Tatsuya Kai

Sakai City Hospital, Sakai, Ōsaka, Japan

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Publications (13)24.57 Total impact

  • Tatsuya Kai · Kinji Ishikawa
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    ABSTRACT: This experiment was designed to determine how the angiotensin-converting enzyme inhibitor, lisinopril, acts on left ventricular wall stress and cardiac polyamine concentrations in Tsukuba hypertensive mice (THMs) carrying both human renin and angiotensinogen genes. Twelve-week-old THMs were treated with either lisinopril or hydralazine, or were left untreated, for 8 weeks. C57BL/6 mice of similar age were used as normal controls. Each group consisted of 14 mice. The systolic blood pressure of each mouse was measured once a week. Mice were euthanized at 20 weeks of age, and the left ventricular weight, left ventricular diameter, left ventricular wall stress, and left ventricular polyamine concentrations were measured. The systolic blood pressure of the untreated group was approximately 35 mmHg higher than that of the C57BL/6 mice. The left ventricular weight, left ventricular diameter, left ventricular wall stress, and left ventricular polyamine concentrations in the untreated group were significantly higher compared to those in the C57BL/6 mice. The lisinopril group had significantly decreased systolic blood pressure and other measurement items, except the left ventricular wall stress, in comparison with the untreated group. The hydralazine group also had significantly decreased systolic blood pressure and left ventricular wall stress when compared with the untreated group, but no significant differences in other measurement items when compared with the untreated group. These findings indicate that lisinopril reduces left ventricular hypertrophy and polyamine concentration without reducing left ventricular wall stress, and that simply decreasing blood pressure does not suppress left ventricular hypertrophy.
    No preview · Article · Dec 2000 · Hypertension Research
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    ABSTRACT: Tsukuba hypertensive mice (THM) are transgenic mice that carry both human renin and angiotensinogen genes and overexpress the human renin-angiotensin system (RAS). In the present study, the effect of lisinopril on deposition of macromolecular iron in renal tissue in THM was evaluated. Twelve-week-old male THM were divided into the following groups: lisinopril dosage group (ACEI group), hydralazine dosage group (hydralazine group), and a no-drug group (control group). Age-matched male C57BL/6 mice (wild group) were used as normal controls. Each mouse was treated with a drug for 8 weeks. All mice were euthanised at 20 weeks of age, and their kidneys were fixed and stained with Berlin-blue. Systolic blood pressure was significantly higher in the control group than in the wild group, and it decreased significantly to similar levels in the ACEI group and the hydralazine group. Iron deposition was observed in proximal renal tubules in the control group and the hydralazine group, but iron deposition was not observed in the ACEI group or the wild group. The results of the study suggest that the RAS plays an important role in the deposition of iron in the proximal renal tubules in THM, and that lisinopril prevents this deposition.
    No preview · Article · Mar 2000 · Nephrology
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    ABSTRACT: 1. The role of the renin–angiotensin system (RAS) in cardiac hypertrophy and nephropathy was examined in Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. 2. Tsukuba hypertensive mice were treated with 20 mg/kg per day lisinopril, 30 mg/kg per day hydralazine or nothing. Administration of drugs was performed for 6 months from 12 weeks of age; water intake and urine volume were measured and urine albumin excretion, heart to bodyweight ratio and the glomerulosclerosis index were examined. 3. Systolic blood pressure was significantly lowered by treatment with lisinopril and hydralazine. Urine volume, water intake and urinary albumin excretion were significantly decreased by lisinopril. When hydralazine was administered to THM, these parameters were transiently decreased, but eventually reached almost the same levels as those in the untreated group. The heart to bodyweight ratio was significantly decreased by lisinopril, but not by hydralazine. The glomerulosclerosis index was significantly lowered by lisinopril, but the index in the hydralazine group was not significantly different from that in the untreated group. 4. These results suggest that the RAS plays an important role in the progression of cardiac hypertrophy in THM. In addition, the RAS may also play an important role in the progression of nephropathy; however, this may also be partially regulated by elevated blood pressure in the short term.
    No preview · Article · Apr 1999 · Clinical and Experimental Pharmacology and Physiology
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    ABSTRACT: Objective: To evaluate the relation of tissue-localized angiotensin II (Ang II) concentration with cardiac hypertrophy and glomerulosclerosis in Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. Design: Thirty THM aged 12 weeks were distributed equally to a lisinopril dosage group, a hydralazine dosage group, and an untreated group. Ten age-matched C57BL/6 mice were used as normal controls. Administration was performed for 8 weeks from 12 weeks of age. All mice were euthanized at 20 week of age, and the heart-to-body weight ratio, the renal glomerulosclerosis score, tissue Ang II concentration and tissue catecholamine concentration were measured. Results: In the untreated group, a significant increase in every examination item was found as compared with that in C57BL/6 mice. In the lisinopril group, the observed value of every item was significantly lower than that in the untreated group. In the hydralazine group, tissue Ang II and catecholamine concentrations and the heart-to-body weight ratio were not different from those in the untreated group. Although the glomerulosclerosis score in the hydralazine group was significantly less than that in the untreated group, this was significantly higher than that in the lisinopril group. Conclusion: Tissue Ang II concentration is more important than hypertension in causing cardiac hypertrophy, and both tissue Ang II level and hypertension are important in causing glomerulosclerosis in THM.
    No preview · Article · Nov 1998 · Journal of Hypertension
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    ABSTRACT: The effects of L-158,809, an angiotensin II type 1 receptor antagonist, on cardiac hypertrophy and nephropathy were examined using Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. Nine male THM aged 20 weeks were assigned to each of a no-dosage group and an L-158,809 dosage group, and L-158,809 was administered for 8 weeks. Nine age-matched male C57BL/6 mice were used as normal control animals. At 28 weeks of age, all of the mice were euthanized. Systolic blood pressure, urinary volume, water intake volume, urinary albumin excretion, heart weight and kidney weight to body weight ratios and a glomerulosclerosis index were measured. In the no-dosage group, the values of all of these parameters were larger than those in the control mice. In the L-158,809 group, all of the parameters showed significant improvement, except for blood pressure, which was not significantly different from that in the no-dosage group. These results suggest that the renin-angiotensin system played a crucial role in the cardiac hypertrophy and nephropathy in THM, and that L-158,809 exhibited strong curative effects on cardiac hypertrophy and nephropathy by blocking the angiotensin II type 1 receptor.
    No preview · Article · Sep 1998 · Japanese Circulation Journal
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    ABSTRACT: Tsukuba hypertensive mice (THMs) are transgenic mice carrying human renin-angiotensin system (RAS) genes. The aim of this study is to evaluate whether renal disorders are present in THMs. Twenty-week-old THMs and C57BL/6 mice (C57s) were used for this study. Each group consisted of 8 mice. Systolic blood pressure, urinary volume, water intake and urinary albumin excretion were measured in each mouse. Each mouse was then euthanized, and the renal glomerulosclerosis index and glomerular size were measured. Systolic blood pressure of THMs was about 40 mmHg higher than that of C57s. Urinary volume, water intake and urinary albumin excretion were significantly higher in THMs than in C57s. The renal glomerulosclerosis index and glomerular size were also significantly higher in THMs than in C57s. These results suggested that an enhanced renin-angiotensin system, including its hypertensive effects, stimulates albuminuria, renal glomerulosclerosis and glomerular hypertrophy in THMs.
    No preview · Article · Aug 1998 · Blood Pressure
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    ABSTRACT: Tsukuba hypertensive mice (THM) are a hypertensive model prepared by mating a transgenic mice with human renin gene and a transgenic mice with human angiotensinogen gene. In the present study, we examined effects of renin-angiotensin system (RAS) on cardiac hypertrophy and renal disorders using Tsukuba hypertensive mice. While THM showed an increase of about 30 mmHg in systolic pressure compared to C57BL/6 mice employed as normal control animals, the increase in blood pressure was not observed in the mice to which either gene was transferred. Urinary volume, water intake volume, urinary albumin excretion, heart to body weight ratio and renal glomerular sclerosis index increased significantly in THM, but none of these parameters showed a significant difference from the C57 mice when they were examined in mice to which either of the genes was transferred. In contrast, when lisinopril was administered to THM, all the parameters decreased significantly without lowering the systolic pressure. From these findings, it was demonstrated that RAS was playing a significant role in cardiac hypertrophy and renal disorders of THM and that lisinopril had inhibitory effects on cardiac hypertrophy and renal glomerular sclerosis by inhibiting RAS.
    No preview · Article · Jun 1998 · Clinical and Experimental Hypertension
  • Tatsuya Kai · Hirofumi Kino · Kinji Ishikawa
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    ABSTRACT: Tsukuba hypertensive mice (THMs) are transgenic mice carrying human renin and angiotensinogen genes. The aim of this study was to evaluate the role of the renin-angiotensin system (RAS) in cardiac hypertrophy and renal disorders in THMs. After a 2-wk control period, 10-wk-old THMs were treated with lisinopril (ACEI group) or hydralazine (hydralazine group) or left untreated (control group) for 8 wk. C57BL/6 mice of similar age (wild group) were used as normal controls. Systolic blood pressure and urinary albumin excretion were measured once a week. All mice were sacrificed at 20 wk of age, and heart to body weight ratio, cardiac myocyte diameter, renal glomerular sclerosis index, and glomerular size were measured. Fibronectin expression was also evaluated. At 20 wk of age, systolic blood pressure and urinary albumin excretion in the control group were significantly higher than those in the wild group and significantly lower than those in the ACEI and hydralazine groups. Heart to body weight ratio and cardiac myocyte diameter were significantly higher in the hydralazine and control groups than in the other groups. Renal glomerular sclerosis index and glomerular size were also significantly higher in the control group than in the other groups, and there were significant differences between the ACEI and hydralazine groups in these variables. Fibronectin expression was marked in the control and hydralazine groups. These findings suggest that the RAS plays an important role in cardiac hypertrophy in THMs, but that both the RAS and elevation of blood pressure contribute to the pathogenesis of renal glomerular sclerosis.
    No preview · Article · Apr 1998 · Hypertension Research

  • No preview · Article · Apr 1998 · American Journal of Hypertension
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    ABSTRACT: Tsukuba hypertensive mice (THM) are transgenic mice carrying both human renin and angiotensinogen genes, and possessing an overexpressing human renin-angiotensin system. The aim of this study is to evaluate the angiotensin II concentration in the heart and kidney in THM. Twenty-week-old male THM and control C57BL/6 mice (C57) were used. Each group consisted of 3 mice. For each mouse, systolic blood pressure, heart to body weight ratio, renal glomerular sclerosis index and angiotensin II concentration in the heart and kidney were measured. Systolic blood pressure of THM was about 40 mmHg higher than that of C57. Heart to body weight ratio and renal glomerular sclerosis index were significantly higher in THM than those in C57. The angiotensin II concentration in THM was about 4 times higher in the heart and about 5 times higher in the kidney compared with that in C57. These results suggest that accelerated tissue angiotensin II production, significant cardiac hypertrophy and renal glomerular sclerosis all occur because of hypertension.
    No preview · Article · Jan 1998 · Blood Pressure

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  • No preview · Article · Jan 1997
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    ABSTRACT: 1. In the present study, we examined the effect of a novel angiotensin II type I receptor antagonist, TCV-116, on carotid neointimal formation after balloon injury in SHR and WKY rats. 2. Oral administration of TCV-116 at a dose of 10mg/kg per day reduced not only systolic blood pressure but also neointimal formation after carotid balloon injury. TCV-116 also suppressed cardiac hypertrophy. An angiotensin-converting enzyme inhibitor, lisinopril (20mg/kg per day), had a similar effect to that of TCV-116. 3. In the WKY experiment, both TCV-116 and lisinopril suppressed neointimal formation as well as systolic blood pressure, but did not suppress cardiac hypertrophy. 4. Although SHR showed markedly enhanced neointimal formation after balloon injury compared with age-matched WKY rat, both TCV-116 and lisinopril showed similar sup-pressive effects on neointimal formation in both SHR and WKY rats. 5. These results confirm the important role of angiotensin II in neointimal formation following balloon injury. Further studies are needed to clarify the mechanism of the difference between SHR and WKY rats in the response of vascular smooth muscle cells.
    No preview · Article · Oct 1995 · Clinical and Experimental Pharmacology and Physiology