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Biomedical subjects

M Sasaguri

Publications and source records attributed to M Sasaguri.

At least 37 records · Page 2Linked to original sources
PubMed1995

Plasma free and sulfoconjugated dopamine before and after a half-marathon.

To elucidate whether increased plasma levels of free dopamine (F-DA) after exercise are due to deconjugation of sulfoconjugated (S-) DA in plasma, we compared the changes in plasma F- and S- DA, as well as changes in both the S- and F- forms of epinephrine (E) and norepinephrine (NE), after running a half-marathon. Free catecholamines (F-CAs) were measured by automated high-performance liquid chromatography (HPLC). Total (F+S) CAs were determined using an efficient deconjugation method as follows; 1200 microliters plasma was incubated with 152 mU arylsulfatase (AS) for 30 min at pH 7.6. The plasma levels of F-CA (pg/ml) (mean +/- SEM) all increased significantly (p < 0.01) after the half-marathon; i.e., F-DA increased from 13.3 +/- 5.7 to 176.3 +/- 32.2; F-E from 58.0 +/- 12.3 to 764.3 +/- 136.4; F-NE from 246.6 +/- 15.2 to 3082.0 +/- 690.3. OF S-CAs, S-E (from 127.8 +/- 26.0 to 1218.2 +/- 190.8) and S-NE (from 717.1 +/- 61.6 to 5586.9 +/- 761.9) also increased, but, in contrast, among the S-CAs, only the increase in S-DA (from 5324.9 +/- 1967.3 to 7359.6 +/- 1627.9) was not statistically significant. Sulfoconjugation may play an important role in inactivating F-DA as well as F-NE and -E, that are released into plasma in response to vigorous exercise. Thus, plasma F-DA is unlikely to be derived through deconjugation of plasma S-DA.

Adult↗
PubMed1994

Central squamous cell carcinoma of the mandible. Computed tomographic findings.

Five cases of central squamous cell carcinoma of the mandible were investigated with the use of computed tomography. Bucco-lingual extent and spread along the mandibular division of the trigeminal nerve were evaluated. Three patients with trismus showed involvement of the masseter or medial pterygoid muscle on computed tomography. Involvement of more than two landmarks along the trigeminal nerve were observed in cases with both paresthesia of the lower lip and severe pain that resembled neuralgia. Perineural invasion was confirmed histologically in four cases, and all of these patients had both severe pain and mandibular canal involvement that could be demonstrated with computed tomography. When localized soft tissue changes are evident along the course of the trigeminal nerve in the region between the mandibular foramen and foramen ovale, ascending perineural spread should be suspected. Computed tomography findings correlated well with clinical symptoms but added information about the spread of the lesion within the surrounding soft tissue.

Carcinoma, Squamous Cell↗
PubMed1994

Angiotensin II formation by an alternative pathway during exercise in humans.

OBJECTIVE: We postulated a 'kinin-tensin system' in which angiotensin II (Ang II) is cleaved by one or more serine protease independent of renin or angiotensin converting enzyme (ACE). The aim was to determine whether this alternative Ang II-forming pathway by serine proteases participates in the rise in plasma levels of Ang II during exercise in humans. DESIGN AND METHODS: The study consisted of two double-blind crossover experiments. in experiment 1 six healthy volunteers who had been taking either placebo (group P) or the ACE inhibitor captopril (150 mg/day for 3 days; group C) performed a cycle ergometer graded exercise test at four different exercise intensities: stage 1, half of the intensity at the blood lactate threshold (WLT); stage 2, the intensity at WLT; stage 3, the intensity at 4 mmol/l blood lactate; and stage 4, an intensity between stage 3 and maximum intensity. In experiment 2 the same volunteers took captopril (150 mg/day for 3 days) and performed exercise at an intensity corresponding to 90% of the 4 mmol/l blood lactate intensity for 30 min during intravenous drip injection of a serine protease inhibitor, nafamostat [NAF; 0.2 mg/kg per h; NAF(+) group] or saline [NAF(-) group]. RESULTS: In experiment 1 plasma Ang II levels increased from at rest to after exercise in both groups P and C. Although there was a significant treatment effect, captopril did not significantly alter the exercise-induced changes in Ang II level. In experiment 2 the increase in Ang II level after 30 min exercise in the NAF(+) group was significantly lower than in the NAF(-) group. CONCLUSIONS: These results suggest the presence of an alternative Ang II-forming pathway independent of ACE, and that one or more NAF-sensitive serine protease is responsible, at least partly, for generating Ang II during exercise.

Adult↗
PubMed1994

Comparative effects of an angiotensin-converting enzyme inhibitor and an angiotensin II antagonist in Dahl rats.

The antihypertensive, cardioprotective, and renoprotective effects of a nonpeptide angiotensin II antagonist (AIIA, CV-11974) and an angiotensin-converting enzyme inhibitor (CEI, captopril) were compared in Dahl salt-sensitive rats. Six-week-old male rats received a high-salt diet (4% NaCl) and were divided into control, CEI, and AIIA groups. The CEI group received captopril (15 mg/kg/day) and the AIIA group received CV-11974 (0.72 mg/kg/day), an active metabolite of the AIIA TCV-116, for 4 weeks by continuous subcutaneous infusion. After 4 weeks, systolic blood pressure (SBP) was significantly lower in the treatment groups than in the control group. The heart weight/body weight ratio and urinary protein excretion were reduced in the treatment groups, and renal damage (glomerular sclerosis score) was reduced by approximately 50%. CV-11974 and captopril were comparable in reducing BP, cardiac hypertrophy, and renal damage, suggesting that the renin-angiotensin (R-A) system is involved in elevating BP and promoting cardiovascular damage, despite suppression of the R-A system in this model. The antihypertensive effect of CEI may be due primarily to inhibition of the action of angiotensin II, while other effects, e.g., potentiation of the kinin system, may be less important.

Angiotensin Receptor Antagonists↗
PubMed1994

Taurine amplifies renal kallikrein and prevents salt-induced hypertension in Dahl rats.

OBJECTIVE: To determine whether taurine reduces blood pressure by stimulating the renal kallikrein-kinin system. METHODS: The effects of taurine on blood pressure, urinary kallikrein activity and renal kallikrein gene expression were investigated in Dahl salt-sensitive (Dahl-S) rats. The specificity of the action of taurine was verified by comparison with the action of beta-alanine, a carboxylic analogue of taurine. The effect of co-administration of the specific bradykinin B2 receptor antagonist Hoe 140 was also examined. RESULTS: Administration of taurine (3% in drinking water) for 4 weeks retarded the development of salt (4% sodium chloride diet)-induced hypertension. Systolic blood pressure at the end of the experiment was significantly higher in control rats than in taurine-treated rats. Urinary sodium excretion was not decreased by the reduction in blood pressure. The heart weight:body weight ratio was significantly lower, and urinary volume and kallikrein excretion were significantly higher, in taurine-treated rats. Renal kallikrein gene expression at weeks 1 and 4 was higher in taurine-treated rats. Systolic blood pressure 3 and 4 weeks after the administration of beta-alanine was slightly, but not significantly, lower than that of untreated rats on a high-salt diet, and was accompanied by a significantly lower body weight. Urinary kallikrein excretion decreased with a high-salt diet regardless of beta-alanine administration. Continuous systemic administration of Hoe 140 did not cause any significant alteration in blood pressure in Dahl-S rats that received taurine with a high-salt diet. Taurine also showed a renoprotective effect, as judged by a reduction in proteinuria. CONCLUSION: These results suggest that taurine is an effective antihypertensive agent for salt-induced hypertension. Although taurine activated renal kallikrein, further studies are required to confirm the participation of activated kallikrein in the antihypertensive, cardioprotective and renoprotective effects of taurine.

Animals↗
PubMed1994

Urinary kallikrein activity is increased during the first few weeks of exercise training in essential hypertension.

OBJECTIVE: To determine whether the renal kallikrein-kinin and dopamine systems participate in lowering blood pressure during mild exercise in hypertensives. DESIGN: After a general clinical observation period of 4 weeks, 27 essential hypertensives were divided into two groups. The exercise group underwent blood lactate threshold exercise, using a cycle ergometer for 60 min three times a week for 10 weeks. The non-exercise group was observed at the outpatient clinic. Blood pressure and humoral parameters were measured at weeks 0, 1, 2, 4 and 10 in both groups. METHODS: Blood pressure was measured indirectly with an automatic blood pressure recorder. Twenty-four-hour urinary kallikrein activity (by kininogenase assay), total or free dopamine and total noradrenaline (by high-performance liquid chromatography) were also measured. RESULTS: In the non-exercise group blood pressure and humoral parameters did not change. In the exercise group the change in resting blood pressure between weeks 0 and 10 was statistically significant. The change in 24-h urinary kallikrein activity of the exercise group was significantly greater than that of the non-exercise group between weeks 0 and 1 and weeks 0 and 2. Moreover, the change in systolic blood pressure (SBP) between weeks 0 and 2 was negatively correlated with the change in urinary kallikrein activity between weeks 0 and 2, the change in total dopamine between weeks 0 and 2 was negatively correlated with the change in diastolic blood pressure in the same period, and the change in SBP between weeks 0 and 10 was positively correlated with the change in total noradrenaline in the same period in the exercise group. Subjects with a relatively high baseline urinary kallikrein activity had a significantly greater change in SBP between weeks 0 and 10 than subjects with a relatively low baseline activity. CONCLUSIONS: The renal kallikrein-kinin and dopamine systems may participate in lowering blood pressure during the first few weeks of exercise training. The subsequent reduction of sympathetic activity may be involved in maintaining the lowered blood pressure. Mild exercise is more effective in reducing blood pressure in hypertensives who have a relatively high basal renal kallikrein-kinin system activity.

Adult↗
PubMed1993

Beneficial effects of a serine protease inhibitor in peripheral vascular disease.

Kallikrein, a serine protease known to generate bradykinin (a vasodilating peptide) in alkaline conditions, also generates angiotensin II (a vasoconstricting peptide) in weak acidic conditions. Based on this previous observation, the present study was performed to determine whether ischemic muscle tissue, in which the regional pH must decrease, produces angiotensin II by kallikrein or a similar enzyme, and whether nafamostat (NAF), a serine protease inhibitor, improves local hemodynamics under ischemic conditions caused by exercise in patients with ischemic peripheral vascular disease. NAF was administered intravenously to 20 patients with peripheral vascular disease. Lower-limb thermograms and blood flow were measured before and after exercise. Femoral venous blood of affected limbs was obtained to measure viscosity and humoral variables (i.e., pH, lactate, angiotensin II and bradykinin). Walking distance and subjective symptoms were also recorded. As a control, the same patients repeated this test with saline infusion on a separate day. NAF significantly increased maximal walking distance, improved subjective symptoms during exercise, and attenuated exercise-induced venous lactate and blood viscosity increases, and pH reduction. The blood viscosity increase correlated with the lactate increase. Pretreatment with NAF also resulted in a higher lower-limb skin temperature, and a greater increase of blood flow in the lower limbs after exercise than did pretreatment with saline. The results suggest that kallikrein-like serine protease may exacerbate ischemic symptoms. Changes in plasma bradykinin and angiotensin II in the femoral vein were not detectable, probably because of the lower levels of these peptides in the peripheral circulation.

Aged↗
PubMed1993

Mandibular reconstruction using hydroxylapatite granules, autogenous bone, and a cervical island skin flap.

Ten patients with gingival carcinoma who were treated by marginal mandibulectomy were reconstructed using hydroxylapatite granules, autogenous bone chips, and a cervical island skin flap. The cervical flap was used to produce a cover and partition, designed to prevent the displacement of the mixture of hydroxylapatite and bone. Reconstruction was successfully achieved in all patients. Loss of height of the reconstructed mandible over an average 18-month follow-up ranged from 8% to 22%. One patient has worn a full denture and five patients wear partial dentures.

Aged↗
PubMed1993

Role of locally formed angiotensin II and bradykinin in the reduction of myocardial infarct size in dogs.

OBJECTIVE: The aim was to investigate the role of local formation of angiotensin II and bradykinin in the reduction of myocardial infarct size. METHODS: Bilaterally nephrectomised male mongrel dogs were used. Effects were compared of pretreatment with three inhibitors of angiotensin II forming enzyme-captopril (an angiotensin converting enzyme inhibitor), nafamostat (a serine protease inhibitor), and chymostatin (a cysteine protease inhibitor)--on left anterior descending coronary artery occlusion. Haemodynamic variables were monitored and blood was collected from the anterior interventricular vein and the aorta. Angiotensin I, angiotensin II, and bradykinin were measured by radioimmunoassay. After 90 min of occlusion, infarct sizes were determined by a macroscopic enzyme technique. RESULTS: Angiotensin II release into the anterior interventricular vein increased from 0.03(SEM 1.19) pg.min-1 (before coronary occlusion) to 4.64(1.37) pg.min-1 (n = 14, p < 0.05), while angiotensin I release and plasma renin activity remained unchanged. The increase in angiotensin II release was inhibited by nafamostat and chymostatin, but not by captopril. Bradykinin release increased from -3.18(2.72) (before coronary occlusion) to 34.7(12.3) pg.min-1 (n = 14 p < 0.05) by 30 min after occlusion. This increase was augmented by captopril, from 4.10(2.86) before occlusion to 97.8(39.6) pg.min-1 at 5 min after occlusion (n = 12, p < 0.05), but not by nafamostat or chymostatin. Infarct size was smaller (p < 0.05) in the captopril group than in the control group. CONCLUSIONS: Angiotensin II is locally produced in the ischaemic heart by both serine protease(s) and chymostatin inhibitable protease(s), but not by angiotensin converting enzyme. From the reduction in myocardial infarct size produced by angiotensin converting enzyme inhibition, it seems that bradykinin accumulation may play a more important role than the suppression of angiotensin II formation.

Angiotensin II↗
PubMed1993

Crossover comparison between the depressor effects of low and high work-rate exercise in mild hypertension.

1. The relationship between work-rate and the antihypertensive effect of exercise in hypertensives, and the mechanism of that effect, were investigated by a crossover clinical trial. 2. Ten mild hypertensives were randomly divided into two groups. One group performed low work-rate exercise (LWE) on a cycle ergometer for 10 weeks (blood lactate threshold; approximately 50% of maximum oxygen consumption [Vo2max]). After a 10 week interval without exercise training, these subjects were then switched to a high work-rate exercise (HWE) regimen (4 mmol/L of blood lactate; approximately 75% of Vo2max) for another 10 weeks. In the other group, the order of exercise training was reversed. Since two patients withdrew from the protocol during HWE periods, statistical analysis was performed on the data from the remaining eight patients. There were no order effects observed in any of the data from the two groups. 3. During both LWE and HWE, resting blood pressure (BP) fell significantly after the initiation of exercise therapy (P < 0.05). Furthermore, the overall effects of 10 weeks of LWE and HWE on BP were not significantly different. 4. The work-rate at the lactate threshold, which reflects physical fitness, had increased significantly by 16 W (P < 0.01) after the LWE period and by 11 W (P < 0.01) after the HWE. 5. During the LWE period, changes in haemodynamic and humoral variables were not significant, except for a reduction in plasma norepinephrine at week 10 (P < 0.05). In the HWE period, changes in haemodynamic and humoral variables were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[A case of idiopathic hyperaldosteronism diagnosed by adrenal imaging].

We report a case of idiopathic hyperaldosteronism (IHA) which was differentiated from an aldosterone producing adenoma by the adrenal imaging techniques with computed tomography (CT) and scintigraphy. In this patient, the high basal aldosterone level with the suppressed plasma renin activity typically indicated the diagnosis of primary aldosteronism. However, the differentiation from an aldosterone producing adenoma by responses of plasma aldosterone levels to upright posture, captopril or adrenocorticotropic hormone (ACTH) administration was not definitive. Abdominal CT revealed bilateral adrenal swelling. Adrenal scintillation scanning with 131I-iodocholesterol showed bilateral uptake even after the administration of dexamethasone. Blood sampling from the right adrenal vein was unsuccessful. Blood pressure and serum potassium levels remained unchanged during dexamethasone administration (2 mg/day) over ten days. After the administration of spironolactone and nisoldipine blood pressure and serum potassium levels were normalized. Adrenal imaging is considered to be very useful for the diagnosis of IHA.

Adrenal Glands↗
PubMed1993

Angiotensin II forming activity of vascular endothelial and smooth muscle cells.

To clarify the role of vascular endothelial cells (VEC) and smooth muscle cells (VSMC) in the generation of angiotensin (Ang) II, we measured the Ang II forming activity of these cells in culture using synthetic Ang I and tridecapeptide renin substrate (13RS). Angiotensin converting enzyme (ACE) activity was demonstrated in both types of cells, and the Ang I converting activity was highly sensitive to an ACE inhibitor. Both VEC and VSMC were able to generate Ang II from 13RS independently of ACE and renin. The activity was partially inhibited by chymostatin. It is suggested that Ang I could be converted to Ang II not only by VEC but also by VSMC. Both VEC and VSMC possess alternate Ang II forming pathways independent of ACE and renin.

Angiotensin II↗
PubMed1992

Active and inactive renin after exercise.

The effects of graded exercise on plasma concentrations of active and inactive renin were studied in seven healthy men. Exercise was performed on a cycle ergometer at four different exercise intensities (corresponding to 30%, 50%, 80% and 87% of VO2max) for 10 min each. Concentrations of active renin and total renin after activation by trypsin were measured by direct immunoradiometric assay. Non-trypsin-activated renin concentration (inactive) was obtained by subtraction. Active renin concentrations at 30%, 50%, 80% and 87% of VO2max were 1.2, 1.9, 3.1 and 4.6 times higher than the control concentration, respectively. Similar increases in plasma renin concentration, determined by conventional enzymatic assay, were observed at every stage. In contrast, changes in inactive renin concentration were not significant at any stage. Significant increases in noradrenaline concentration were found at every exercise stage, but adrenaline, aldosterone and lactate concentrations were significantly elevated only after exercise at 50%, 80% and 87% of VO2max. The similarity between the changes in concentration of active renin and noradrenaline would suggest that sympathetic nerve activity may have been responsible either for the release of active renin or for the conversion of inactive renin to its active form in the kidney.

Adult↗
PubMed1992

Clinical symptoms of open lock position of the condyle. Relation to anterior dislocation of the temporomandibular joint.

Nine cases of open lock position of the condyle of the temporomandibular joint (TMJ) are reported. In two patients recurrent dislocation of the TMJ was diagnosed clinically, and four had previous episodes of anterior dislocation. An arthrotomographic examination revealed that the condyles of the affected TMJs were located anterior to the anterior bands of the disks at an open-mouth position. An arthrographic fluoroscopic examination showed that the anterior bands mechanically obstructed the anteriorly displaced condyles from posterior movement into the articular fossae to various degrees at open-mouth position. One cause of anterior dislocation of the TMJ is thought to be fixation of the condyle in the open lock position resulting from a disturbance of a neuromuscular mechanism. In the two patients with dislocation, occlusal treatment eliminated muscular symptoms and the dislocations completely disappeared.

Adult↗
PubMed1992

Regulation of bradykinin-induced chloride secretion in a human epithelial cell line.

The chloride secretory response to bradykinin in T84 cells is regulated. The efflux rate of 125I from these cells can be used to measure this response, and to demonstrate that the sensitivity to bradykinin varies with time in culture. The response in NuT84 cells is greater than that in T84, and can be blocked by the B2 receptor antagonist HOE-140.

Bradykinin↗
PubMed1992

Cardioprotection of ACE inhibitor in ischemic heart is not dependent on the local angiotensin II formation.

Angiotensin II (AII) and bradykinin (BK) release into anterior interventricular vein (AIV) increased significantly 30 minutes after left anterior descending artery (LAD) occlusion in the absence of kidneys. Captopril enhanced BK release, but did not suppress the increase of AII release. Nafamostat suppressed both releases. Infarct size was significantly reduced by captopril but not by nafamostat. These results suggest that cardioprotective effect of captopril might be dependent on local BK accumulation, but not on suppression of local AII generation.

Angiotensin II↗
PubMed1991

Human renin activation by protease from the renin granule fraction of the dog kidney cortex.

To clarify the possible conversion of prorenin in renin granules where conversion reportedly occurred, we investigated whether the renin granule fraction of the kidney could activate prorenin to the active form. Renin granules were isolated from the dog kidney cortex by discontinuous sucrose density gradient centrifugation. Human active renin was quantified by immunoradiometric assay which could detect only the human active renin but not the inactive human renin or dog renin. Inactive renin from human amniotic fluid was incubated with the subcellular fraction of the dog kidney cortex. The renin granule fraction that showed the highest renin activity stimulated the inactive renin to become the active form. The membrane preparation obtained from the renin granule fraction by freezing and thawing the fraction in low osmolarity retained the activity of renin activation. Other subcellular fractions showed less renin activation. The optimal pH for renin activation by the membrane was pH 5.0 to 6.0. The activation depended on the time of incubation and concentration. The activation was inhibited by N-ethylmaleimide but not by EDTA or serine protease inhibitors. These results suggest that renin is processed by a membrane bound protease in renin granules.

Amniotic Fluid↗