Publications by authors named "Shiono S"

Using a radioimmunoassay for alpha-rat atrial natriuretic polypeptide (alpha-rANP), tissue levels of alpha-rANP-like immunoreactivity (-LI) in the rat spinal cord and autonomic ganglia were investigated. The alpha-rANP-LI level was higher in the more caudal parts of the spinal cord and the highest in the sacral spinal cord. alpha-rANP-LI was also detected in the superior cervical and coeliac ganglia.

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To investigate whether vasopressin is involved in the secretory mechanism of atrial natriuretic polypeptide (ANP), effects of arginine-vasopressin (AVP) administered iv on plasma ANP levels were studied in conscious, unrestrained rats. The administration of 100 ng and 1 microgram of AVP caused a dose-dependent increase of the plasma ANP level, which was blocked by a V1-receptor antagonist of AVP, and was attenuated by 5 ml blood volume reduction before the stimulation. The injection of less than 10 ng of AVP induced no significant effects on ANP secretion.

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Using synthetic beta-human atrial natriuretic polypeptide (beta-hANP), an antiparallel dimer of alpha-hANP, and radioimmunoassay (RIA) for alpha-ANP which also detects beta-hANP, we investigated the disappearance profile and the change in the molecular form of exogenously added beta-hANP in human plasma in vitro, compared with those of alpha-hANP. The ANP-like immunoreactivity (ANP-LI) level in beta-hANP-added human plasma exhibited slower disappearance than that in alpha-hANP-added plasma during the incubation at 37 degrees C. High performance-gel permeation chromatography and reverse phase-high performance liquid chromatography coupled with RIA revealed that beta-hANP (6K) was converted into a smaller peptide with an approximate molecular weight of 3K corresponding to alpha-hANP during the incubation.

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The structure-activity relationship of atrial natriuretic polypeptides (ANPs) in the central action was investigated by examining the suppressive effects of the intracerebroventricular (i.c.v.

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Biologically active peptides isolated in the peripheral organs often distribute in the central nervous system and vice versa. Accumulating evidence supports the concept that the effects of centrally active peptides are often, although not always, complementary to their peripheral actions. Atrial natriuretic polypeptide (ANP) is one of these biologically active peptides.

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Biologically active peptides isolated from peripheral organs often occur in the central nervous system, and vice versa. There is evidence that the effects of centrally active peptides are often, although not always, complementary to their peripheral actions. Atrial natriuretic polypeptide (ANP) is one of these biologically active peptides.

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The effects of intracerebroventricular injection of atrial natriuretic polypeptide (ANP) and angiotensin II (AII) on the concentration of dopamine, noradrenaline, serotonin and their primary metabolites in the rat brain were studied using high performance liquid chromatography with electrochemical detection. ANP (2 and 5 micrograms) decreased the level of dopamine and its metabolite in the septum and hypothalamus. In contrast, AII (100 ng) increased their levels in these brain regions.

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In order to clarify the role of atrial natriuretic polypeptide (ANP) in the brain on regulation of blood pressure and urine output, we examined the effects of intracerebroventricular (i.c.v.

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To elucidate the pathophysiological role of atrial natriuretic polypeptide (ANP) in the brain in hypertension, the tissue concentrations and contents of alpha-rat ANP-like immunoreactivity (alpha-rANP-Ll) in the hypothalamus and septum of 4-week or 18-week-old spontaneously hypertensive rats (SHR) were studied using a radio-immunoassay (RIA) for alpha-rANP and compared with those of age-matched Wistar-Kyoto rats (WKY). The concentration and content of alpha-rANP-Ll in these regions of both 4-week and 18-week-old SHR were significantly higher that those of WKY (P less than 0.05).

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We have previously shown that atrial natriuretic polypeptide is present in the brain with the highest concentration in the hypothalamus and septum and that intracerebroventricular injection of atrial natriuretic polypeptide inhibits water drinking induced by centrally injected angiotensin II or 24-hour water deprivation in rats. To study further the role of brain atrial natriuretic polypeptide in the control of water and electrolyte balance, the effect of chronic intracerebroventricular infusion of atrial natriuretic polypeptide on salt appetite in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats was examined with a free-choice, two-bottle preference test. The intracerebroventricular infusion of 100 ng/hour and 500 ng/hour of alpha-human atrial natriuretic polypeptide preferentially suppressed the intake of 0.

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Effects of Bay K 8644, a voltage-sensitive calcium channel agonist, on atrial natriuretic polypeptide (ANP) secretion from isolated rat hearts perfused with Krebs-Henseleit solution were investigated. After a ninety-min period for stabilization, coronary sinus effluents were collected every two min and ANP levels were measured by radioimmunoassay. The basal secretory rate of ANP was 1.

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To evaluate whether extracellular and intracellular calcium ion may be involved in the regulation of TSH secretion in response to TRH in human subjects, the TSH blood level was determined in normal man before and after administration of two kinds of calcium ion antagonists, nifedipine that blocks transmembrane influx of calcium ion and nicorandil that inhibits mobilization of intracellular calcium ion. Administration of nifedipine and nicorandil significantly decreased the blood level of TSH stimulated by TRH, although calcium ion antagonists did not affect the basal level of TSH. The blood level of neither T4, T3, free T4, free T3, nor reverse T3 was altered by administration of calcium ion antagonists.

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The effect of intracerebroventricular administration of atrial natriuretic polypeptide on blood pressure was studied in conscious, unrestrained rats. The intracerebroventricular injection of alpha-human atrial natriuretic polypeptide did not promote any significant change in basal blood pressure, whereas it attenuated central angiotensin II-induced pressor response in a dose-dependent manner. The plasma atrial natriuretic polypeptide level did not change after the central administration of alpha-human atrial natriuretic polypeptide.

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Evidence for a voltage-dependent regulatory (inhibitory) site on the nicotinic acetylcholine receptor to which acetylcholine binds was obtained in membrane vesicles prepared from the Torpedo californica electric organ. Two rate coefficients, JA and alpha, which pertain to the receptor-controlled ion flux, were measured. A 1000-fold concentration range of acetylcholine was used in a transmembrane voltage (Vm) range from 0 to -48 mV under a voltage-clamped condition at pH 7.

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Using reverse phase high performance liquid chromatography (RP-HPLC) coupled with two radioimmunoassays for atrial natriuretic polypeptide (ANP) with different specificities, we investigated the nature of alpha-rat ANP-like immunoreactivity (alpha-rANP-LI) with a low molecular weight in the rat brain. Two major peaks with alpha-rANP-LI in the extract from rat whole brains were eluted in the vicinity of the elution position of synthetic alpha-rANP, a 28-amino acid polypeptide. These two components co-migrated with synthetic alpha-rANP (4-28) and alpha-rANP (5-28), respectively.

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Using a specific radioimmunoassay (RIA) for alpha-rat atrial natriuretic polypeptide (alpha-rANP), we have demonstrated the presence of a considerable amount (6.10 +/- 0.38 ng/g) (mean +/- SE) of alpha-rANP-like immunoreactivity (alpha-rANP-LI) in the rat lung, the first organ through which atrial natriuretic polypeptide (ANP) released from the heart passes.

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We have analysed the pharmacokinetics of alpha-human atrial natriuretic polypeptide (alpha-hANP) in healthy subjects, using a two-compartment open model following bolus intravenous injection. The plasma half-times for the fast and slow components were 1.7 +/- 0.

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Does the acetylcholine receptor have a specific regulatory (inhibitory) site for the natural receptor ligand acetylcholine? This paper deals with this question. The inhibition of acetylcholine-receptor function by diverse organic cations including local anesthetics such as procaine has been well documented. Evidence indicates that these compounds are noncompetitive inhibitors, enter the open-channel form of the receptor, and block it and that the extent of this blockage depends on the transmembrane voltage of the cell.

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