonidine gave rise to elevation of blood glucose and decreased insulin secretion. When the response of insulin secretion to glucose administration during clonidine therapy was compared with that after 12 days of wash-out for clonidine in this patient (who was then receiving phentolamine mesylate), there was a marked suppression of insulin secretion to stimulation by intravenous glucose during oral clonidine therapy. This result indicates that the decreased insulin secretion associated with oral clonidine therapy is very unlikely to be due to any direct action of clonidine on beta cells of the pancreatic islets and may be due to suppression of catecholamine release via central alpha-adrenergic receptor stimulation.

Blood Glucose↗
PubMed1986

Effect of morphine on hypothalamic corticotropin-releasing factor (CRF) and pituitary-adrenocortical activity.

The effects of intraperitoneal and intra-third ventricular administration of morphine on the hypothalamic corticotropin-releasing factor (CRF) and the pituitary-adrenocortical activity were examined in unanesthetized, freely moving rats. Hypothalamic CRF was measured by rat CRF radioimmunoassay. Intraperitoneal or intra-third ventricular administration of morphine increased blood concentrations of ACTH and corticosterone while intraperitoneal administration tended to increase CRF concentration in the whole hypothalamus including the median eminence and intra-third ventricular administration increased CRF concentration in the hypothalamus excluding the median eminence. However, morphine seemed to inhibit the increase in CRF concentration in the hypothalamus induced by the ether-laparotomy stress. The main site of morphine action on the hypothalamo-pituitary-adrenocortical system seemed to be in the hypothalamic area.

Adrenocorticotropic Hormone↗