Lisinopril Reduces Left Ventricular Hypertrophy and Cardiac Polyamine Concentrations without a Reduction in Left Ventricular Wall Stress in Transgenic Tsukuba Hypertensive Mice.

Kai, Tatsuya; Ishikawa, Kinji

doi:10.1291/hypres.23.625

Cited by 6 publications

(4 citation statements)

References 45 publications

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“…It has been reported that there is a close relationship between wall stress and cardiac hypertrophy (21). However, Kai and Ishikawa has reported that lisinopril reversed cardiac remodeling without a reduction in LV wall stress in transgenic hyprertensive mice (22). This report supports our present results.…”

Section: Discussionsupporting

confidence: 91%

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

et al. 2002

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Studies have shown that the renin-angiotensin system (RAS) plays an important role in cardiac remodelinginduced by hypertension. However, the role of this system on myocyte remodeling remains unclear. In the present study, we have assessed the effect of perindopril, an angiotensin converting enzyme (ACE) inhibitor, in spontaneously hypertensive rats (SHRs) as a means to evaluate the role of RAS in myocyte remodeling. We also investigated the effect of blockade on myocyte remodeling. We used female SHRs at

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Section: Discussionsupporting

confidence: 91%

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

et al. 2002

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“… 37 The serum concentration of AngII is 4 to 5 times higher in THM than in the C57BL/6 mice. 38 , 39 Because nutrition of articular cartilage is provided by diffusion from vessels in subchondral bone and bone marrow and percolation through synovial fluid, 40 it is possible that the high serum AngII concentration upregulated the AT1R in chondrocytes in articular cartilage. Together, the mechanical stresses induced by forced running and higher serum and cartilage concentrations of AngII in the THM might have resulted in synergistic upregulation of AT1R expression.…”

Section: Discussionmentioning

confidence: 99%

Activation of the renin-angiotensin system in mice aggravates mechanical loading-induced knee osteoarthritis

et al. 2018

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Epidemiological studies have shown an association between hypertension and knee osteoarthritis (OA). The purpose of this study was to investigate whether activation of the renin–angiotensin system (RAS) can aggravate mechanical loading-induced knee OA in mice. Eight-week-old male Tsukuba hypertensive mice (THM) and C57BL/6 mice were divided into four groups: i) running THM group, ii) running C57BL/6 mice group, iii) non-running THM group, and iv) non-running C57BL/6 mice group. Mice in the running group were forced to run (25 m/min, 30 min/day, 5 days/week) on a treadmill. All mice in the four groups (n=10 in each group) were euthanized after 0, 2, 4, 6, or 8 weeks of running or natural breeding. Cartilage degeneration in the left knees was histologically evaluated using the modified Mankin score. Expression of Col X, MMP-13, angiotensin type 1 receptor (AT1R), and AT2R was examined immunohistochemically. To study the effects of stimulation of the AT1R in chondrocytes by mechanical loading and/or Angiotensin II (AngII) on transduction of intracellular signals, phosphorylation levels of JNK and Src were measured in bovine articular chondrocytes cultured in three-dimensional agarose scaffolds. After 4 weeks, the mean Mankin score for the lateral femoral condylar cartilage was significantly higher in the THM running group than in the C57BL/6 running group and non-running groups. AT1R and AT2R expression was not detected at 0 weeks in any group but was noted after 4 weeks in the THM running group. AT1R expression was also noted at 8 weeks in the C57BL/6 running group. The expression levels of AT1R, COL X, and MMP-13 in chondrocytes were significantly higher in the THM running group than in the control groups. Positive significant correlations were noted between the Mankin score and the rate of AT1R-immunopositive cells, between the rates of AT1R- and Col X-positive cells, and between the rates of AT1Rand AT2R-positive cells. The phosphorylation level of JNK was increased by cyclic compression loading or addition of AngII to the cultured chondrocytes and was reversed by pretreatment with an AT1R blocker. A synergistic effect on JNK phosphorylation was observed between compression loading and AngII addition. Transgene activation of renin and angiotensinogen aggravated mechanical load-induced knee OA in mice. These findings suggest that AT1R expression in chondrocytes is associated with early knee OA and plays a role in the progression of cartilage degeneration. The RAS may be a common molecular mechanism involved in the pathogenesis of hypertension and knee OA.

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“…11 Furthermore, a direct comparison of hydralazine and lisinopril at doses that lower blood pressure equally also shows additional effects of ACE inhibitors unrelated to blood pressure effects. 12 In another study, Kauser et al 13 reported that apoE KO mice treated with L-N-arginine methyl ester (L-NAME) at doses that do not raise blood pressure still have increased lesion areas. These results agree with ours in that the predominant effect of NOS inhibition on atherogenesis seems independent of blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Hypertension Does Not Account for the Accelerated Atherosclerosis and Development of Aneurysms in Male Apolipoprotein E/Endothelial Nitric Oxide Synthase Double Knockout Mice

et al. 2001

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Background-Apolipoprotein E (apoE)/endothelial nitric oxide synthase (eNOS) double knockout (DKO) mice demonstrate accelerated atherosclerosis and develop abdominal aortic aneurysms and aortic dissection, suggesting a role for eNOS in suppressing atherogenesis. To test whether accelerated atherosclerosis and aortic aneurysms were due to hypertension, we administered hydralazine to male apoE/eNOS DKO mice to reduce blood pressure. Methods and Results-Male apoE/eNOS DKO mice were treated with hydralazine in their drinking water (250 mg/L) using a dose that lowers the blood pressure to levels seen in apoE KO mice. The mice were fed a Western-type diet for 16 weeks, and lesion formation was assessed by inspection of the vessel and staining with Sudan IV. Hydralazinetreated, normotensive male apoE/eNOS DKO mice developed increased aortic lesion areas (30.0Ϯ2.8%, nϭ11) compared with male apoE KO mice (14.6Ϯ0.8%, nϭ7). The extent of lesion formation was not significantly different from male apoE/eNOS DKO mice that were not given hydralazine (28.3Ϯ3.1%, nϭ9). Four of 11 hydralazine-treated male apoE/eNOS DKO mice developed abdominal aortic aneurysms. Conclusions-Hypertension is not required for the accelerated atherosclerosis seen in apoE/eNOS DKO animals, and control of hypertension during a 16-week period does not prevent aortic aneurysm formation.

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Lisinopril Reduces Left Ventricular Hypertrophy and Cardiac Polyamine Concentrations without a Reduction in Left Ventricular Wall Stress in Transgenic Tsukuba Hypertensive Mice.

Cited by 6 publications

References 45 publications

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

Perindopril Reverses Myocyte Remodeling in the Hypertensive Heart

Activation of the renin-angiotensin system in mice aggravates mechanical loading-induced knee osteoarthritis

Hypertension Does Not Account for the Accelerated Atherosclerosis and Development of Aneurysms in Male Apolipoprotein E/Endothelial Nitric Oxide Synthase Double Knockout Mice

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