Yuji Ito

Kanazawa University, Kanazawa, Ishikawa, Japan

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Publications (10)22.8 Total impact

  • Yuji Ito · Ryoyu Takeda · Yoshiyu Takeda
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    ABSTRACT: Screening for primary aldosteronism was historically recommended in patients with moderate to severe and/or resistant hypertension. Patients with mild hypertension and normotensive subjects were therefore excluded from the screening. However, a considerable number of normotensive individuals without hypokalaemia may have subclinical forms of primary aldosteronism. In this review, we describe evidence supporting the idea that primary aldosteronism is not only confined to patients with moderate to severe and/or resistant hypertension, but also exists in patients with mild hypertension and even in those with normotension. We discuss possible aetiologies, screening and diagnostic techniques and treatment options of the normotensive form of primary aldosteronism. The natural history, adverse effects and best treatment of this disease still remain to be resolved. The long-term follow-up studies of normotensive primary aldosteronism patients who receive neither adrenal surgery nor treatment with mineralocorticoid receptor antagonists might help to solve these problems.
    Best Practice & Research: Clinical Endocrinology & Metabolism 08/2012; 26(4):485-95. DOI:10.1016/j.beem.2011.11.006 · 4.91 Impact Factor
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    ABSTRACT: Recent studies have reported a high prevalence of primary aldosteronism among patients with severe hypertension. However, the prevalence of this disease among normotensive and mildly hypertensive patients has not been determined. The aim of this study was to examine the prevalence of primary aldosteronism among prehypertensive and stage 1 hypertensive subjects. A total of 292 adult subjects with hypertension or prehypertension was screened for primary aldosteronism. Subjects with a plasma aldosterone concentration (ng per 100 ml) to plasma renin activity (ng ml(-1) h(-1)) ratio (ARR) above 20 underwent confirmatory captopril suppression testing. A total of 54 subjects (18.5%) had an ARR above 20. A captopril suppression test was performed in 17 of 54 subjects with probable primary aldosteronism. The test confirmed the diagnosis of primary aldosteronism in 11 (64.7%) of 17 patients, giving a least prevalence of 3.8% for this disease. The 11 patients with primary aldosteronism had a mean ± s.d. systolic blood pressure of 139 ± 4 mm Hg, diastolic blood pressure of 95 ± 10 mm Hg and serum potassium of 4.46 ± 0.48 mEq l(-1) at the time of screening test. The prevalence of primary aldosteronism as could be assessed in this study was at least 6.8% in prehypertensive patients, 3.3% in stage 1 hypertensive patients and 3.1% in stage 2 hypertensive patients. In conclusion, this study suggests a high prevalence of primary aldosteronism among prehypertensive and stage 1 hypertensive Japanese patients. Significant numbers of prehypertensive individuals may have subclinical forms of this disease.
    Hypertension Research 10/2010; 34(1):98-102. DOI:10.1038/hr.2010.166 · 2.94 Impact Factor
  • Annals of the New York Academy of Sciences 12/2006; 707(1):60 - 73. DOI:10.1111/j.1749-6632.1993.tb38042.x · 4.31 Impact Factor
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    ABSTRACT: We assessed the effect of an opener of ATP-sensitive K+ channel, levcromakalim (BRL 38227, (−)6-cyano-3,4-dihydro-2,2-dimethyl-trans-4-(2-oxo-1-pyrrolidyl)-2H/it-1-benzopyran-3-ol) on seizure threshold and severity of the hippocampus-generating partial seizures in rats. For comparison, an ATP-sensitive K+ channel blocker, glibenclamide; K+ channel blocker, tetraethylammonium; Ca2+ channel antagonist, nimodipine and Ca2+ channel agonist, (±)-BAY K 8644 (1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl)-phenyl]-3-pyridinecarboxylic acid methyl ester) were also examined. Seizure threshold was determined using pulse number threshold and seizure severity was ascertained using afterdischarge duration. Levcromakalim decreased afterdischarge duration at 10 nmol i.c.v. and decreased pulse number threshold at 100 nmol i.c.v. Tetraethylammonium at 10 nmol i.c.v. increased afterdischarge duration selectively and at 100 nmol i.c.v. induced spontaneous seizures. Glibenclamide (1–100 nmol i.c.v.) failed to change pulse number threshold and afterdischarge duration. Nimodipine (40 mg/kg i.p.) decreased afterdischarge duration and pulse number threshold. BAY K 8644 (1 mg/kg i.p.) decreased pulse number threshold and increased afterdischarge duration. In addition, voltage-clamp recording from neuroblastoma × glioma hybrid cells indicates that levcromakalim inhibited the fast component of Ca2+-dependent K+ currents, in addition to the inhibition of T- and L-types of voltage-dependent Ca2+ currents reported (Ito et al., FEBS Lett. 262, 313, 1990). These results suggest that levcromakalim shows anti- and proconvulsive actions in the hippocampus-generating partial seizures in rats and these effects might be, at least partly, caused by inhibiting Ca2+ channel and Ca2+-dependent K+ channel, respectively.
    European Journal of Pharmacology 10/1996; 311(1-311):37-44. DOI:10.1016/0014-2999(96)00400-1 · 2.68 Impact Factor
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    ABSTRACT: 1. We measured the urinary excretion of 19-noraldosterone in the spontaneously hypertensive rat (SHR) and stroke-prone SHR (SHRSP) during the development of hypertension and compared these measurements with Wistar-Kyoto (WKY) rats. 2. 19-Noraldosterone in rat urine was confirmed using HPLC-MS. Urine samples were collected from 4 and 9 week old SHR (n = 12), SHRSP (n = 12) and WKY rats (n = 9). 19-Noraldosterone was measured by specific radio immunoassay after purification of the urine extracts with HPLC. 3. There were no significant differences in plasma corticosterone among SHR, SHRSP and WKY rats at 4 and 9 weeks of age. Aldosterone levels were increased in the prehypertensive SHR and SHRSP. Nine week old SHRSP showed high plasma concentration of aldosterone compared with SHR or WKY rats of the same age. 4. Urinary excretion of 19-noraldosterone was increased in 4 week old SHR (15 +/- 4.2 pmol/day) and SHRSP (17 +/- 5.0 pmol/day) compared with WKY rats (9 +/- 3.9 pmol/day) at the same age. Nine week old SHR showed decreased urinary excretion of 19-noraldosterone compared with WKY rats at the same age. Urinary levels of 19-noraldosterone were higher in SHRSP (11 +/- 4.9 pmol/day) than in SHR (7 +/- 4.0 pmol/day) at 9 weeks of age. 5. Adrenal mineralocorticoids are suggested to be responsible for the abnormal vascular reactivity observed in SHRSP. Relatively elevated levels of 19-noraldosterone in SHRSP may contribute to malignant hypertension in this model.
    Clinical and experimental pharmacology & physiology. Supplement 01/1996; 22(1):S20-2. DOI:10.1111/j.1440-1681.1995.tb02882.x
  • Japanese Heart Journal 01/1995; 36(4):515-515. DOI:10.1536/ihj.36.515 · 0.40 Impact Factor
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    ABSTRACT: FK 506 is a powerful new immunosuppressant that is more effective in preventing and treating allograft rejection than cyclosporine (CyA). This study was undertaken to examine the effect of FK 506 on stimulation of endothelin-1 (ET-1) mRNA and secretion of ET-1 in human endothelial cells (EC) compared with the effects of CyA. The dose of 0.1 microM of CyA used in clinical practice induced expression of ET-1 mRNA and increased secretion of ET-1 in EC. The same dose of FK 506 had the same effect. A clinical dose of 0.01 microM of FK 506 did not induce expression of ET-1 mRNA and did not increase the secretion of ET-1 in EC. These findings suggest that the lower incidence of complications seen with FK 506 is due in part to its use at a lower clinical dose compared with that of CyA.
    Journal of Cardiovascular Pharmacology 02/1993; 22 Suppl 8:S310-2. DOI:10.1097/00005344-199322008-00081 · 2.11 Impact Factor
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    ABSTRACT: 1. The second-messengers system of bradykinin (BK) receptors was examined in NG108-15 neuroblastoma x glioma hybrid cells. 2. An application of BK induced an immediate outward (K+) current and acetylcholine (ACh) release, which are generated through inositol 1,4,5-trisphosphate (InsP3)-dependent Ca2+ ions. 3. Application of phorbol dibutyrate (a protein kinase C activator) produced a voltage-dependent inward current and inhibited another K+ (M)-current. 4. A similar current response has been produced by ACh in NG108-15 cells transfected with rodent muscarinic ACh receptor I and III subtype genes. 5. These results suggest a dual and time-dependent role for these two intracellular messengers in the control of neuronal signalling by BK and ACh.
    Comparative Biochemistry and Physiology Part C Comparative Pharmacology and Toxicology 02/1991; 98(1):129-37. DOI:10.1016/0742-8413(91)90189-Z
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    ABSTRACT: Extracellular perfusion with the antihypertensive agent cromakalim produced an inhibition of 22-66% in the low-threshold transient Ca2+ (T-like) current in NG108-15 hybrid cells. Cromakalim suppressed the high-threshold and long-lasting Ba2+ current (L-like Ca2+ current) by 29-73%, but had almost no effect on the high-threshold and inactivating Ba2+ current (N-like Ca2+ current). IC50 for T-like and L-like currents was the same at about 100 microM. The inhibitory effect developed relatively fast and was reversible. These results indicate that cromakalim can selectively inhibit the activity of inward Ca2+ currents.
    FEBS Letters 04/1990; 262(2):313-6. DOI:10.1016/0014-5793(90)80217-7 · 3.34 Impact Factor
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    ABSTRACT: FK 506 is a powerful new immunosuppressant that is more effective in preventing and treating allograft rejection than cyclosporine (CyA). This study was undertaken to examine the effect of FK 506 on stimulation of endothelin-1 (ET-1) mRNA and secretion of ET-1 in human endothelial cells (EC) compared with the effects of CyA. The dose of 0.1 [mu]M of CyA used in clinical practice induced expression of ET-1 mRNA and increased secretion of ET-1 in EC. The same dose of FK 506 had the same effect. A clinical dose of 0.01 [mu]M of FK 506 did not induce expression of ET-1 mRNA and did not increase the secretion of ET-1 in EC. These findings suggest that the lower incidence of complications seen with FK 506 is due in part to its use at a lower clinical dose compared with that of CyA. (C) Lippincott-Raven Publishers.
    Journal of Cardiovascular Pharmacology 22. · 2.11 Impact Factor