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Biomedical subjects

K Tateishi

Publications and source records attributed to K Tateishi.

At least 73 records · Page 4Linked to original sources
PubMed1992

Role of NK-1 receptor in central cardiovascular regulation in rats: studies on a novel non-peptide antagonist, CP-96,345, of substance P NK-1 receptor.

CP-96,345[(2S,3S)-cis-2-(diphenylmethyl)-N-[(2-methoxyphenyl)- methyl]-1-azabicyclo [2.2.2] octan-3-amine] was recently discovered to be a nonpeptide substance P (SP) antagonist. We examined the effects of CP-96,345 on the central cardiovascular responses to tachykinin peptides in anesthetized rats. CP-96,345 (200 nmol, i.c.v.) inhibited the pressor responses of the NK-1 receptor-selective agonist GR 73632 (0.5 nmol, i.c.v.) and SP (7 nmol, i.c.v.). It also inhibited the increase in blood pressure elicited by neurokinin A (7 nmol, i.c.v.). However, it had no effect on the earlier pressor response induced by neuropeptide gamma (l nmol, i.c.v.) or by a selective NK-3 agonist senktide (1 nmol, i.c.v.). These findings suggest that SP (i.c.v.) induces pressor responses via the NK-1 receptor, and that the pressor response to neurokinin A may also be mediated by the NK-1 receptor in the brain.

Animals↗
PubMed1992

Pertussis toxin non-sensitive G protein mediates cholinergic stimulation for secretion of pancreastatin and somatostatin from QGP-1N cells.

To clarify the possible role of a guanine nucleotide-binding protein (G-protein) in the signal transducing system activated by carbachol, actions of carbachol on human pancreastatin producing cell line (QGP-1N) were compared with those of fluoride, a well-known activator of stimulatory (Gs) or inhibitory (Gi) G protein. 10(-5) M of carbachol as well as 20 mM of NaF stimulated secretion of pancreastatin and somatostatin and intracellular Ca2+ mobilization. These secretion and Ca2+ mobilization were not modified by pertussis toxin, an inhibitor of Gi protein. These results suggest that pancreastatin and somatostatin secretions from QGP-1N are regulated by acetylcholine through a muscarinic receptor coupled to the activation of polyphosphoinositide breakdown by a G protein, which appears to be fluoride sensitive but is other than a Gi-like protein.

Calcium↗
PubMed1992

Degradation of human pancreastatin-52 by human kidney extract.

We examined the in vitro degradation of human pancreastatin-52 (hPST-52) and a larger molecular form (approximate 15 kDa) of human PST by an enzyme extract from human kidney. The PST-degrading activity was determined from the amount of immunoreactive PST remaining after incubation of hPST-52 or the larger molecular form with the enzyme extract. Human PST-52 was degraded to smaller molecular forms within 30 min, but the larger molecule was not degraded within 90 min. Phosphoramidon, an inhibitor of endopeptidase, metal ion chelators (EDTA and 1, 10-phenanthroline) and Cu2+ prevented the degradation of hPST-52. These results indicated that the enzyme in the kidney extract degraded hPST-52 and smaller forms of the peptide, but had no effect on the 15 kDa form.

Chromatography, Gel↗
PubMed1992

Decreased numbers of cholecystokinin-immunoreactive nerve cells in the cerebral cortex of LEC rats with a hereditary hepatitis.

The distribution of CCK-immunoreactive cells was investigated by the indirect fluorescence method in the cerebral cortex of LEC (Long-Evans Cinnamon) rats which have recently been introduced as a model of jaundice and hepatic encephalopathy. Reduction of CCK-immunoreactive nerve cells was observed in the brains of LEC rats with stage III to V hepatic encephalopathy in comparison with the rats without hepatic encephalopathy. These observations were confirmed by counting the CCK-positive nerve cells at magnification x 125. 3 microscopic fields per animal were immunostained and CCK-immunoreactive nerve cells counted. The number of CCK-immunoreactive cells per field was 28.5 +/- 0.7 (mean +/- SEM, n = 5) in rats without hepatic encephalopathy, and 14.1 +/- 2.0 (n = 3) in rats with stage III to V hepatic encephalopathy. Thus, the number of CCK-immunoreactive nerve cells was significantly less in rats with stage III to V hepatic encephalopathy (p less than 0.05). A decrease in CCK-immunoreactive nerve cells was not observed in the rats with stage I or II hepatic encephalopathy. This study shows that there is a relationship between the severity of hepatic encephalopathy and the number of CCK-immunoreactive nerve cells in the cerebral cortex.

Animals↗
PubMed1991

Distribution of neurokinin A-like and neurokinin B-like immunoreactivity in human peripheral tissues.

Using specific radioimmunoassay and immunocytochemistry for neurokinin A (NKA) and neurokinin B (NKB), distribution and localization of the two peptides in human peripheral tissues were studied. Both NKA-like immunoreactivity (NKA-LI) and NKB-like immunoreactivity (NKB-LI) were present in the walls of the gut and gall bladder and in the pancreas. In the gut, the values for NKA-LI were 0.56-35.73 pmol/g wet weight, while those in pancreas and gall bladder were 0.64-0.68 and 0.36 pmol/g wet weight, respectively. The values of NKB-LI were 0.45-2.66 pmol/g wet weight in the gut, 0.93-1.65 pmol/g wet weight in the pancreas, and 0.30 pmol/g wet weight in the gall bladder. The immunocytochemical reactivity to both peptides was localized to ganglia of the submucosal and myenteric nerve plexuses in the gut wall, and to neurons in the muscle layer and mucosa of the gut wall. Weak but positive NKA-LI appeared in nerve cells of the pancreas, while NKB-LI was not detectable in the pancreas. Conversely, in the gall bladder wall, NKA-LI was undetectable while a very faint NKB-LI was found in the muscle layer. The localization of NKA corresponded closely to that of NKB in the tissues although the relative concentrations of the peptides varied from organ to organ.

Digestive System↗
PubMed1991

Reduced somatostatin-like immunoreactivity in the brain of LEC rats with hepatic encephalopathy.

Somatostatin-14-like immunoreactivity (S14LI) and somatostatin-28(1-12)-like immunoreactivity (S28(1-12)LI) in the brain of LEC (Long Evans Cinnamon) rats with hepatic encephalopathy were measured. Significant reduction of both S14LI and S28(1-12)LI was observed in the hypothalamus, medulla oblongata, striatum and spinal cord. Both of the immunoreactivities in the hypothalamus of these rats were approx. 50% of those in LEC rats without hepatic encephalopathy. The amounts of reduction of S14LI significantly correlated with those of reduction of S28(1-12)LI. No significant difference in gel chromatographic profiles of S14LI and S28(1-12)LI was observed between LEC rats with and without hepatic encephalopathy. These results suggest that the reduction of somatostatin-like immunoreactivity in LEC rats with hepatic encephalopathy may be caused by a decrease in production of prosomatostatin rather than altered degradation.

Animals↗
PubMed1991

Reduced cholecystokinin in the brain of LEC rats with hepatic encephalopathy.

Levels of cholecystokinin (CCK) immunoreactivity and distribution of CCK immunoreactive cells were studied in the cerebral cortex of LEC (Long Evans Cinnamon) rats with hepatic encephalopathy. CCK immunoreactivity in water extract of cerebral cortex of LEC rats with hepatic encephalopathy (n = 7) was 41.5 +/- 2.6 (mean +/- S.E.M. pmol/g wet wt.) and that of LEC rats without encephalopathy (n = 8) was 67.1 +/- 6.9, the difference being significant (P less than 0.01). CCK immunoreactive cells assessed by immunohistochemistry were also markedly decreased in the cortex of LEC rats with hepatic encephalopathy of stage IV. Thus, CCK reduction was observed in the cerebral cortex of LEC rats with hepatic encephalopathy which are provided as a model for analysis of the pathogenesis of acute hepatic encephalopathy.

Amino Acids↗
PubMed1991

The central pressor actions of a novel tachykinin peptide, gamma-preprotachykinin-(72-92)-peptide amide.

Intracerebroventricular (i.c.v.) injections of a novel tachykinin peptide, gamma-preprotachykinin-(72-92)-peptide amide (neuropeptide gamma, NP gamma), caused dose-dependent increases in blood pressure. The NP gamma-induced pressor responses (1 microgram i.c.v.) were blocked by peripheral administration of pentolinium (10 mg/kg i.v.) and phentolamine (10 mg/kg i.v.), but were not inhibited by a vasopressin antagonist. These results suggest that central NP gamma increases the blood pressure via sympathetic nerve activity.

Animals↗
PubMed1991

Immunohistochemical study of the distribution of pancreastatin in endocrine tumors of the pancreas and in normal pancreatic tissue: analysis of autopsy cases.

Using sixteen cases (sixteen lesions) of endocrine tumor of the pancreas, found in 1,300 consecutive autopsy cases (661 men and 639 women; mean age, 79.0 years), we examined distribution patterns of pancreastatin (PST) in these endocrine tumors and in normal tissues around them, using immunohistochemical staining. In addition, the distribution patterns of PST was compared with those of insulin (INS), glucagon (GLU), somatostatin (SOM), and pancreatic polypeptide (PP), in these tissues. Normal islets of Langerhans were stained completely and evenly for PST. Two endocrine tumors did not stain for PST at all, six were partially stained, and eight were stained as densely as normal islets, or even more densely. Acinar cells were only partially stained for PST in 11 cases and showed scattered staining in three cases. Epithelial cells of ducts or ductuli were partially stained for PST in 10 cases and showed scattered staining in three cases. Distribution patterns of PST coincided with that of INS in 56% (9/16) of cases, GLU in 81% (13/16), SOM in 31% (5/16), and PP in 31% (5/16). In the eight tumors that were stained at least as densely for PST as normal islets, the staining pattern did not coincide with that of INS in any case (0%), coincided with that of GLU in all 8 cases (100%), and coincided with those of SOM and PP in one case each (13%). Therefore, the distribution of GLU-producing cells (A cells) coincided most closely with that of PST. It is concluded that most PST is secreted from A cells in human pancreas.

Adenoma, Islet Cell↗
PubMed1991

Acetylcholine regulates pancreastatin secretion from the human pancreastatin-producing cell line (QGP-1N).

Studies were made of pancreastatin (PST) secretion from a human PST-producing cell line (QGP-1N) in response to various secretagogues. Cells with immunoreactivity for PST were observed in monolayer cultures of QGP-1N cells. Carbachol stimulated PST secretion and the intracellular Ca2+ mobilization concentration dependently in the range of 10(-6)-10(-4) M. The PST secretion and Ca2+ mobilization induced by carbachol were inhibited by atropine. The calcium ionophore (A23187) stimulated PST secretion. However, cholecystokinin and gastrin-releasing peptide did not stimulate either PST secretion or Ca2+ mobilization. Secretin also did not stimulate PST secretion. The glucose concentration in the culture medium had no effect on PST secretion. These results suggest that PST secretion is mainly regulated by acetylcholine through a muscarinic receptor, and that an increase in intracellular Ca2+ plays an important role in stimulus-secretion coupling in QGP-1N cells.

Acetylcholine↗
PubMed1991

[Eosinophil activation in acute asthma attacks evaluated by electronmicroscopic findings of eosinophils and the concentration of eosinophil cationic protein in sputum].

We evaluated the activation of eosinophils in the airways of patients with acute asthma attacks by measuring the concentration of sputum eosinophil cationic protein (ECP) and changes in the electron densities of the eosinophil specific granules in sputum. In six hospitalized patients with asthmatic attacks, sputum samples were collected for seven consecutive days after admission and were used for the evaluation of eosinophil activation. The concentration of sputum ECP, the incidence of changes in the electron densities of eosinophil specific granules and the severity of asthma attacks were highest on the day of admission and decreased in association with each other after treatment. A significant correlation was found between the concentration of sputum ECP and the incidence of changes in the electron densities of eosinophil specific granules. These findings suggest that the eosinophils in the airways are markedly activated and degranulated in asthma attacks.

Adult↗
PubMed1991

[Fundamental studies on measurement of the eosinophil cationic protein in sputum from patients with bronchial asthma].

One of the characteristics of patients with bronchial asthma is activation of eosinophils in the bronchi, which can be evaluated by measuring concentrations of the cationic granule proteins. Sputum seems to be the best material to evaluate the activation of eosinophils in the bronchi because it can be collected easily from the same patient every day even if he (she) has an asthmatic attack. Recently it has become possible to measure the concentration of the eosinophil cationic protein (ECP) thanks to the availability of the ECP RIA kit. However no fundamental studies have been carried out on the handling of sputum samples, and whether only ECP released into sputum is measured. We prepared supernatants of sputum samples according to the method of Gleich and others by adding the same volume of physiological saline, mixing it for one minute by a vortex mixer and centrifuging at 40000 Xg, 4 C, for 30 minutes. We found that the measurement of ECP is not inhibited by materials in sputum supernatants through a dilution test and a recovery test. We also found that the followings did not influence the measurement of ECP; the times of dilution, the duration from collection to handing of sputum, the solution added to sputum, and the gravity of centrifugation. In addition, it was suggested that only ECP released into sputum is measurable from the results of an electron microscopic study and the measurement of ECP after centrifugation following the addition of white blood cells to sputum.

Asthma↗
PubMed1990

Distribution and localization of neurokinin A-like immunoreactivity and neurokinin B-like immunoreactivity in rat peripheral tissue.

Using specific radioimmunoassays and immunocytochemistry for neurokinin A (NKA) and neurokinin B (NKB), distribution and localization of these peptides in rat peripheral tissues were studied. NKA-like immunoreactivity (NKA-LI) was present in highest levels of 15.7-23.9 pmol/g wet wt. and NKB-like immunoreactivity (NKB-LI) was in levels of 0.33-0.67 pmol/g wet wt., throughout the gastrointestinal tract involving stomach, duodenum, jejunum, ileum and colon. Immunocytochemical analysis of gastrointestinal tract revealed that NKA-LI and NKB-LI localized in ganglia of both the submucosal and myenteric plexuses as well as varicose neurons in the mucosa and the muscle layer of the small and large intestine. On the other hand, high levels of NKB-LI were observed in oesophagus (0.83 +/- 0.08 pmol/g wet wt.), adrenal (1.02 +/- 0.21), head of pancreas (0.73 +/- 0.06) and kidney (0.98 +/- 0.05). The present study shows the difference of localization of NKA-LI and NKB-LI in peripheral tissues and suggests that NKB may have some physiological role differing from that of NKA in peripheral tissues.

Animals↗
PubMed1990

Role of central tachykinin peptides in cardiovascular regulation in rats.

The mechanisms of action of tachykinin peptides thought to be involved in central cardiovascular regulation were examined. Intracerebroventricular injections (i.c.v.) of tachykinin peptides caused dose-dependent increases in blood pressure and heart rate. The pressor responses to substance P (SP) (10 micrograms, i.c.v.) and neurokinin A (NKA) (10 micrograms, i.c.v.) were blocked by peripheral administration of pentolinium or phentolamine, and partially attenuated by adrenalectomy. In contrast, the only initial pressor response to the neurokinin B (NKB) analogue senktide (10 micrograms, i.c.v.) was blocked by pentolinium or phentolamine. The pressor response to senktide was inhibited by pretreatment with a vasopressin V1 receptor antagonist (d(CH2)5OMe(Tyr)AVP) (10 micrograms/kg, i.v.), and senktide (10 micrograms, i.c.v.) caused an increase in plasma vasopressin level. However, the vasopressin antagonist did not influence the SP- and NKA-induced pressor responses. These results suggest that central SP and NKA increase the blood pressure and heart rate via sympathetic nerve activity, whereas central NKB increases the blood pressure mainly via release of vasopressin from the hypothalamus.

Adrenal Glands↗
PubMed1990

Elevated plasma levels of pancreastatin (PST) in patients with non-insulin-dependent diabetes mellitus (NIDDM).

Pancreastatin (PST) is known as the peptide which inhibits first phase of glucose-stimulated insulin secretion. Fasting plasma PST levels and responses of PST after oral glucose ingestion in patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied with human PST-specific radioimmunoassay. Fasting plasma PST in NIDDM patients was not different from healthy controls, although a slightly higher level of PST was observed in patients treated with sulfonylurea among NIDDM patients. No significant increase in plasma PST was observed after a glucose ingestion in healthy controls. In contrast, plasma PST levels in NIDDM patients rose significantly after glucose ingestion. These results suggest a possible pathophysiological role for PST in NIDDM.

Administration, Oral↗
PubMed1990

Isolation and characterization of a tumor-derived human protein related to chromogranin A and its in vitro conversion to human pancreastatin-48.

A protein with pancreastatin-like immunoreactivity has been isolated and purified from liver metastasis of a patient with insulinoma. NH2-terminal residue analysis, in conjunction with the use of antibodies that are specific for the C-terminal amide peptide of porcine pancreastatin, identified this protein as a 186-amino-acid protein corresponding to human chromogranin A-116-301 (the fragment corresponding to the positions from 116 to 301 of human chromogranin A). Digestion of this protein with trypsin yielded a 48-amino-acid peptide with the retention of full pancreastatin activity. Serum from patient with insulinoma contains a peptide specie(s) that comigrates with the 48-amino-acid pancreastatin, suggesting that this peptide might be a physiologically important circulation form of pancreastatin in humans. A sensitive radioimmunoassay was established using antibody developed against a synthetic 29-amino-acid peptide amide of pancreastatin. Immunocytochemical staining revealed that a major population of human pancreatic islet cells were immunoreactive to the antiserum but with varying intensity of staining. Pancreastatin-like immunoreactivity was not observed in exocrine acinar cells.

Adenoma, Islet Cell↗