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T Emori

Publications and source records attributed to T Emori.

At least 19 recordsLinked to original sources
PubMed1992

Cellular mechanism of thrombin on endothelin-1 biosynthesis and release in bovine endothelial cell.

We have studied the cellular mechanism responsible for induction of preproendothelin (preproET)-1 mRNA and release of ET-1 by thrombin in cultured bovine endothelial cells (ECs). Thrombin induced an immediate and dose-dependent formation of inositol-1,4,5-trisphosphate (IP3) with a concomitant increase in intracellular Ca2+ concentration ([Ca2+]i). The thrombin-induced ET-1 release was abolished either by a phospholipase C inhibitor, a protein kinase C (PKC) inhibitor, or an intracellular Ca(2+)-chelator, whereas a Ca(2+)-channel antagonist was ineffective. A selective thrombin inhibitor (argatroban) decreased IP3 formation and the increase in [Ca2+]i and ET-1 release stimulated by thrombin. Northern blot analysis revealed that thrombin-induced expression of preproET-1 mRNA was inhibited completely by a PKC inhibitor and partially by argatroban. These data suggest that thrombin is involved in the mechanism of preproET-1 mRNA expression and subsequent ET-1 release, possibly through activation PKC and mobilization of intracellular Ca2+ resulting from the receptor-mediated phosphoinositide breakdown in ECs.

Animals↗
PubMed1992

Concomitant expression of receptor subtype and isopeptide of endothelin by human adrenal gland.

We studied whether specific receptors for endothelin (ET) isopeptide exist in human aldosterone-producing adenoma and normal adrenal cortex, and whether ET isopeptides are produced by human adrenal gland. Competitive binding studies using [125I]ET-1 as a radioligand revealed the presence of a single class of high-affinity binding sites for ET-1 with the apparent KD of 70 +/- 31 pM and Bmax of 226 +/- 139 fmol/mg protein in adenoma membranes almost comparable to those in adjacent normal cortex. The apparent Ki for ET-2 and ET-3 were 89 +/- 33 pM and 82 +/- 16 pM, respectively. Northern blot analysis of poly(A)+ RNA of adenoma and adjacent normal cortex using cDNAs for ET receptor subtype (ETA, ETB) and ET isopeptide (ET-1, ET-3) as probes revealed that ETA and ETB receptors as well as ET isopeptides (preproET-1, preproET-3) are concomitantly expressed in both tissues. Our data demonstrate for the first time that ET receptor subtype (ETA and ETB) and ET isopeptide (ET-1 and ET-3) are concomitantly expressed by human adrenal cortex, suggesting the potential role of ETs as a local mediator in human adrenal gland.

Adenoma↗
PubMed1992

Induction of TU abnormalities in patients with torsades de pointes.

1. TU abnormalities could be induced by the specific interventions in the majority of the patients with TDP in chronic stage: isoproterenol in congenital long QT patients, disopyramide in Ia-related TDP patients, and slow heart rate in bradycardia-related TDP patients. 2. Humps in MAP could be recorded in all patients with congenital long QT syndrome by isoproterenol, in half of the patients with Ia-related TDP by disopyramide, but in none of the control patients by these agents. 3. The results suggested that TU abnormalities and the occurrence of hump in MAP were hypersensitive reactions. 4. The results also suggested that specific intervention was not enough for the appearance of marked TU abnormalities in some TDP patients, especially in Ia-related TDP patients. Additional aggravating factors were probably required for marked TU abnormalities and the occurrence of TDP in these patients.

Action Potentials↗
PubMed1992

Effects of three distinct natriuretic peptides on receptor binding and guanylate cyclase activities in rat glioma cells.

Receptor binding and cyclic GMP generation by three distinct natriuretic peptides (ANP, BNP, CNP) were studied in a cultured rat glioma cell line (C6). Binding studies revealed the presence of high-affinity binding sites for three natriuretic peptides with almost comparable affinities. In contrast, CNP and BNP were almost equipotent in stimulating intracellular cyclic GMP generation over the low concentration range, but CNP caused further elevation in the high concentration range, whereas ANP was minimally effective. Our data suggest that the glioma cells possess receptors more responsive to CNP than ANP and BNP despite no apparent correlation between receptor binding affinities and cyclic GMP responses.

Animals↗
PubMed1992

Recovery functions of common peroneal, posterior tibial and sural nerve somatosensory evoked potentials.

We studied recovery functions of the somatosensory evoked potentials (SEPs) of common peroneal (CPN), posterior tibial (PTN) and sural nerves (SN) using a paired conditioning-test paradigm. The interstimulus interval (ISI) of paired stimuli ranged from 2 to 400 msec. In all SEPs with ISIs of 12-20 msec, the amplitude recovery was close to or beyond 100% of the control response, though their latencies and wave forms were not the same as the control. Further increases of the ISI resulted in significant depression of SEP (late phase suppression), most markedly in CPN, and less prominently in SN-SEP. With a longer than 50 msec ISI there was progressive recovery of SEP, but full recovery differed depending on the nerve stimulated; 400 msec ISI was required for CPN-, 250 msec for PTN- and 100 msec for SN-SEP. The peroneal nerve block by local anesthetic injected just distal to the stimulus electrodes abolished the late phase SEP suppression observed before the nerve block. These findings suggest that the late phase SEP suppression is attributable to the "secondary" afferents as a result of activation of peripheral receptors (muscle, joint and/or cutaneous) by the efferent volley initiated from the stimulus point. The greater and longer duration of peripheral receptor activation in CPN than in PTN or SN stimulation could explain the more pronounced and the longer duration of late phase suppression in CPN-SEP.

Adult↗
PubMed1992

L-arginine infusion induces hypotension and diuresis/natriuresis with concomitant increased urinary excretion of nitrite/nitrate and cyclic GMP in humans.

1. The vascular endothelium produces endothelium-derived relaxing factor (EDRF) or nitric oxide (NO), which exerts vasodilation through cyclic guanosine monophosphate (cGMP) as a second messenger. To determine whether EDRF has any vasodilating and natriuretic action in man, the present study examined the effects of L-arginine (L-Arg), a substrate for NO, on the responses of mean blood pressure (MBP) and heart rate (HR); plasma concentrations of cGMP, atrial natriuretic factor (ANF) and nitrite/nitrate (NOx); urinary excretion of sodium, cGMP and NOx; and urinary flow in eight normal male subjects. These parameters were compared with those following saline infusion in the same subjects. Clearance of para-aminohippuric acid (PAH) and inulin was studied in five normal subjects. 2. Infusion of L-Arg (30 g) caused a significant fall in MBP (-8 mmHg) with a concomitant rise in HR (10 beats/min), while saline infusion had no effects on these parameters. 3. Neither L-Arg nor saline infusion caused appreciable changes in plasma concentrations of ANF or NOx. Plasma cGMP concentrations increased significantly during (1.7-fold) and after (1.9-fold) L-Arg infusion, but only slightly (1.3-fold) during saline infusion. 4. Urine flow increased more remarkably following L-Arg infusion than that following saline infusion. Remarkable increases in urinary excretion of sodium and fractional excretion of sodium were observed after L-Arg infusion compared with those after saline infusion. Natriuresis was associated with enhanced urinary excretion of cGMP and Nox. Urinary Nox excretion showed positive correlations with urinary flow (r = 0.69, P less than 0.001) and with urinary cGMP excretion (r = 0.60, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Induction of endothelin-1 gene by angiotensin and vasopressin in endothelial cells.

To elucidate the cellular mechanism of endothelin-1 biosynthesis induced by angiotensin and vasopressin, we first cloned and sequenced full-length bovine preproendothelin-1 complementary DNA (cDNA) from a cultured bovine carotid artery endothelial cell cDNA library. The predicted bovine preproendothelin-1 consists of 202 amino acid residues and has a high percentage of homology to human, porcine, and rat preproendothelin-1 (70%, 81%, and 77%, respectively). Big endothelin-1, an intermediate form, consists of 39 residues differing only at position Val28 from porcine (Ile28) and His27 from rat (Arg27). The predicted 21-residue mature endothelin-1 is identical to human, porcine, rat, canine, and mouse endothelin-1. Northern blot analysis with the cloned cDNA as a probe demonstrated that a single 2.3-kb preproendothelin-1 messenger RNA (mRNA) is expressed not only in endothelial cells, but also in various bovine tissues, including lung, brain, heart, intestine, kidney, ovary, and urinary bladder. Angiotensin II and arginine vasopressin immediately and dose-dependently induced expression of preproendothelin-1 mRNA, whose effects were abolished by specific receptor antagonists. These findings suggest that stimulation of endothelin-1 secretion from endothelial cells by both agonists may be principally due to induction of preproendothelin-1 mRNA.

Amino Acid Sequence↗
PubMed1992

Ataxic hemiparesis following thalamic lacunar infarction.

A 60-year-old man developed left hemiparesis and homolateral ataxia with normal sensation and normal somatosensory evoked potentials. A lacunar infarct with gadolinium enhancement in the right dorsolateral part of the thalamus was demonstrated on magnetic resonance imaging. Thalamic lesion is a relatively rare cause of ataxic hemiparesis; most of the reported cases of ataxic hemiparesis caused by thalamic lesion were accompanied by sensory disturbances. This is an interesting case which suggested that the thalamic lesion could be responsible for the ataxic hemiparesis without a sensory disturbance.

Ataxia↗
PubMed1992

Circulating and excreted forms of atrial natriuretic peptide in healthy subjects and patients with renal diseases.

The immunoreactivity of plasma and urine atrial natriuretic peptide (ANP) was measured in patients with renal disease and in healthy volunteers. The molecular forms of ANP in these subjects were estimated by gel permeation chromatography and reverse phase high performance liquid chromatography. No significant increase in plasma ANP was observed in patients with nephrotic syndrome or non-oliguric chronic renal failure compared to healthy volunteers. However, plasma ANP levels were significantly increased in patients on hemodialysis (normal 18.6 +/- 11.4 fmol/ml; hemodialysis 91.2 +/- 69.9 fmol/ml, p < 0.01). Chromatographic analyses revealed that plasma ANP consisted of only alpha-ANP or combined alpha- and gamma-ANP in healthy volunteers and in nephrotic patients, whereas beta-ANP frequently appeared in the plasma of both dialyzed and non-dialyzed chronic renal failure patients. Excreted forms, except in subjects free from renal disease where gamma-ANP may serve as a potential marker of glomerular injury in humans.

Adult↗
PubMed1991

Endothelin-3 stimulates production of endothelium-derived nitric oxide via phosphoinositide breakdown.

Cultured bovine endothelial cells (EC) have specific receptors for endothelin (ET)-3 functionally coupled to phosphoinositide breakdown. We studied whether ET-3 stimulates synthesis of nitric oxide (NO), an endothelium-derived relaxing factor that activates soluble guanylate cyclase in EC, and whether the ET-3-induced NO formation involves G-proteins. ET-3 dose-dependently stimulated production of intracellular cGMP in EC, of which effects were abolished by pretreatment with NG-monomethyl L-arginine, an inhibitor of NO synthesis, and methylene blue, an inhibitor of soluble guanylate cyclase. The stimulatory effects of ET-3 on cGMP production, inositol trisphosphate formation and increase in cytosolic free Ca2+ concentration were similarly blocked by pretreatment with pertussis toxin (PTX). These data suggest that ET-3 induces synthesis of NO mediated by phosphoinositide breakdown via PTX-sensitive G-protein in EC.

Animals↗
PubMed1991

The silent period produced by electrical stimulation of mixed peripheral nerves.

The electromyographic silent period (SP) produced by electrical stimulation of the median and ulnar nerve, before and after lidocaine block of the ulnar nerve at the elbow, was recorded in the voluntarily contracting abductor pollicis brevis (APB) muscle of 4 normal subjects. Prior to block, stimulation of the corresponding segment in either nerve (e.g., wrist and elbow) elicited SPs with similar end points. With more proximal stimulation, the SPs consistently ended earlier. Following the block, ulnar nerve stimulation below the elbow failed to elicit a SP in any subject, despite a mechanical twitch caused by the antagonistic contraction of adductor pollicis muscle. Ulnar nerve stimulation above the block elicited a SP in all subjects similar to the preblock SP. In all 4 subjects, submaximal median nerve stimulation at the wrist produced an H-reflex, followed by a SP in the absence of the direct M-response. This SP, due to selective activation of sensory fibers, lacked a collision component, but, was otherwise similar to the SP elicited by supramaximal wrist stimulation. These findings indicate that the ascending volley following electrical stimulation of a mixed peripheral nerve produces the SP without apparent contribution from the descending motor volley.

Adult↗
PubMed1991

Recovery functions of fast frequency potentials in the initial negative wave of median SEP.

Following far-field potential of P14 after median nerve stimulation, we identified several small wavelets, designated here as fast frequency potentials or FFP, over the ascending and descending phases of the major negative wave of 'N20.' In 10 normal subjects who had well defined FFP, namely N16, N17, N18 and N19, we studied recovery functions of FFP by applying paired (condition and test) stimuli of various interstimulus intervals (ISIs) ranging from 3 to 150 msec. Recovery of FFP was determined by the difference wave forms, i.e., subtracting the response of conditioning stimuli from the response to paired stimuli. Measuring latencies and amplitude of FFP and also of the far-field potential of P14, we found recoveries of P14 and each FFP to be different; P14 recovered with the shortest ISI while progressively longer ISIs were required for full recovery of the later FFP. This finding suggests the existence of progressively increased number of interspersed synapses from the early to late FFP. It is unlikely that FFP represents passage of the afferent volley from one anatomical site to the next, but rather that they are cortically generated via a closely situated polysynaptic network. The polysynaptic nature of FFP is consistent with the observation that they disappear in sleep and also during anesthesia. The study indicates that FFPs represent different physioanatomical systems from the primary negative wave of 'N20' that results from specific sensory input to the primary sensory cortex.

Adolescent↗
PubMed1991

Urinary excretion of endothelin-1 in normal subjects and patients with renal disease.

To elucidate the pathophysiological significance of urinary endothelin-1 (ET-1), we measured urinary excretion of ET-1-like immunoreactivity (L1) in 17 patients with renal disease and 9 normal subjects. Twenty-four hour urinary ET-1-L1 excretion in patients with renal disease (358 +/- 68 ng, mean +/- SE) was significantly (P less than 0.005) greater than that of normal subjects (77 +/- 5 ng). In patients with renal disease. ET-1-L1 clearance (CET) exceeded creatinine clearance (CCR); CET/CCR (305 +/- 81%) was significantly (P less than 0.005) greater than that of normal subjects (43 +/- 13%). The 24-hour urinary excretion of ET-1-L1 in patients with renal disease showed significant correlation with that of N-acetyl-beta-D-glucosaminidase (r = 0.587, P less than 0.05), beta 2-microglobulin (r = 0.614, P less than 0.01) and albumin (r = 0.484, P less than 0.05). Intravenous infusion of saline (500 ml) in seven normal subjects did not affect urinary ET-1 excretion rate. These data suggest that urinary excretion of ET-1 derives mainly from renal tubular secretion at least in patients with renal disease, and that degradation and/or reabsorption of ET-1 at the tubular site may also contribute to the renal handling of ET-1. Therefore, urinary excretion of ET-1 should serve as a potential marker for renal injury.

Acetylglucosaminidase↗
PubMed1991

Endothelin-3 stimulates prostacyclin production in cultured bovine endothelial cells.

Among three endothelin (ET) isopeptides, ET-3 shows the most potent initial depressor response through endothelium-dependent mechanism. We have recently reported that ET-3 induces receptor-mediated phosphoinositide breakdown, which increases the intracellular Ca2+ concentration [( Ca2+]i) and stimulates synthesis of endothelium-derived relaxing factor (EDRF), or nitric oxide (NO), in endothelial cells (ECs). We examined whether ET-3 has any effect on synthesis of prostacyclin, a potent vasodilator prostanoid in bovine ECs. ET-3 dose-dependently (10(-10) - 10(-8) M) stimulated the formation of 6-keto-prostaglandin F1 alpha, a stable metabolite of prostacyclin, in culture media of ECs, whose stimulatory effect was inhibited by indomethacin, a cyclooxygenase inhibitor. These data suggest that ET-3 stimulates, in addition to EDRF (NO), the synthesis and release of prostacyclin.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Cellular mechanism of endothelin-1 release by angiotensin and vasopressin.

Release of endothelin-1, a novel potent vasoconstrictor peptide originally isolated from endothelial cells, from cultured bovine endothelial cells has been shown to be stimulated by arginine vasopressin and angiotensin II. To elucidate the cellular mechanism by which endothelin-1 is released by these vasoconstrictors, we tested the effects of several compounds on the agonist-induced endothelin-1 release and studied the changes of cytosolic free Ca2+ concentrations and phosphoinositide breakdown by these agonists in cultured bovine endothelial cells. Protein kinase C inhibitors (H-7, staurosporine), an intracellular Ca2+ chelator, and an inhibitor of phospholipase C (neomycin), all abolished the agonist-induced endothelin-1 release, whereas the Ca2+ channel blocker nicardipine was ineffective. Although synthetic 1,2-diglyceride (diolein) dose dependently stimulated endothelin-1 release, downregulation of protein kinase C after pretreatment with phorbol ester resulted in decreased effects to increase endothelin-1 release by the agonists. Both arginine vasopressin and angiotensin II induced immediate and transient increases in intracellular Ca2+ levels of fura-2-loaded endothelial cells as well as formation of inositol trisphosphate; the agonist-induced intracellular Ca2+ increases were not affected either by nicardipine or by chelating extracellular Ca2+. The arginine vasopressin- and angiotensin II-induced intracellular Ca2+ increases, inositol trisphosphate formation, and endothelin-1 release were completely abolished by V1-receptor antagonist and saralasin, respectively. It is concluded that arginine vasopressin and angiotensin II stimulate the release of endothelin-1 by a common mechanism, involving receptor-mediated mobilization of intracellular Ca2+ and activation of protein kinase C in endothelial cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

The effect of stimulus rate upon common peroneal, posterior tibial, and sural nerve somatosensory evoked potentials.

We examined the effect of stimulus rate on somatosensory evoked potentials (SEPs) following stimulation of the common peroneal nerve (CPN) at the knee, and the posterior tibial nerve (PTN) and sural nerve (SN) at the ankle. We measured the amplitude of P40-N50 and N50-P60 in the PTN-SEP and corresponding amplitude of CPN-SEP and SN-SEP at the rate of 2.3, 3.4, 4.1, and 5.1 Hz. When the stimulation rate was increased from 2.3 to 5.1 Hz, the P40-N50 amplitude decreased by 50% for the CPN-SEP and 20% for the PTN-SEP. Also, the N50-P60 amplitude was reduced by 30% in the CPN-SEP and 20% in the PTN-SEP. In contrast, this change in stimulus rate produced no significant amplitude decline in the SN-SEP. Blocking the peroneal nerve with lidocaine just distal to the stimulating electrodes eliminated the descending peroneal nerve volley and abolished the amplitude attenuation observed with the faster stimulus rate. The findings suggest that at higher rates of stimulation, the afferent volleys induced by the movements that follow mixed nerve stimulation interfere with the SEP produced by electrical activation of the sensory afferents. The interference is greater when the more proximal site of the mixed nerve is stimulated.

Adult↗
PubMed1991

[Cardiac pacing].

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Arrhythmias, Cardiac↗