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M Katori

Publications and source records attributed to M Katori.

At least 91 records · Page 5Linked to original sources
PubMed1994

[Observation of the rat gastric mucosal microcirculation by vital-microscopy].

The greater curvature of the stomach of fasted rats was cut under urethane anesthesia (1.25 g/kg, i.p.). The dorsal side of the glandular stomach was fixed in a plastic chamber by facing the mucosal side to the chamber and perfused with warm Tyrode solution at 37 degrees C. A window made by partial removal of the serosa, the muscularis externa and the submucosa allowed us to observe the basal part of the mucosal microcirculation through the muscularis mucosae. Images of the microcirculation were transmitted through a TV camera to a TV monitor screen and recorded on videotapes by a videotape-recorder. The diameters of the arterioles, collecting venules and venules were measured by an image analyzer. Arterioles, running along the muscularis mucosae, responded to acetylcholine and epinephrine applied on the window, by dilatation and constriction, respectively, but the collecting venules and venules showed no changes in diameter. Application of 50% ethanol on the mucosal side caused dilatation of the arterioles and constriction of the collecting venules and venules. This method may be useful for analyzing the mechanisms of gastric mucosal injury and those of the effects of vasoactive agents on the gastric mucosal microcirculation.

Animals↗
PubMed1994

Diuretic and natriuretic effect of ebelactone B in anesthetized rats by inhibition of a urinary carboxypeptidase Y-like kininase.

Ebelactone B (EB) (10(-7)-10(-5) M) inhibited dose-dependently carboxypeptidase (CP) Y-like exopeptidase, one of the major kininases separated from rat urine, whereas it inhibited neither CPA, CPB or neutral endopeptidase (NEP). Degradation of bradykinin (BK) to BK-(1-8) in rat urine was completely inhibited by EB (10(-5) M) with the increased generation of BK-(1-7). Intraduodenal administration of EB (3 mg/kg) to anesthetized rats caused marked diuresis (by 110%) and natriuresis (130%), in parallel with the increase in urinary kinin levels (110%). Intravenous infusion of a BK antagonist, Hoe140 (3 mg/kg/hr), strongly blocked both EB-induced diuresis and natriuresis. EB may be a novel type of diuretic and natriuretic agent that acts by increasing urinary kinin levels.

Amino Acid Sequence↗
PubMed1993

Poststatin, a novel inhibitor of bradykinin-degrading enzymes in rat urine.

Incubation of bradykinin with rat urine resulted in the successive degradation of bradykinin to bradykinin-(1-8), bradykinin-(1-7) and bradykinin-(1-6). In contrast, in rat plasma, bradykinin was degraded via either bradykinin-(1-8) or bradykinin-(1-7) to bradykinin-(1-5). Phosphoramidon (1 mM) partially inhibited the degradation of bradykinin by rat urine, as well as the conversion of bradykinin-(1-7) to bradykinin-(1-6). D,L-2-Mercaptomethyl-3-guanidinoethylthiopropanoic acid (1 mM) and captopril (1 mM) did not have a significant effect on any of the degradation steps in rat urine. In contrast, all of the degradation steps in urine, namely, from bradykinin to bradykinin-(1-8), from bradykinin-(1-8) to bradykinin-(1-7) and from bradykinin-(1-7) to bradykinin-(1-6), were markedly inhibited by poststatin (1 mM), even though this compound was reported originally to be a novel inhibitor of post-proline cleaving enzyme. Poststatin (1 mM) did not inhibit the degradation of bradykinin in rat plasma. These results indicate that poststatin is an effective inhibitor of kinin-degrading enzyme in rat urine.

Amino Acid Sequence↗
PubMed1993

Detection of the degradation products of bradykinin by enzyme immunoassays as markers for the release of kinin in vivo.

We developed an enzyme immunoassay (EIA) specific for Arg1-Pro2-Pro3-Gly4-Phe5 ([1-5]-BK) for determination of the levels of this peptide in biological fluids. Previously developed EIAs for bradykinin (BK) and for des-Phe8-Arg9-BK ([1-7]BK) were also used. Incubation of rat plasma with glass powder resulted in the transient appearance of BK. A degradation product, [1-7]BK, could be detected in the incubation mixture for a longer period of time. When compared with BK and [1-7]BK, a larger amount of [1-5]BK was detectable even longer. In carrageenan-induced pleurisy in rats, which was associated with a peak rate of plasma exudation 5 hr after administration of carrageenan, BK was undetectable (< 160 pg/rat) in the pleural exudates. By contrast, [1-7]BK was detectable over the entire course of the inflammatory response. A larger amount of [1-5]BK was detectable. The peak level of [1-5]BK was 6050 +/- 1050 pg/rat, 5 hr after administration of carrageenan. Inhibition of the generation of BK by intrapleural administration of soy bean trypsin inhibitor (0.3 mg/rat) 30 min before collection of pleural fluid resulted in significant reductions in the levels of both [1-7]BK (by 51-65%) and [1-5]BK (by 63-79%) in the exudates 3, 7 and 19 hr after administration of carrageenan. Intraperitoneal administration of captopril (10 mg/kg) caused a marked reduction (by 98%) in levels of [1-5]BK in exudates 3 hr after administration of carrageenan. The reduction was accompanied by an increase in the level of BK up to 1250% of that in untreated rats. These results indicate that the newly developed EIA for [1-5]BK might be a useful tool for verifying the release of kinin in vivo.

Amino Acid Sequence↗
PubMed1993

Immediate inhibitory effect of methylprednisolone suleptanate (U-67590A) on antigen-induced cutaneous and airway anaphylactic responses in guinea-pigs.

1. Inhibitory effects of water-soluble glucocorticoids administered intravenously were examined on skin and airway reactions caused by antigen challenge or chemical mediators in guinea-pigs. 2. Methylprednisolone suleptanate (U-67590A) which is an analogue of methylprednisolone, produced immediate inhibition of 3-h and 7-day homologous passive cutaneous anaphylaxis (PCA) reactions, but not of histamine- or bradykinin-induced cutaneous vascular permeability, when administered 10 min before antigen challenge. In contrast, methylprednisolone succinate (MP) or dexamethasone (DXM) administered 10 min before antigen challenge failed to show an immediate inhibitory effect on the PCA or mediator-induced reactions. When administered 1 to 5 h before antigen challenge, all the steroids used in this study reduced both PCA and mediator-induced reactions. 3. Pretreatment with cycloheximide almost completely abolished the late inhibition of 3-h PCA and histamine reactions produced by U-67590A or MP, but it did not affect the immediate inhibition of 3-h PCA produced by U-67590A. 4. U-67590A also demonstrated immediate inhibitory effects on antigen-induced bronchoconstriction in guinea-pigs actively sensitized with ovalbumin even when administered 10 min before antigen challenge, whereas MP and DXM failed to show the immediate inhibitory effect. When administered 3 h before antigen challenge, all the steroids used in this study reduced the response to antigen. 5. The late inhibitory effect of U-67590A administered 3 h before antigen challenge was almost completely abolished by treatment with cycloheximide or 17 alpha-methyltestosterone, whereas the immediate inhibition produced by U-67590A administered 10 min before challenge was not affected by this treatment. 6. U-67590A administered 10 min or 3 h before challenge did not affect the bronchoconstriction induced by histamine or leukotriene D4.7. Release of histamine from lung fragments of sensitized guinea-pigs in vitro was inhibited by U-67590A.8. The present experiments indicate that U-67590A demonstrated dual, immediate and late, inhibitory effects. The former are independent of protein synthesis and may be associated with non-genomic direct action on the mediator-releasing process without affecting mediator-induced reactions. The latter share common inhibitory actions with other glucocorticoids which are dependent on protein synthesis through gene expression.

Airway Resistance↗
PubMed1993

High sensitivity to salt in kininogen-deficient brown Norway Katholiek rats.

Brown Norway Katholiek rats, which have very low levels of plasma kininogens, excreted a much smaller amount of kinin in the urine than normal rats of the same strain. The systolic blood pressure of 7-week-old kininogen-deficient rats fed low (0.3%) NaCl diets (131 +/- 4 mm Hg, n = 12) was not different from that in normal rats. Two percent NaCl diets given from 7 weeks of age for 4 weeks caused rapid increases in blood pressure (167 +/- 4 mm Hg, n = 12, 9 weeks old) in deficient rats, although the same diets induced no blood pressure increase in normal rats. Urinary excretion of active kallikrein and prokallikrein remained constant in both rat groups throughout NaCl loading. During this period, the deficient rats secreted less urine (9 weeks old, P < .05) and less urinary sodium (11 weeks old, P < .05). Serum levels of sodium in deficient rats were higher (P < .05) than in normal rats at 9 weeks of age. Intracellular concentrations of sodium in the erythrocytes of deficient rats were higher (P < .05) than in normal rats throughout NaCl loading. Subcutaneous infusion of bovine low molecular weight kininogen with an osmotic pump in NaCl-loaded deficient rats induced a reduction (P < .01) in blood pressure and increases (P < .05) in urine volume and urinary sodium and kinin levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 or of aprotinin in NaCl-loaded normal rats induced a hypertensive response. This antagonist treatment reduced urine volume and urinary sodium. These results indicate that the lack of kinin generation observed in the kininogen-deficient rats was related through sodium retention to the hypertensive response to NaCl loading.

Aging↗
PubMed1993

The presence of two sites of action of endothelins in the isolated rabbit iris sphincter and dilator muscles.

The contractile activity of endothelins (ETs) and their effect on twitch contraction evoked by electrical field stimulation were studied in the isolated rabbit iris sphincter and dilator muscles using the isometric tension recording method. ET-1, ET-2 and ET-3 caused slow contractile response of the sphincter as well as the dilator muscles, with sphincter muscle EC50 values of 37.3, 58.0 and 84.3 nM, and dilator muscle values of 31.7, 69.0 and 224.4 nM, respectively. These contractile responses were not affected by atropine (1 microM), prazosin (1 microM) or indomethacin (1 microM). ET-1 and ET-3 slightly but significantly inhibited the fast cholinergic component of twitch contraction of the sphincter muscle evoked by field stimulation, without affecting the response to carbachol. However, ET-1 did not affect the slow substance P-ergic component of twitch contraction of this preparation. In the dilator muscle, ET-1 and ET-3 had little effect on the contraction induced by phenylephrine but reduced the amplitude of the twitch contraction evoked by the field stimulation. The inhibitory effect of ETs on the dilator muscle was antagonized by pretreatment with BQ-123 (100 nM), which is a selective ETA receptor antagonist. Pretreatment with indomethacin (1 microM) also attenuated the inhibitory effect of ETs on the twitch contraction. These results suggest that ETs may have two sites of action, pre- and post-synaptic effects, on the rabbit iris sphincter muscle as well as the dilator muscle. All three ET isopeptides may have direct contractile activity on the smooth muscles of the sphincter as well as the dilator without mediation by prostaglandins or neuronal mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Transmigration routes and a delayed systemic hypotension in rats after intraperitoneal injection of endotoxin from Escherichia coli.

An intraperitoneal injection of endotoxin (ETX; 3 mg/kg) to rats caused gradual decrease in the systemic arterial blood pressure for up to 3 hr, together with decrease in heart rate, increase in hematocrit, and changes in the core temperature (an initial increase and a subsequent decrease). Pretreatment of rats with indomethacin (10 mg/kg, p.o.) prevented the decrease in the systemic blood pressure and the changes in other three parameters. The intraperitoneal injection of ETX also induced a gradual increase in exudation of plasma for up to 3 hr, with increased levels of prostaglandin (PG) E2 and 6-keto-PGF1 alpha in the peritoneal exudate. Indomethacin inhibited the exudation of plasma. The levels of ETX in the arterial and portal venous plasmas began to increase 5 min after the intraperitoneal injection of ETX, and reached levels on the order of micrograms per milliliter plasma 10-20 min after the injection. The levels of ETX in the right and left thoracic lymph nodes, but not in the mesenteric lymph nodes, increased in parallel with those in the systemic arterial plasma. In conclusion, the delayed hypotension may be attributable to the mesenteric vasodilatation induced by PGs generated in the peritoneal cavity, and the ETX injected entered the systemic circulation mainly through lymphatic vessels, but in the initial stage, a part of ETX may be transmigrated into portal vein through damaged intestine.

Animals↗
PubMed1992

Inhibition site of dexamethasone on extravasation of polymorphonuclear leukocytes in the hamster cheek pouch microcirculation.

A video system was used to investigate the inhibitory effect(s) of the glucocorticoid dexamethasone (DEX) on polymorphonuclear leukocyte (PMN) extravasation in the microcirculation of hamster cheek pouch. DEX was given intraperitoneally at 0.1 or 0.3 mg/kg body weight 2 h before induction of extravasation by topical application of leukotriene B4 (LTB4) or formyl-methionyl-leucyl-phenylalanine (fMLP) on the microvasculature. The number, time course, and behavior of PMNs were examined in the following five steps of extravasation: (1) rolling on the venular endothelium, (2) adhesion on the endothelium, (3) passage between the endothelial cells, (4) staying in the venular wall, and (5) migration from the venular wall into the interstitial space. In either the presence or absence of DEX, topical application of LTB4 (15 pmol/50 microliters) or fMLP (10 nmol/50 microliters) caused an increase in the number of PMNs that adhered to the venules. Thus, DEX did not inhibit the adhesion of PMNs on the endothelial cells. The adhered PMNs induced by these chemoattractants became gradually smaller, finally disappearing in the vascular lumen, as observed on the monitor screen. The whole process took about 10 min. This passage of PMNs between the endothelial cells was also not inhibited by DEX, as over 90% of the adhered PMNs passed through the endothelial cells and advanced to the next step of extravasation in the presence or absence of DEX. When these chemoattractants were applied to DEX-untreated animals, the PMNs that passed through the endothelial cells stayed for about 30 min in the venular wall. Thereafter, PMNs migrated into the interstitial space. The numbers of PMNs in the interstitial space were counted at 30, 60, and 90 min after the application of chemoattractants. In the DEX-untreated animals, PMNs in the interstitial space started to appear by 30 min, and thereafter the number further increased. However, in the DEX-treated animals, the number of PMNs at 60 and 90 min was significantly suppressed. Since DEX may inhibit the synthesis and/or release of a proteinase(s) in the PMN granules, which would normally degrade the basement membrane, this inhibition may be due to the inability of PMNs to penetrate the basement membrane.

Animals↗
PubMed1992

A useful and sensitive method for demonstration of the involvement of either kallikrein-kinin system in pathological states.

In rat carrageenin-induced pleurisy, bradykinin (BK) was hardly able to be detected (< 160 pg per rat) in the exudates. In contrast, des-Phe8-Arg9-BK (des-8,9-BK) level, determined by an enzyme immunoassay (EIA) newly developed, was larger in the exudate and the levels were kept throughout the entire course of this inflammation. Arg-Pro-Pro-Gly-Phe ([1-5] BK) level, measured by an EIA newly developed, was much higher than that of des-8,9-BK in the exudate. Intrapleural administration of soy bean trypsin inhibitor (0.3 mg per rat) reduced the levels of both des-8,9-BK and [1-5] BK in the exudates. Reduction in the residual levels of plasma prekallikrein (P-Kall) and high-molecular-weight-kininogen (HMW-K), not low-molecular-weight-kininogen (LMW-K), were accompanied with increase in these BK degradation products, indicating that plasma prekallikrein was activated in the pleural cavity. On the other hand, intravenous injection of acetaldehyde to rats pretreated with disulfiram resulted in the significant increase in the levels of [1-5] BK in the blood, which was accompanied with reduction in the residual levels of LMW-K, not of HMW-K and P-Kall in plasma. These results indicated that the detection of BK degradation products was a good marker for the kinin release in vivo and that the concomitant reduction of the precursor proteins allowed us to identify the type of kallikrein-kinin systems relevant to the kinin release.

Acetaldehyde↗
PubMed1992

Suppression of myoelectrical activity of gastric smooth muscle by endogenous gastric prostaglandin E2.

The myoelectrical activity of the gastric smooth muscle, recorded by a bipolar electrode placed at the gastric antrum in rats, could be recorded when the stomach was distended with 5 ml of physiological saline. This activity may be induced by a mucosal reflex and was inhibited both by atropine and by pirenzepine. Replacement of physiological saline with solutions of NaCl suppressed this myoelectrical activity. This suppression was dependent on the concentrations of NaCl in the solutions, from 0.3 to 1.0 M. Pretreatment with indomethacin (10 mg/kg, intravenous) completely prevented this suppression induced by different concentrations of NaCl solutions. Intragastric administration of 1.0 M NaCl in solution caused an increase in the levels of PGE2 in the gastric lumen. Intragastric administration of OU-1308, a synthetic derivative of PGE1, also suppressed the myoelectrical activity in a dose-dependent manner. It is concluded that the suppression of gastric myoelectrical activity by hyperosmolar NaCl may be attributable to the generation of endogenous PGE2 in the stomach.

Alprostadil↗
PubMed1992

Increased secretion of glandular-kallikrein in the bronchial washings induced by intravenous injection of leukotriene C4 in guinea-pigs.

1. Intravenous administration of leukotriene C4 (LTC4) and LTD4 (1-10 nmol kg-1) caused a dose-dependent increase in secretion of glandular-kallikrein in the bronchial washings of guinea-pigs, as measured by cleavage of a synthetic substrate and the formation of kinin. LTC4 was more potent than LTD4 and pilocarpine was much less potent than peptide leukotrienes on a molecular basis. 2. The increases in levels of glandular-kallikrein in the bronchial washings that were induced by LTC4 (3 nmol kg-1, i.v.) were almost completely inhibited by pretreatment with an antagonist of leukotrienes (ONO-1078), with an antagonist of thromboxane (S-1452), with an inhibitor of thromboxane synthetase (OKY-046), with indomethacin, with atropine or with scopolamine. These results indicate that the LTC4-induced increase in levels of glandular-kallikrein may have been mediated by the formation of thromboxane and the release of acetylcholine. 3. The increases in levels of glandular-kallikrein in the bronchial washings induced by STA2 (20 pmol kg-1, i.v.), a stable analogue of thromboxane A2, were completely blocked by pretreatment with atropine, whereas increases induced by pilocarpine (41 mumol kg-1, i.v.) were not blocked by pretreatment with indomethacin, although such increases were inhibited by atropine. This result indicates that secretion of kallikrein stimulated by LTC4 may have been mediated by the successive formation of thromboxane A2 and release of acetylcholine. 4. Intravenous administration of bradykinin (3-30 nmol kg-1) caused a dose-dependent increase in levels of glandular-kallikrein in the bronchial washings. This increase was completely inhibited by pretreatment with atropine, with indomethacin or with an antagonist of thromboxane.5. The increases in levels of glandular-kallikrein in the bronchial washings induced by LTC4 (3 nmol kg'- , i.v.) and pilocarpine (41 flmol kg- 1, i.v.) were significantly inhibited by pretreatment with an antagonist of bradykinin. These results suggest that intravenous LTC4 may increase secretion of glandular-kallikrein via formation of thromboxane A2 and release of acetylcholine in that order, and kinin released by kallikrein may enhance the rate of secretion of glandular-kallikrein.

Acetylcholine↗
PubMed1992

[Thrombus models and mechanisms of action of anti-platelet drugs].

Thrombus formation is initiated by platelet aggregation, followed by activation of the blood coagulation system, so that anti-thrombotic drugs can be classified into anti-platelet drugs, anti-coagulation drugs and fibrinolytic drugs. A variety of thrombus models in animals have been reported. Microthrombus formation in arterioles in the microcirculation is useful for analyzing the nature of the thrombus and the process of thrombus formation. Platelet aggregation can be divided into two types: (a) reversible aggregation (Rev-Aggr), in which platelets do not release their granular contents and are able to return to the resting discoid shape and (b) irreversible aggregation (Irrev-Aggr), in which platelets release their granular contents. Irrev-Aggr is inhibited by aspirin and not by PGI2 at the maximum aggregation, whereas Rev-Aggr is not inhibited by aspirin and inhibited by PGI2 even at the maximum aggregation. Thrombi corresponding to either type of platelet aggregation can be produced in arterioles in the microcirculation. An ADP-induced thrombus, which is composed of Rev-Aggr of platelets and disaggregated automatically, is not inhibited by indomethacin, but inhibited by PGI2. In contrast, a stable thrombus, which is composed of Irrev-Aggr of platelets and keeps its initial shape for a longer period, is sensitive to indomethacin, but resistant to PGI2. Thus, anti-thrombotic drugs should be developed and used for targeting the individual processes of thrombus formation.

Animals↗
PubMed1992

A stable metabolite, Arg-Pro-Pro-Gly-Phe, of bradykinin in the degradation pathway in human plasma.

Degradation of bradykinin (BK) in human plasma was investigated by searching for a stable metabolite as a marker of kinin release in vivo. BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK). Des-9-BK was degraded to [1-5]BK without an increase in des-8,9-BK, and des-8,9-BK was also degraded to [1-5]BK. D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK. The half lives of BK, des-9-BK, des-8,9-BK and [1-5]BK under the present experimental conditions were 60 min, 90 min, 14 min and 4.2 hr, respectively. Among the metabolites, [1-5]BK was the most stable one and may be used as a marker for BK production in vivo.

Adult↗
PubMed1992

Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats.

Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in Brown Norway (BN) kininogen-deficient rats (BN-Ka) and normal rats from the same strain (BN-Ki) after nephrectomy. Systolic blood pressure, which was determined by the tail-cuff method, of BN-Ki increased gradually during this treatment. In contrast, the blood pressure of mutant BN-Ka increased rapidly 2 weeks after the onset of the treatment. Urinary excretion of active kallikrein and prokallikrein increased at the same degree in rats of both strains during this treatment. Significant increase in urinary sodium excretion was observed with a tendency to increase in urine volume during the treatment in normal BN-Ki rats, whereas both parameters were essentially not increased in mutant BN-Ka rats, which could not generate urinary kinin. Aprotinin infusion by osmotic minipump to normal BN-Ki rats during the DOCA-salt treatment resulted in significant further increase in the systolic blood pressure.

Animals↗
PubMed1992

Influence of a kinin antagonist on acute hypotensive responses induced by bradykinin and captopril in spontaneously hypertensive rats.

We have evaluated the effects of a B2 receptor antagonist (B5630) of kinins on BK and captopril-induced acute hypotensive responses in anaesthetized SHR. Intravenous treatment of BK (1.0 microgram) and captopril (0.3 mg/kg) caused significant (p < 0.05) fall in the SBP and DBP. Whereas BK caused greater fall in the SBP (p < 0.05), DBP (p < 0.01) and duration of hypotension (p < 0.05) when administered after captopril (Fig 1 and 2). All the hypotensive effects of BK and captopril were significantly antagonised (p < 0.05) in the presence of B5630 (2.0 mg/kg). Further, the duration of hypotensive responses of BK and captopril were blocked (p < 0.05) by B5630. The agonists and BK-antagonist did not cause significant (p > 0.05) alterations in HR during the entire investigation. These findings provide evidence to support the suggestion that B2 receptor might be involved in the regulation of the hypotensive actions of BK and captopril. Kinins should also have valuable functions in the antihypertensive property of captopril-like drugs.

Animals↗
PubMed1992

Plasma exudation by activated plasma kallikrein after intraperitoneal injection of lambda-carrageenin or endotoxin in rats.

The experimental study was carried out to examine whether intraperitoneal injection of carrageenin or endotoxin activates plasma kallikrein-kinin system to induce plasma exudation in rats. Intraperitoneal injection of 2% lambda-carrageenin induced plasma exudation in the peritoneal cavity by activation of plasma prekallikrein. Intraperitoneal injection of endotoxin (3mg/kg) also resulted in intraperitoneal plasma exudation, but plasma kallikrein-kinin system did not seem to be involved.

Animals↗