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M Katori

Publications and source records attributed to M Katori.

At least 73 records · Page 4Linked to original sources
PubMed1996

Failure of the oxytocin-induced increase in secretion of urinary kallikrein in young spontaneously hypertensive rats.

Urinary kallikrein excretion during oxytocin (OT) infusion were studied in anesthetized (sodium pentobarbital, 50 mg/kg, i.p.) young (4-weeks-old) spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). OT-infusion (30 nmol/kg/30 min) to WKY significantly increased urinary excretion of the active kallikrein from the basal levels (25.4 +/- 5.6 10(-2) x AU/15 min, n = 5) to 37.3 +/- 5.0 10(-2) x AU/15 min (P < 0.05, n = 5) and 50.7 +/- 17.1 10(-2) x AU/15 min (P < 0.05, n = 5) 15 and 30 min after the start of OT-infusion, respectively. In SHR, OT-infusion did not increase the urinary excretion of active kallikrein, but did decrease the urine volume and sodium excretion. The concentration of the active kallikrein in the kidney of WKY was not changed by OT-infusion, but that of SHR was slightly increased. The OT-infusion resulted in significantly higher concentrations of the active kallikrein in SHR kidney than in WKY kidney. These results suggest that less excretion of urinary kallikrein in SHR during OT-infusion may be attributable to a lower response in the secretion of kallikrein from the kidney.

Animals↗
PubMed1996

Pharmacological characterization of endothelin receptors in the rabbit iris sphincter muscle: suggestion for the presence of atypical receptors.

Pharmacological profiles of endothelin (ET) receptors in the isolated rabbit iris sphincter were characterized. ET isopeptides caused dose-dependent contraction of the preparation. The respective EC50 values for ET-1, ET-2 and ET-3 were 39.4, 58.0 and 84.3 nM, so that ET-1 was twice as potent as ET-3. Sarafotoxin (SRTX) -b, an ET(A)/ET(B) non-selective agonist, caused very potent contraction with an EC50 of 1.13 nM. However, selective ET(B) receptor agonists SRTX-c and IRL 1620 showed no contractile activity up to 1 microM. BQ-123, a selective ET(A) receptor antagonist, shifted the dose-response curves of ET isopeptides to the right. The pA2 value for ET-1 was 5.52 with a slope of 1.06, which is not different from unity, and the pK(B) value for ET-2 was 5.06. Interestingly, very low doses of BQ-123 antagonized responses to ET-3 and SRTX-b, with a Schild plot slope of approximately 0.7 which is significantly different from unity, suggesting receptor heterogeneity. The abscissal intercepts of the Schild plots were -9.29 for ET-3 and -8.53 for SRTX-b. FR 139317, another ET(A) receptor antagonist, also preferentially antagonized responses to ET-3. RES-701-1, a selective ET(B) receptor antagonist, did not shift dose-response curves for ET-1 and ET-3. These results suggest that ET receptors in the rabbit iris sphincter muscle cannot be classified into the ET(A), ET(B) or ET(C) receptor subtypes, so far established. When compared to the established receptor subtypes, ET receptors in this preparation were quite different from the ET(B) receptor, but apparently showed a pharmacological profile most similar to the ET(A) receptor, suggesting the presence of heterogeneous and atypical ET(A) receptors.

Animals↗
PubMed1996

Calcitonin gene-related peptide induced relaxation of the rabbit iris dilator muscle.

Calcitonin gene-related peptide (CGRP) and Substance P (SP) -immunoreactive nerves have been found in the anterior uvea of various mammalian species. Although SP is known to play a major role in control of pupil motility in rabbits, little is known about the effect of CGRP on the iris smooth muscles. We isolated iris sphincter and dilator muscles from rabbit eyes and investigated the mechanical responses and intracellular cyclic AMP (cAMP) levels in these muscles. CGRP (up to 0.1 microM) had no effect on either the resting muscle tone or the amplitude of contraction evoked by field stimulation of the sphincter. On the other hand, CGRP (0.1 microM) relaxed dilator muscle which had been pre-contracted by phenylephrine and reduced the amplitude of contraction evoked by field stimulation. These responses were antagonized by CGRP (8-37), a CGRP antagonist. The phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX), dose-dependently inhibited the contraction evoked by field stimulation. However, 3 microM IBMX had no effect on CGRP inhibition of twitch contraction in this preparation. CGRP had little effect on cAMP production in dilator muscle either with or without IBMX. In conclusion, the miosis which occurs during an ocular inflammatory response, when both CGRP and SP are thought to be released from terminals of sensory neurons, results from CGRP relaxation of the dilator and from the strong contractile effect of SP on the sphincter. Adenylate cyclase activation does not seem to be involved in the relaxant effect of CGRP on the dilator.

1-Methyl-3-isobutylxanthine↗
PubMed1996

Inhibitory effects of a phosphate diester of alpha-tocopherol and ascorbic acid (EPC-K1) on myocardial infarction in rats.

The inhibitory effect of a phosphate diester of alpha-tocopherol and ascorbic acid (EPC-K1) was examined in myocardial infarction induced in rats, in comparison with a selective 5-lipoxygenase inhibitor, AA-861. EPC-K1 significantly reduced the infarct size at 24 and 48 h after ligation, whereas AA-861 reduced it only at 48 h after ligation. In in-vitro experiments, EPC-K1 inhibited not only superoxide anion generation (IC50 = 4.2 x 10(-5) M), but also acid phosphatase activity (IC50 = 2.4 x 10(-5) M) in rat polymorphonuclear leukocytes in a concentration-dependent manner, while AA-861 showed marginal effects on both actions. These results indicated that EPC-K1 induced cardioprotective effects by affecting neutrophil functions by inhibition of generation of superoxide-anion generation and acid-phosphatase activity. The mechanism of the reduction of the infarct size by EPC-K1 differed from that of AA-861, which latter inhibited 5-lipoxygenase and the formation of leukotriene B4.

Animals↗
PubMed1995

Ebelactone B, an inhibitor of urinary carboxypeptidase Y-like kininase, prevents the development of deoxycorticosterone acetate-salt hypertension in rats.

Kininogen-deficient Brown Norway Katholiek rats (BN-Ka) excrete little urinary kinin, compared with normal rats of the same strain (BN Kitasato rats (BN-Ki)). Deoxycorticosterone acetate-salt treatment increased systolic blood pressure in both rats, but much faster in BN-Ka than in BN-Ki. Daily subcutaneous administration of ebelactone B (15 and 5 mg/kg/day), a rat urinary carboxypeptidase Y-like kininase inhibitor, significantly reduced systolic blood pressure in BN-Ki, but not in BN-Ka. This treatment significantly increased urinary Na+ excretion and reduced Na+ concentration in the erythrocytes in BN-Ki, but not in BN-Ka. An angiotensin-converting enzyme inhibitor, lisinopril (5 mg/kg/day s.c.), did not reduce the systolic blood pressure in either BN-Ki or BN-Ka. These results suggested that ebelactone B has promise as a preventive agent for the development of hypertension acting through the inhibition of urinary kinin degradation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Evaluation of plasma 11-dehydro-thromboxane B2 as an indicator for thromboxane A2 synthesis in vivo in laboratory animals.

Since thromboxane (TX) B2 is not a reliable indicator of TXA2 generation in vivo, because of artifactual TXA2 generation during blood collection, we tested the feasibility of replacing TXB2 with 11-dehydro (dh)-TXB2 as the indicator. Plasma levels of TXB2 and 11-dh-TXB2 were measured after i.v. administration of TXB2 to rabbits, guinea pigs, rats, dogs and a monkey, and after i.v. infusion of collagen in rabbits. In the rabbits and dogs, 2,3-dinor-TXB2 levels were also measured. After intravenous injection of TXB2 (10 micrograms/kg) in rabbits, the ratio of the area under the curve (AUC) of 11-dh-TXB2 to that of TXB2 (1.94) was far higher than the AUC ratio between 2,3-dinor-TXB2 and TXB2 (0.42). When endogenous TXA2 was generated by infusion of collagen (2 mg/kg/5 min), the plasma level of 11-dh-TXB2 was significantly increased, and had a longer half-life than TXB2. In the guinea pigs, rats and monkey, the peak plasma levels of 11-dh-TXB2 were significantly increased after injection of TXB2 (10 micrograms/kg, i.v.), whereas the AUC ratios of 11-dh-TXB2/TXB2 were less than one fourth of that in rabbits. No significant increase in 11-dh-TXB2 was observed after TXB2 injection (10 micrograms/kg) in dogs, but the 2,3-dinor-TXB2 level rose significantly, its AUC ratio to TXB2 being 0.29, comparable with that in rabbits. The order of the 11-dh-TXB2/TXB2 AUC ratios was: rabbits > guinea pigs > monkey > rats >> dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Direct observation of microcirculation of the basal region of rat gastric mucosa.

We modified and improved techniques for the intravital microscopic observation of the rat gastric microcirculation. The stomach of anesthetized rats was cut along the greater curvature, and the posterior wall of the glandular stomach was fixed in a chamber with the serosal side up and perfused with warmed Tyrode's solution. A portion of the muscularis externa was resected with the serosa to make an observation window. Vascular casts were studied histologically after the injection of Monastral blue B gelatin solution. Vascular casts revealed that most of the microvasculature observed in the window was not located in the submucosa, but in the basal part of the mucosa. Microscopic observation showed that the basal mucosal arterioles branched to form the mucosal capillaries, and the collecting venules from the mucosal surface were seen in cross-sections to drain into the venules located in the basal mucosa, without penetrating the muscularis mucosae. Topical application of acetylcholine (0.03-10 microM) to the window dilated the arterioles, and topical application of epinephrine (0.03-3 microM) constricted them dose-dependently without affecting the collecting venules and the venules. This method made possible the direct observation of the microvasculature in the basal mucosa of the stomach, in which common microvessel characteristics were shown.

Acetylcholine↗
PubMed1995

Contribution of bradykinin to heat-induced substance P release in the hind instep of rats.

To investigate the possible contribution of the bradykinin (BK) system to heat-induced substance P (SP) release from the peripheral endings of primary afferent nerves, we used the high molecular weight (HMW) and low molecular weight (LMW) kininogen-deficient rat strain (Brown Norway-Katholiek, B/N-Ka) and the normal rat strain (Brown Norway-Kitasato, B/N-Ki). We found that immersion of the paw of B/N-Ki rats in water of 47 degrees C for 20 min led to significant increases of BK, SP and Evans blue extravasation in the s.c. perfusate, and that similar treatment resulted in significantly lower levels in B/N-Ka rats. Local application of BK (10(-4) M) to the s.c. perfusate and intra-arterial infusion of BK 10(-5) mol/kg) increased Evans blue extravasation and SP release evoked by heat stimulation, respectively, in B/N-Ka rats to similar levels to those in B/N-Ki rats after heat-stimulation without BK treatment. These results indicate that BK released into the extravascular space by noxious stimulation is involved in SP release from the peripheral endings of capsaicin-sensitive primary sensory neurons.

Animals↗
PubMed1995

Approaches to the development of novel antihypertensive drugs: crucial role of the renal kallikrein-kinin system.

The renal kallikrein-kinin system has been shown to be important in the development of hypertension, but its precise role remains to be determined. The recent use of mutant rats that are deficient in plasma kininogens and hence incapable of generating kinin in the renal tubules has facilitated elucidation of the involvement of kinin in hypertension. In this article, Masataka Majima and Makoto Katori provide evidence that the renal kallikrein-kinin system plays a crucial role in the development of hypertension and discuss a novel rationale for developing effective new antihypertensive drugs.

Animals↗
PubMed1995

Oxytocin-induced natriuresis mediated by the renal kallikrein-kinin system in anesthetized male rats.

Intravenous infusion of oxytocin (OT) (10-100 nmol/kg/30 min) to 8-week-old anesthetized male rats resulted in a dose-dependent increase in urine volume, which showed a peak value 30-45 min after the start of OT-infusion. Urinary excretions of sodium, chloride and potassium were also increased by OT, showing peak values at 30-45 min, without any increase in the creatinine level. The natriuresis by OT was accompanied by increased excretion of urinary active kallikrein, which showed a peak value 15 min after the start of OT-infusion. The urinary kinin level was also increased. Intravenous infusion of a kallikrein inhibitor, aprotinin (15 mg/kg/90 min), when started 30 min before the OT-infusion, significantly inhibited the OT-induced increase in urine volume and urinary excretion of sodium, chloride and potassium. Intravenous infusion of a bradykinin B2 antagonist, Hoe 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]BK, 4.5 mg/kg/90 min), when started 30 min before the OT-infusion, significantly inhibited the OT-induced increases in urine volume and urinary excretion of sodium and chloride, but not that of potassium. These results indicate that the OT-infusion induces natriuresis in male rats, and more than half of the natriuresis is mediated by a concomitant increase in excretion of urinary active kallikrein and the kinin generated.

Anesthesia↗
PubMed1995

Increase in vascular sensitivity to angiotensin II and norepinephrine after four-day infusion of 0.3 M sodium chloride in conscious kininogen-deficient brown Norway Katholiek rats.

Kininogen-deficient Brown Norway Katholiek (deficient BN-Ka) rats excreted a small amount of kinin in their urine, compared with normal BN Kitasato (normal BN-Ki) rats from the same strain. Intraarterial (i.a.) infusion (6 ml/kg/hr) of conscious deficient BN-Ka rats with 0.15 M NaCl did not increase mean arterial blood pressure (MBP) [from 103 +/- 2 (pre) to 93 +/- 6 mmHg (day 4)] and did not cause sodium accumulation in the serum, cerebrospinal fluid or erythrocytes, but 0.3 M NaCl infusion significantly increased MBP from 104 +/- 3 (pre) to 130 +/- 5 mmHg (day 4) with increased sodium levels in the serum, cerebrospinal fluid and erythrocytes. Infusion of 0.3 M NaCl in normal BN-Ki rats neither increased MBP nor accumulated sodium. The dose-response curve of the increase in MBP for angiotensin II injection (i.a., bolus, 1-1000 pmol/kg) in 0.3 M NaCl-infused deficient BN-Ka rats shifted to the left by a factor of 10 compared with that in 0.15 M NaCl-infused deficient BN-Ka rats, and that for norepinephrine injection shifted to the left by a factor of 30. Normal BN-Ki rats did not show any enhancement in MBP elevation with 0.3 M NaCl. These results suggest that the sodium accumulation attributable to a lack of kinin generation may be related to increased vascular reactivity to angiotensin II and norepinephrine.

Angiotensin II↗
PubMed1995

Induction of cyclooxygenase type-2 (COX-2) in rat endometrium at the peak of serum estradiol during the estrus cycle.

We investigated the induction of cyclooxygenase (COX) in rat endometrium during the estrus cycle. The estrus cycle was divided into five stages (proestrus, estrus, diestrus-1, diestrus-2, diestrus-3) by cytological observation of vaginal smears. COX-1 was detected in the endometrium during all five stages of the estrus cycle. In contrast, COX-2 in the endometrium was detectable only in three stages (diestrus-3, proestrus, estrus) and showed a peak at diestrus-3, coinciding with the peak in serum estradiol level, suggesting the estradiol-dependent induction of COX-2.

Animals↗
PubMed1995

Effects of MK-447 on thrombin-induced aggregation, secretion of ATP, and [Ca2+]i mobilization in rabbit platelets.

AIM: To study the effects of MK-447 on aggregation release reaction and intracellular calcium mobilization by thrombin. METHODS: Aggregation and release reaction were assessed by light transmission and ATP content in rabbit citrate platelet-rich plasma (PRP), and cytosolic-free calcium was measured by fluorescence and imaging. RESULTS: MK-447 (2-aminomethyl-4-t-butyl-6-iodophenol hydrochloride) induced a decrease in light transmission (DLT), so called platelet shape change, without detectable aggregation and secretion of ATP, and increased intracellular calcium concentration ([Ca2+]i) slightly in washed single platelet loaded with Fura 2, the peak value being about 160 nmol.L-1. These effects were not inhibited by egtazic acid 3 mmol.L-1 or indometacin 3 mumol.L-1. The pretreatment of PRP with MK-447 700 mumol.L-1 reduced the DLT by thrombin, potentiated and enhanced thrombin-induced aggregation and secretion of ATP in a concentration-dependent manner. Thrombin-induced [Ca2+]i mobilization (peak value: 369 +/- 45 nmol.L-1) was further enhanced by the administration of MK-447 at 2 min before the addition of thrombin, and the peak value reached 623 +/- 121 nmol.L-1 (P < 0.01). CONCLUSION: MK-447-induced platelet shape change was involved in intracellular calcium release in this preparation. MK-447 enhanced thrombin-induced aggregation and release reaction and these effects of MK-447 on aggregation and release reaction by thrombin might result from the synergistic effect of intracellular calcium mobilization.

Adenosine Triphosphate↗
PubMed1995

Different responses of arterioles and venules in rat gastric mucosal microcirculation to endothelin-1 and endothelin-3.

Responses of the microvessels in the basal part of the gastric mucosa of anesthetized rats to endothelin (ET)-1 and ET-3 were examined by intravital microscopy. The posterior wall of the stomach, which was incised along the greater curvature, was secured in an observation chamber and superfused with Tyrode's solution, and the microcirculation was observed through a window made by removing a limited area of smooth-muscle layers with the serosa and submucosal tissue. Topical application of the same ranges of ET-1 and ET-3 (0.1-10 microM, 20 microliters) to the window dose-dependently constricted collecting venules and venules downstream. The constriction was inhibited by BQ-123, an ETA receptor antagonist, but the equipotency of ET-1 and ET-3 did not support the presence of the ETA receptor (tentatively called ETR-m). Arterioles were constricted through ETR-m, particularly at higher doses (> 3 microM), but 1 microM ET-1 dilated the arterioles by generating prostaglandin through BQ-123-sensitive ET receptor (tentatively called ETR-e), as shown by the inhibition of dilatation by indomethacin. Furthermore, the dilatation component of the arteriolar smooth-muscle responses to ET-1 and ET-3 was elicited by BQ-123 and was inhibited by NG-monomethyl-L-arginine (L-NMMA), indicating the generation of nitric oxide. This dilating effect of the endothelins was mediated by the ETB receptor.

Animals↗
PubMed1995

Degradation of bradykinin in human urine by carboxypeptidase Y-like exopeptidase and neutral endopeptidase and their inhibition by ebelactone B and phosphoramidon.

Incubation of bradykinin with human urine resulted in a successive degradation of bradykinin-(1-8), bradykinin-(1-7), bradykinin-(1-6), and bradykinin-(1-5). Although D,L-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid (100 microM) and captopril (100 microM) did not have any significant effect on bradykinin degradation in human urine, the neutral endopeptidase inhibitor phosphoramidon (100 microM), a carboxypeptidase Y-like exopeptidase inhibitor ebelactone B (100 microM), and o-phenanthroline (100 microM) significantly inhibited bradykinin degradation by 36%, 38% and 48% respectively. The combination of phosphoramidon and ebelactone B completely (by 95%) inhibited bradykinin degradation in human urine. At pH 5, bradykinin degradation was performed by carboxypeptidase Y-like exopeptidase; at pH 7, this degradation was performed by neutral endopeptidase in addition to carboxypeptidase Y-like exopeptidase. From these results, it can be concluded that carboxypeptidase Y-like exopeptidase and/or neutral endopeptidase certainly have a role in kinin degradation in human urine under neutral and acid pH conditions.

Adult↗
PubMed1995

Calcium mobilization in density subpopulations of rabbit washed platelets.

To estimate the responsiveness of an individual platelet, rather than a group of platelets, we determined the intracellular calcium concentration ([Ca2+]i) of single platelets using digital imaging microscopy after density fractionation. The mean [Ca2+]i of non-fractionated resting single platelets was 74.0 +/- 4.2 nM (n = 71). Immediately after thrombin stimulation (100 mu/ml), [Ca2+]i increased markedly in the entire cytoplasm, reaching maximum levels of 400-1000 nM, and decreased slightly thereafter. These maximum levels varied markedly from cell to cell in non-fractionated platelets. Although there was no significant difference in the resting levels of [Ca2+]i of single platelets even after density fractionation, the peak [Ca2+]i levels after thrombin stimulation (10 and 100 mu/ml) in platelets with higher density ( > 1.062) were significantly higher than those in platelets with intermediate density (1.052-1.061) or lower density ( < 1.051). This higher responsiveness of higher-density platelets in calcium mobilization was accompanied by higher aggregability and higher reactivity in the release reaction. These results suggest that higher responsiveness in higher-density platelets may be explained by the higher reactivity in [Ca2+]i mobilization.

Animals↗
PubMed1994

Hypertension induced by a nonpressor dose of angiotensin II in kininogen-deficient rats.

Brown Norway Katholiek rats with 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 (132 +/- 2 mmHg, n = 7) was not different from that of normal rats. Angiotensin II (Ang II) (20 micrograms/d SC) from 7 weeks of age for 2 weeks with a micro-osmotic pump caused significant increases in blood pressure (181 +/- 5 mm Hg, n = 7, 9 weeks old) in the deficient rats, although the same treatment induced no blood pressure increase in the normal rats. Also during this period, the deficient rats had significantly higher heart rates, tended to excrete less urinary sodium, and showed significantly higher sodium levels in serum, erythrocytes, and cerebrospinal fluid compared with the normal rats. Ang II increased urinary excretion of aldosterone in both deficient and normal rats (P < .05). Spironolactone treatment (50 mg/kg per day) for 7 days in deficient rats restored blood pressure and heart rate to normal levels and significantly reduced sodium levels in erythrocytes and cerebrospinal fluid. Subcutaneous infusion of bovine low-molecular-weight kininogen with an osmotic pump in Ang II-treated deficient rats induced significant reductions in blood pressure, heart rate, and erythrocyte sodium levels. By contrast, subcutaneous infusion of the bradykinin antagonist Hoe 140 in Ang II-treated normal rats induced a hypertensive response in parallel with significant increases in heart rate and erythrocyte sodium level. These results suggest that the lack of kinin generation observed in the kininogen-deficient rats may cause the hypertensive response during the administration of a nonpressor dose of Ang II mainly through sodium retention probably caused by aldosterone release.

Aldosterone↗