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Biomedical subjects

T Izawa

Publications and source records attributed to T Izawa.

At least 55 records · Page 3Linked to original sources
PubMed1996

Pulpal blood flow assessed by laser Doppler flowmetry in a tooth with a horizontal root fracture.

Horizontal root fractures of both maxillary central incisors were diagnosed radiographically; neither responded to electric pulp testing nor to cold testing. The pulp of the right incisor was necrotic, whereas the pulpal status of the left incisor was uncertain. Pulpal blood flow of the teeth was measured with laser Doppler flowmetry. The blood flow of the left central incisor was 4.0. Eight months after the injury, a local anesthetic with a vasoconstrictor was administered to confirm pulp vitality. The blood flow of the tooth was decreased to 51% of the preanesthesia value after the local anesthesia. At 19 months after the injury, it responded to both the electric pulp test and cold test. Laser Doppler flowmetry is a noninvasive method of evaluating the blood flow status in human teeth, and it may provide a clinically reliable method of assessing pulpal vitality.

Adolescent↗
PubMed1996

The rab16B promoter of rice contains two distinct abscisic acid-responsive elements.

To localize abscisic acid (ABA)-inducible gene expression of rab16 genes, rab16A promoter was linked to the gusA reporter gene encoding beta-glucuronidase and introduced into rice (Oryza sativa L.) plants. The activity of rab16A promoter was induced by ABA and osmotic stresses in various tissues of vegetative and floral organs. In anthers and embryos, rab16A promoter was active in the absence of ABA. To elucidate cis-elements of the rab16 promoter that confer ABA-inducible expression, variously modified 40-bp fragments (-264 to -225) of the rab16B promoter were fused to a truncated (-46 bp) cauliflower mosaic virus 35S minimal promoter, and their activities in protoplasts were analyzed. The transient assays revealed that the 40-bp fragment consists of two separate ABA-responsive elements, motif 1 (AGTACGTGGC) and motif III (GCCGCGTGGC). Motif I and motif III are both required for ABA induction; however, each can substitute for the other. Further analyses of these motifs indicated that motif III has a distinct DNA sequence specificity as an ABA-responsive element from motif I, suggesting that the two motifs interact with different transcription factors in vivo.

Abscisic Acid↗
PubMed1996

Glucocorticoid-mediated generation of suppressor macrophages with high density Fc gamma RII during acute cold stress.

Acute cold stress induces adherent cells with suppressor function, resulting in immunosuppression. Glucocorticoids (GC) are known as an inhibitor of the immune system and are increased by stress through stimulation of the hypothalamic-pituitary-adrenal axis. To elucidate the mechanisms underlying acute cold stress-induced immunosuppression, functions and surface phenotypes of murine peritoneal cells of the monocyte/macrophage lineage from acute cold-stressed mice (5 C for 3 or 24 h) in addition to the role of GC in the immunomodulation were investigated. Flow cytometric analysis revealed that the proportion of MAC-1+ cells with a high density of Fc gamma RII (Fc gamma RIIbright cells) was markedly increased in the peritoneal exudate cells from acute cold-stressed mice. These Fc gamma RIIbright cells were also stained with F4/80, a monoclonal antibody directed specifically against the mouse mature macrophages. The prominent suppressor activity for Concanavalin A (Con A) responses of control spleen cells was found in Fc gamma RIIbright cells, whereas MAC-1+ cells, with a low density of Fc gamma RII (Fc gamma RIIdull cells), from the stressed mice did not suppress the Con A responses. Fc gamma RIIbright cells from control mice also suppressed the Con A responses; the inhibitory effect was considerably less than that of cells from acute cold-stressed mice. As was anticipated, serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of GC receptor messenger RNA was observed in Fc gamma RIIbright cells from these mice. The increase in Fc gamma RIIbright cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of Fc gamma RIIbright cells in peritoneal exudate cells of control mice. These results suggest that the generation of Fc gamma RIIbright suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated to a greater or lesser degree by the action of GC through the GC receptor.

Acute Disease↗
PubMed1996

Decreased vascular sensitivity after acute exercise and chronic exercise training in rat thoracic aorta.

The effects of acute and chronic physical exercise on the sensitivity of isolated aorta to norepinephrine were investigated. After chronic exercise, the EC50 values for norepinephrine increased 3.1-fold and 2.3-fold in endothelium-intact and in endothelium-denuded aorta, respectively. The attenuated sensitivity of aorta to norepinephrine after chronic exercise was still evident in endothelium-denuded aorta, but to a lesser extent than in endothelium-intact aorta. After acute exercise, in control rats, the EC50 values increased 7.8-fold and 5.4-fold in endothelium-intact and endothelium-denuded aorta, respectively. The attenuated sensitivity of aorta to norepinephrine after an acute exercise was still evident in endothelium-denuded aorta. In trained rats, the EC50 values increased 2.3-fold and 2.6-fold in endothelium-intact and endothelium-denuded aorta, respectively. Thus, acute exercise was less effective in trained than in control rats. No significant difference in 60 mM KCl-induced tension between control and trained rats was observed with or without endothelium after acute and chronic exercise. The results suggest that levels of endothelium-dependent releasing factor may increase in response to norepinephrine after acute and chronic exercise. In addition, the attenuated sensitivity of aorta to norepinephrine after acute and chronic exercise may also result from the change(s) in the receptor sites. However, the degree of desensitization caused by acute exercise was less in the rats adapted to chronic exercise than in the sedentary control rats.

Adrenergic alpha-Agonists↗
PubMed1995

Effects of KRN4884, a novel K channel opener, on the cardiovascular system in anesthetized dogs: a comparison with levcromakalim, nilvadipine, and nifedipine.

Pharmacological profiles of KRN4884, 5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine+ ++, were evaluated in in vitro and in vivo experiments. In rat isolated aorta, KRN4884 (10(-10)-10(-5) M) produced a concentration-dependent relaxation. Pretreatment with glibenclamide (10(-7)-10(-6) M) produced a rightward shift of the concentration-response curve for KRN4884. In anesthetized dogs, KRN4884 (3 and 10 micrograms/kg intravenously, i.v.), levcromakalim (3 and 10 micrograms/kg i.v.), nilvadipine (1-10 micrograms/kg i.v.), and nifedipine (1-10 micrograms/kg i.v.) produced decreases in mean blood pressure (MBP), total peripheral vascular resistance (TPR), and coronary vascular resistance (CVR), and increases in aortic blood flow (AoF) and coronary blood flow (CBF). The percentage decrease in CVR was greater than that in TPR with KRN4884 and levcromakalim, but nilvadipine and nifedipine showed no significant differences between CVR and TPR in percentage decreases. Heart rate (HR) was slightly increased by KRN4884 but was not affected by levcromakalim, nilvadipine, or nifedipine. Left ventricular dP/dt (LVdP/dt) was reduced only by nifedipine in a dose-dependent manner. The duration of the hypotensive action of KRN4884 was longer than those of levcromakalim and nifedipine and was similar to that of nilvadipine. The duration of the decreases in TPR and CVR induced by KRN4884 was longer than those induced by levcromakalim and nifedipine and shorter than that induced by nilvadipine. These results suggest that the cardiovascular effects of KRN4884 are very similar to those of the K channel opener levcromakalim and Ca channel blockers such as nilvadipine and nifedipine. However, the hypotensive effects of KRN4884 are long-acting in comparison with those of levcromakalim and the selective effect of KRN4884 on coronary vasculature is greater than those of nilvadipine and nifedipine.

Anesthesia↗
PubMed1995

Effect of Kil769, a novel K(+)-channel opener, on sensitivity to Ca2+ of contractile elements and inositol phosphate formation in porcine coronary artery.

To determine whether Kil769, a novel K(+)-channel opener, acts intracellularly in vasorelaxation, we compared the effects of Kil769 on force of contraction, intracellular Ca2+ concentration ([Ca2+]i) and inositol phosphate (IP1) formation with those of Ca(2+)-channel blockers in isolated porcine coronary artery. Kil769 (10 microM) and verapamil (1 microM), which produced submaximal relaxation, reduced the increase in [Ca2+]i and force of contraction induced by 25 mM KCl. Verapamil reduced [Ca2+]i and the force of contraction to a similar extent but Kil769 reduced force of contraction more strongly than it did [Ca2+]i. Kil769 also inhibited U46619 (9,11-dideoxy-9 alpha,11 alpha-methano-epoxy-PGF2 alpha)-induced IP1 formation and glibenclamide blocked its inhibitory effect. These results suggest that the opening of K+ channels induced by Kil769 reduces the Ca2+ sensitivity of contractile elements and inositol phospholipid hydrolysis which is related to the Ca2+ release from intracellular storage.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Acute or chronic exercise alters angiotensin II-induced contraction of rat aorta.

Chronic exercise substantially shifted the dose-response curve for angiotensin II (ANG II)-induced contractions to the right with increases in the EC50 value in both endothelium-intact and endothelium-denuded aortae. An acute endurance exercise also caused a 3-fold increase in the EC50 value in both endothelium-intact and endothelium-denuded aortae from sedentary control rats. Whereas, no substantial increase in the EC50 value was observed in trained rats after an acute endurance exercise. Thus, chronic exercise attenuates ANG II receptor-mediated contraction of rat aortae. An acute exercise also caused the reduced responses to ANG II in sedentary control rats but not in chronically exercise-trained rats.

Angiotensin II↗
PubMed1994

Pharmacological analysis of the inhibitory effects of KRN2391 on endothelin-1-induced contraction in isolated large coronary artery of the pig.

1. The relaxant effect of KRN2391, N-cyano-N'-(2-nitroxyethyl)-3-pyridine-carboximidamide-mo nomethanesulfonate (with both K+ channel opener and nitrate actions), nifedipine (Ca2+ channel blocker), nitroglycerin (nitrate) and cromakalim (K+ channel opener) were investigated in isolated porcine large coronary arteries contracted by endothelin-1. These drugs inhibited endothelin-1-induced contraction in a concentration-dependent manner. 2. The relaxation induced by KRN2391 was nearly complete at their maximum effects, but nifedipine and cromakalim could not produce complete relaxation. 3. The concentration-relaxation curves for KRN2391 underwent a rightward shift in the presence of methylene blue or glibenclamide. The concentration ratios of KRN2391 calculated based on EC50 values were 2.8 and 3.7 in the presence of methylene blue and glibenclamide, respectively. 4. The concentration-relaxation curves for nitroglycerin and cromakalin underwent a rightward shift in the presence of methylene blue and glibenclamide, respectively, and the concentration ratios of nitroglycerin and cromakalim were 12.0 and 6.3. 5. These relaxant effects of KRN2391 and nitroglycerin on endothelin-1-induced contraction of porcine coronary artery were greater than those of cromakalim and nifedipine. This potent relaxant action of KRN2391 on endothelin-induced contraction is thought to be based on both a nitrate action and a K+ channel opening action.

Animals↗
PubMed1994

Comparative analysis of vasodilating mechanisms of Ki1769, Ki3315 and KRN2391, pyridinecarboximidamide derivatives, in porcine isolated coronary artery.

1. The vasodilating mechanisms of pyridinecarboximidamide derivatives which have a nitroxyl group (KRN2391), a phenyl group (Ki1769) or a hydroxyl group (Ki3315) were studied in porcine isolated coronary artery. 2. KRN2391 (10(-6) M) increased cyclic GMP formation but did not affect intracellular cyclic AMP level. Ki1769 (10(-5) M) and Ki3315 (10(-3) M) had no effect on intracellular cyclic GMP and cyclic AMP levels. 3. Despite producing submaximal relaxation at KRN2391 (10(-6) M) and nitroglycerin (10(-6) M), the increase in cyclic GMP caused by KRN2391 was lower than that caused by nitroglycerin. 4. Methylene blue (10(-5) M) inhibited KRN2391- and nitroglycerin-induced relaxations but did not affect Ki1769- and Ki3315-induced relaxation. 5. Glibenclamide (10(-6) M) inhibited KRN2391-, Ki1769- and Ki3315-induced relaxation but did not affect nitroglycerin-induced relaxation. 6. These results suggest that the nitroxyl group of KRN239 contributes to its nitrate action and the pyridinecarboximidamide moiety plays an important role of developing a K channel opening action.

Animals↗
PubMed1994

Cardiovascular effects of KRN2391, nitroglycerin and cromakalim in dihydroergotamine-treated pithed rats.

1. The effects of KRN2391 on the cardiovascular system were compared with those of nitroglycerin and cromakalim in pithed rats treated with dihydroergotamine (DHE) in order to examine the effects of these drugs on venous blood vessels. 2. DHE (100 micrograms/kg, i.v.) produced increases in mean blood pressure (MBP), cardiac output (CO) and central venous pressure (CVP) without changes in total peripheral vascular resistance (TPR) and heart rate (HR) based on venoconstriction. The DHE-treated pithed rats, nitroglycerin (30 micrograms/kg, i.v.) decreased CO and CVP whereas cromakalim (30 micrograms/kg, i.v.) produced a slight increase in CO followed by a decrease and did not affect CVP. KRN2391 (30 micrograms/kg, i.v.) produced a decrease in CVP without affecting CO. Decreases in MBP and TPR were induced by all drugs. 3. These results suggest that nitroglycerin acts predominantly as a venodilator and KRN2391 and cromakalim showed a venodilating action in addition to an arterial dilating action in DHE treated pithed rats. However, the venodilating action of KRN2391 in this condition is more potent than that of cromakalim.

Animals↗
PubMed1994

Vasospasmolytic effect of KRN2391 on 3,4-diaminopyridine-induced rhythmic contraction of porcine coronary artery.

1. In the present study, we examined the vasospasmolytic effect of KRN2391 on rhythmic contractions of porcine coronary artery caused by 3,4-diaminopyridine (3,4-DAP) compared with cromakalim and nitroglycerin. 2. KRN2391 at 10(-7) showed a tendency to prolong the cycle length and at 10(-6) M completely eliminated rhythmic contractions in all preparations. The elimination by 10(-6) M KRN2391 was antagonized by either oxyhemoglobin (10(-5) M) or glibenclamide (3 x 10(-6)) although not completely. 3. Cromakalim at 10(-5) M and nitroglycerin at 10(-7) M completely eliminated 3,4-DAP-induced rythmic contractions in all preparations. The elimination by cromakalim and nitroglycerin was completely antagonized by glibenclamide and oxyhemoglobin, respectively. 4. The present study suggests that the vasospasmolytic effect of KRN2391 on 3,4-DAP-induced rhythmic contractions is based on its nitrate action and K channel opening action.

4-Aminopyridine↗
PubMed1994

Pharmacological analysis of the effect of KRN2391 on coronary vasculature in perfused rat heart.

1. The antagonism by glibenclamide of the effects of KRN2391, cromakalim and nifedipine on coronary flow (CF) were compared in isolated perfused rat hearts. 2. KRN2391, cromakalim and nifedipine increased CF in a concentration-dependent manner. In the presence of glibenclamide, the concentration-effect curves on CF for KRN2391 and cromakalim shifted to the right but that for nifedipine did not change. 3. The EC50 values increased about 6.6-fold for KRN2391 and 19.0-fold for cromakalim in the presence of glibenclamide. 4. These results suggest that the increase in CF induced by KRN2391 is due to both glibenclamide-sensitive and insensitive mechanisms.

Animals↗
PubMed1994

Plant bZIP proteins gather at ACGT elements.

ACGT cis-acting DNA sequence elements have been identified in a multitude of plant genes regulated by diverse environmental, physiological, and environmental cues. In vivo transient and transgenic plant expression studies have shown that these ACGT elements are necessary for maximal transcriptional activation. Plants possess a conserved family of DNA-binding proteins specific for these DNA sequence motifs. Well-defined in terms of nucleotide sequence required for protein/DNA interactions and transcriptional activation, various ACGT elements have been used as molecular probes to clone sequence-specific DNA binding proteins. All plant DNA-binding proteins specific for ACGT elements belong to the bZIP classification. Most recombinant bZIP proteins can interact with ACGT elements derived from different plant genes, albeit with different affinity. Systematic protein/DNA binding studies have shown that sequences flanking the ACGT core affect bZIP protein binding specificity. These studies have provided the basis for a concise ACGT nomenclature and defined high-affinity A-box, C-box, and G-box elements. Plant bZIP factors can be classified according to their quantitative binding affinities for high-affinity ACGT elements. Potential molecular mechanisms that may control how plant bZIP proteins activate plant gene expression are discussed.

Amino Acid Sequence↗
PubMed1994

The rice bZIP transcriptional activator RITA-1 is highly expressed during seed development.

Systematic protein-DNA binding studies have shown that plant basic leucine zipper (bZIP) proteins exhibit a differential binding specificity for ACGT motifs. Here, we show that the rice transcription activator-1 (RITA-1) displays a broad binding specificity for palindromic ACGT elements, being able to bind A-, C-, and G-box but not T-box elements. By using gel mobility shift assays with probes differing in sequences flanking the hexameric core, we identified high-affinity A-, C-, and G-box binding sites. Quantitative and competition DNA binding studies confirmed RITA-1 specificity for these sites. Using rice protoplasts as a transient expression system, we demonstrated that RITA-1 can transactivate reporter genes possessing high-affinity but not low-affinity RITA-1 binding sites. Our results established a direct relationship between in vivo transactivation and in vitro binding activity. Transient expression assays that demonstrated the ability of RITA-1 to transactivate a construct containing rita-1 5' flanking sequences suggest that the factor may be autoregulated. Histochemical analysis of transgenic rice plants showed that a rita-1-beta-glucuronidase transgene is expressed in aleurone and endosperm cells of developing rice seeds. We propose that RITA-1 plays a role in the regulation of rice genes expressed in developing rice seeds.

Amino Acid Sequence↗
PubMed1994

Differential vasodilator properties of KRN2391, cromakalim, nitroglycerin and nifedipine in rabbit isolated femoral artery and vein.

1. The selectivity for artery and vein of KRN2391, cromakalim, nitroglycerin and nifedipine was examined in isolated femoral artery and vein preparations of the rabbit. 2. All drugs produced a concentration-dependent relaxation in both femoral artery and vein. 3. Nitroglycerin was more potent in femoral vein than in femoral artery at all concentrations. The EC50 value obtained in the vein was about 14 times smaller than that obtained in artery. 4. Cromakalim and nifedipine were almost equipotent on both vascular preparations. Cromakalim at the highest concentration (10(-5) M) produced 88 and 78% relaxation in femoral artery and vein, respectively. The maximum relaxation induced by nifedipine (10(-6) M) was less than 50% in both preparations. 5. KRN2391 was active at a lower concentration in the vein than in the artery and its maximum relaxation at 10(-5) M was about 90% in both preparations. 6. Glibenclamide (10(-6) M) inhibited the vasorelaxation caused by KRN2391 in both artery and vein. Methylene blue (10(-5) M) also inhibited the relaxant action of KRN2391 but this action was slight in the artery. 7. These results suggest that KRN2391 and nitroglycerin are more potent in the vein than in the artery and cromakalim and nifedipine are equipotent in both. It is considered that the relaxation induced by low concentrations of KRN2391 reflects predominantly its action as a nitrate and that at high concentrations it acts as a K+ channel opener in addition to its nitrate action. The different vascular selectivities of these drugs are thought to relate to the differences in their mechanisms of action in vascular smooth muscle.

Animals↗
PubMed1994

Increase in cytosolic free Ca2+ in corticotropin-stimulated white adipocytes.

The mechanism of the adrenal corticotropin hormone (ACTH)-stimulated increase in cytosolic free Ca2+ concentration ([Ca2+]i) was investigated in rat white adipocytes. ACTH at concentrations > 10 mU/ml caused a rapid and transient increase in [Ca2+]i followed by a small but sustained elevation of [Ca2+]i. A similar phenomenon was also induced by alpha-adrenergic or synthetic ACTH stimulation. The effect of norepinephrine (NE) plus ACTH on [Ca2+]i was nearly additive. Pertussis toxin completely blocked the ability of ACTH or NE to increase [Ca2+]i. NE but not ACTH caused a significant increase in inositol 1,4,5-trisphosphate levels. ACTH caused a rapid and transient accumulation of [3H]arachidonic acid (AA) and a marked loss of [3H]AA from phosphatidylinositol (PI) and phosphatidylcholine (PC) 10 s after stimulation. Neither a lipoxygenase inhibitor nor a dual inhibitor of cyclooxygenase and lipoxygenase blocked the increases in [Ca2+]i and the accumulation of [3H]AA in response to ACTH. On the other hand, either pertussis toxin or phospholipase A2 inhibitor drastically blocked both parameters in response to ACTH. These results indicate that ACTH stimulates AA release from PC and PI via the activation of phospholipase A2 coupled with pertussis toxin-sensitive GTP-binding protein(s), which leads to an increase in [Ca2+]i in rat white adipocytes.

Acetophenones↗
PubMed1994

Ca2+ and lipolysis in adipocytes from exercise-trained rats.

The effects of Ca2+ on lipolysis and protein kinase activity in adipocytes from exercise-trained rats were investigated. Chronic exercise significantly increased lipolytic responses to norepinephrine and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). The inhibitory effects of N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide (W-7), a calumodulin inhibitor, on norepinephrine- and dibutyryl cAMP-stimulated lipolysis were significantly greater in trained than in sedentary rats. Training did not alter cAMP-dependent protein kinase activity. However, the inhibitory effect of W-7 on cAMP-dependent protein kinase activity was much greater in trained than in sedentary rats. The basal intracellular free Ca2+ concentration ([Ca2+]i) was significantly higher in trained than in sedentary rats. The rapid and transient increases in [Ca2+]i due to adrenocorticotropic hormone and phenylephrine from basal levels were significantly lower in trained than in sedentary rats. However, the higher basal [Ca2+]i level in trained rats led to increases in sustained [Ca2+]i levels after stimulation. We concluded that in trained rats the regulation of protein kinase activity by cAMP depends to a greater degree on Ca(2+)-calmodulin complex than it does in sedentary rats and that training alters adipocyte intracellular Ca2+ homeostasis, including [Ca2+]i responsiveness to hormones.

Adipocytes↗