The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform

Li Yan-hua - One of the best experts on this subject based on the ideXlab platform.

  • Effect of rosiglitazone on serum MMP-2 and TIMP-1 in Diabetic Hypertension
    Chinese Journal of Diabetes, 2008
    Co-Authors: Li Yan-hua
    Abstract:

    Objective To observe the effect of rosiglitazone on MMP-2 and TIMP-1 in the patients with Diabetic Hypertension.Methods 40 Diabetic patients with essential Hypertension(DMEH)were divided into 2 groups:(1)group A(n=20)without rosiglitazone treatment;(2)group B(n=20)undergoing rosiglitazone treatment.ELISA method was adopted to determine the levels of MMP-2 and TIMP-1,and the differences in MMP-2 and TIMP-1 between pre-and post-use of rosiglitazone were observed.Results At 16 weeks of the treatment by rosiglitazone,the level of MMP-2 was higher after treatment than before treatment [(37.9±3.9)vs(27.5±4.3)μg/L,P0.05],and the level of TIMP-1 was lower after treatment than before treatment[(410±81)vs(468±101)μg/L,P0.01].Conclusions Rosiglitazone not only improves blood sugar and blood pressure,but also raises the level of MMP-2 and reduces the level of TIMP-1.

Miki Nagase - One of the best experts on this subject based on the ideXlab platform.

  • Mineralocorticoid receptor blockade suppresses dietary salt-induced ACEI/ARB-resistant albuminuria in non-Diabetic Hypertension: a sub-analysis of evaluate study
    Hypertension Research, 2019
    Co-Authors: Mitsuhiro Nishimoto, Hiroshi Ohtsu, Takeshi Marumo, Wakako Kawarazaki, Nobuhiro Ayuzawa, Kohei Ueda, Daigoro Hirohama, Fumiko Kawakami-mori, Shigeru Shibata, Miki Nagase
    Abstract:

    Excessive dietary salt intake can counteract the renoprotective effects of renin–angiotensin system (RAS) blockade in hypertensive patients with chronic kidney disease (CKD). In rodents, salt loading induces Hypertension and renal damage by activating the mineralocorticoid receptor (MR) independently of plasma aldosterone levels. Thus, high salt-induced resistance to RAS blockade may be mediated by MR activation. To test this, a post hoc analysis of the Eplerenone Combination Versus Conventional Agents to Lower Blood Pressure on Urinary Antialbuminuric Treatment Effect (EVALUATE) trial was conducted. Thus, 304 non-Diabetic hypertensive patients on RAS-blocking therapy were divided into tertiles according to salt intake (estimated 24-h urinary sodium excretion at baseline) and compared in terms of percent reduction in urinary albumin-to-creatinine ratio (UACR) at 52 weeks relative to baseline. The eplerenone-treated patients in the highest sodium excretion tertile exhibited significantly greater reduction in UACR than the placebo subjects in the same tertile (−22.5% vs. +21.8%, p   =  0.02). This disparity was not observed in the lowest (−10.2% vs. −0.84%, p   =  0.65) or middle (−19.5% vs. +9.5%, p   =  0.22) tertiles. Similar systolic blood pressure changes were observed. In the whole cohort, reduction in UACR correlated positively with reduction in systolic blood pressure ( r ^2 = 0.04, p  = 0.02). These results support the hypothesis that excessive salt intake can enhance resistance to RAS blockade by activating MR. They also suggest that eplerenone plus RAS blockade may be effective for CKD in hypertensive patients, especially those with excessive salt intake.

  • mineralocorticoid receptor blockade suppresses dietary salt induced acei arb resistant albuminuria in non Diabetic Hypertension a sub analysis of evaluate study
    Hypertension Research, 2019
    Co-Authors: Mitsuhiro Nishimoto, Hiroshi Ohtsu, Takeshi Marumo, Wakako Kawarazaki, Nobuhiro Ayuzawa, Kohei Ueda, Daigoro Hirohama, Shigeru Shibata, Fumiko Kawakamimori, Miki Nagase
    Abstract:

    Excessive dietary salt intake can counteract the renoprotective effects of renin–angiotensin system (RAS) blockade in hypertensive patients with chronic kidney disease (CKD). In rodents, salt loading induces Hypertension and renal damage by activating the mineralocorticoid receptor (MR) independently of plasma aldosterone levels. Thus, high salt-induced resistance to RAS blockade may be mediated by MR activation. To test this, a post hoc analysis of the Eplerenone Combination Versus Conventional Agents to Lower Blood Pressure on Urinary Antialbuminuric Treatment Effect (EVALUATE) trial was conducted. Thus, 304 non-Diabetic hypertensive patients on RAS-blocking therapy were divided into tertiles according to salt intake (estimated 24-h urinary sodium excretion at baseline) and compared in terms of percent reduction in urinary albumin-to-creatinine ratio (UACR) at 52 weeks relative to baseline. The eplerenone-treated patients in the highest sodium excretion tertile exhibited significantly greater reduction in UACR than the placebo subjects in the same tertile (−22.5% vs. +21.8%, p = 0.02). This disparity was not observed in the lowest (−10.2% vs. −0.84%, p = 0.65) or middle (−19.5% vs. +9.5%, p = 0.22) tertiles. Similar systolic blood pressure changes were observed. In the whole cohort, reduction in UACR correlated positively with reduction in systolic blood pressure (r2 = 0.04, p = 0.02). These results support the hypothesis that excessive salt intake can enhance resistance to RAS blockade by activating MR. They also suggest that eplerenone plus RAS blockade may be effective for CKD in hypertensive patients, especially those with excessive salt intake.

Carl Erik Mogensen - One of the best experts on this subject based on the ideXlab platform.

  • Vascular impact of anti-hypertensive treatment and renal protection
    Current medical research and opinion, 2005
    Co-Authors: Carl Erik Mogensen
    Abstract:

    Hypertension contributes to the progression of renal disease by accelerating structural changes in the kidney, leading to a progressive decline in glomerular filtration rate. Hypertension and microvascular changes can create a vicious circle, leading to further renal damage and increases in blood pressure. Prevention of renal damage is a priority, especially in the growing number of patients with Diabetic Hypertension. Angiotensin receptor blocking drugs and ACE inhibitors have been shown to display renoprotective effects, and ACE inhibitors reduce the risk of microalbuminuria, the initial step in renal disease in diabetes. Impressive results have been obtained with a low-dose combination of the ACE-inhibitor perindopril and the diuretic indapamide, which not only gave superior reductions in blood pressure to enalapril, but also a 24% greater reduction in albumin excretion. Perindopril/indapamide also showed a trend towards reducing cardiovascular events. There is evidence from animal studies that this combination protects both renal structure and function.

  • Protection rénale: données récentes en faveur d’une nouvelle approche — l’étude PREMIER
    American Journal of Cardiovascular Drugs, 2004
    Co-Authors: Carl Erik Mogensen
    Abstract:

    Microalbuminuria is a strong marker for progressive renal damage and an increased risk of mortality, especially from cardiovascular disease, in patients with type 1 or type 2 diabetes and Hypertension. The benefits of blood pressure reduction in patients with diabetes and Hypertension are well known and a range of treatments have been shown to be effective in reducing the microalbuminuria associated with Diabetic Hypertension. The PREMIER study compared the effects of 12 months’ therapy daily with a combination treatment consisting of an ACE inhibitor (2 mg perindopril) plus a diuretic (0.625 mg indapamide) with those of daily ACE inhibitor monotherapy with 10 mg enalapril, in patients with type 2 diabetes and Hypertension. The decreases in systolic and diastolic blood pressure produced by a low-dose combination perindopril/indapamide (PER/IND) (14.8 and 8.8 mm Hg, respectively) were significantly greater (systolic = −3.0 mm Hg [95% CI, −5.6, -0.4], p = 0.012 and diastolic = −1.5 mm Hg [95% CI, −3.0, −0.10], p = 0.019) than those produced by enalapril (12.3 and 7.3 mm Hg, respectively). The albumin excretion rate (AER) decreased significantly more with PER/IND (−42% [95% CI, −50% to −33%]) than with enalapril (−27% [95% CI, −37% to −16%]) giving an adjusted additional decrease of 24% (95% CI, −38% to −8%, p=0.002) for PER/IND. The effect of PER/IND on AER was independent of its effect on blood pressure. Recent guidelines recommend that combination therapy with a diuretic and an ACE inhibitor should be initiated early in Diabetic Hypertension. The results of the PREMIER study validate these recommendations and show that combination treatments such as PER/IND should be viewed as the most appropriate treatment for patients with diabetes and Hypertension, particularly those with microalbuminuria. La microalbuminurie est un puissant marqueur d’altération progressive de la fonction rénale et de risque accru de mortalité, notamment par affection cardiovasculaire, chez les patients atteints de diabète de type 1 ou 2 et d’Hypertension artérielle. Les effets bénéfiques liésàl’abaissement de la pression artérielle chez les patients diabétiques présentant une Hypertension artérielle sont bien établis, et différents protocoles thérapeutiques ont fait la preuve de leur efficacite à réduire la microalbuminurie associée à l’Hypertension artérielle chez les sujets diabétiques. L’étude PREMIER visait à comparer les effets de l’administration quotidienne, sur une période de 12 mois, d’une association thérapeutique constituée d’un inhibiteur de l’enzyme de conversion (IEC) (le perindopril 2 mg) et d’un diurétique (l’indapamide 0,625 mg)àceux d’un IEC, l’énalapril 10 mg, administré quotidiennement en monothérapie chez des patients atteints de diabète de type 2 et d’Hypertension artérielle. Les diminutions de la pression artérielle systolique et diastolique induites par une association faiblement dosée de perindopril/indapamide (PER/IND) (14,8 et 8,8 mmHg respectivement) ont été significativement supérieures [systolique = −3,0 mmHg (IC à 95 %: −5,6 à −0,4), p = 0,012; et diastolique = −1,5 mmHg (IC à 95 %: −3,0 à −0,10), p = 0,019] à celles engendrées par l’énalapril (respectivement 12,3 et 7,3 mmHg). Le taux d’excrétion d’albumine (TEA) a été abaissé de façon significativement plus marquée par PER/IND [−42 % (IC à 95 %: −50 % à −33 %)] que par l’énalapril [−27 % (IC à 95 %: −37 % à −16 %]), cela s’étant traduit par une diminution supplémentaire ajustée de 24 % (IC à 95 %: −38 % à −8 %; p = 0,002) en faveur de PER/IND. L’effet exercé par PER/IND sur le TEA s’est révéle indépendant de son action sur la pression artérielle. Les recommandations récemment publiées stipulent que les patients diabétiques atteints d’Hypertension artérielle doivent être précocement traités par une association thérapeutique constituée d’un diurétique et d’un IEC. Les résultats de l’étude PREMIER valident ces recommandations et montrent que les associations thérapeutiques telles que PER/IND doivent être considérées comme le mode de traitement le plus pertinent chez les patients présentant un diabète associé à une Hypertension artérielle, surtout lorsqu’il existe une microalbuminurie.

Mitsuhiro Nishimoto - One of the best experts on this subject based on the ideXlab platform.

  • Mineralocorticoid receptor blockade suppresses dietary salt-induced ACEI/ARB-resistant albuminuria in non-Diabetic Hypertension: a sub-analysis of evaluate study
    Hypertension Research, 2019
    Co-Authors: Mitsuhiro Nishimoto, Hiroshi Ohtsu, Takeshi Marumo, Wakako Kawarazaki, Nobuhiro Ayuzawa, Kohei Ueda, Daigoro Hirohama, Fumiko Kawakami-mori, Shigeru Shibata, Miki Nagase
    Abstract:

    Excessive dietary salt intake can counteract the renoprotective effects of renin–angiotensin system (RAS) blockade in hypertensive patients with chronic kidney disease (CKD). In rodents, salt loading induces Hypertension and renal damage by activating the mineralocorticoid receptor (MR) independently of plasma aldosterone levels. Thus, high salt-induced resistance to RAS blockade may be mediated by MR activation. To test this, a post hoc analysis of the Eplerenone Combination Versus Conventional Agents to Lower Blood Pressure on Urinary Antialbuminuric Treatment Effect (EVALUATE) trial was conducted. Thus, 304 non-Diabetic hypertensive patients on RAS-blocking therapy were divided into tertiles according to salt intake (estimated 24-h urinary sodium excretion at baseline) and compared in terms of percent reduction in urinary albumin-to-creatinine ratio (UACR) at 52 weeks relative to baseline. The eplerenone-treated patients in the highest sodium excretion tertile exhibited significantly greater reduction in UACR than the placebo subjects in the same tertile (−22.5% vs. +21.8%, p   =  0.02). This disparity was not observed in the lowest (−10.2% vs. −0.84%, p   =  0.65) or middle (−19.5% vs. +9.5%, p   =  0.22) tertiles. Similar systolic blood pressure changes were observed. In the whole cohort, reduction in UACR correlated positively with reduction in systolic blood pressure ( r ^2 = 0.04, p  = 0.02). These results support the hypothesis that excessive salt intake can enhance resistance to RAS blockade by activating MR. They also suggest that eplerenone plus RAS blockade may be effective for CKD in hypertensive patients, especially those with excessive salt intake.

  • mineralocorticoid receptor blockade suppresses dietary salt induced acei arb resistant albuminuria in non Diabetic Hypertension a sub analysis of evaluate study
    Hypertension Research, 2019
    Co-Authors: Mitsuhiro Nishimoto, Hiroshi Ohtsu, Takeshi Marumo, Wakako Kawarazaki, Nobuhiro Ayuzawa, Kohei Ueda, Daigoro Hirohama, Shigeru Shibata, Fumiko Kawakamimori, Miki Nagase
    Abstract:

    Excessive dietary salt intake can counteract the renoprotective effects of renin–angiotensin system (RAS) blockade in hypertensive patients with chronic kidney disease (CKD). In rodents, salt loading induces Hypertension and renal damage by activating the mineralocorticoid receptor (MR) independently of plasma aldosterone levels. Thus, high salt-induced resistance to RAS blockade may be mediated by MR activation. To test this, a post hoc analysis of the Eplerenone Combination Versus Conventional Agents to Lower Blood Pressure on Urinary Antialbuminuric Treatment Effect (EVALUATE) trial was conducted. Thus, 304 non-Diabetic hypertensive patients on RAS-blocking therapy were divided into tertiles according to salt intake (estimated 24-h urinary sodium excretion at baseline) and compared in terms of percent reduction in urinary albumin-to-creatinine ratio (UACR) at 52 weeks relative to baseline. The eplerenone-treated patients in the highest sodium excretion tertile exhibited significantly greater reduction in UACR than the placebo subjects in the same tertile (−22.5% vs. +21.8%, p = 0.02). This disparity was not observed in the lowest (−10.2% vs. −0.84%, p = 0.65) or middle (−19.5% vs. +9.5%, p = 0.22) tertiles. Similar systolic blood pressure changes were observed. In the whole cohort, reduction in UACR correlated positively with reduction in systolic blood pressure (r2 = 0.04, p = 0.02). These results support the hypothesis that excessive salt intake can enhance resistance to RAS blockade by activating MR. They also suggest that eplerenone plus RAS blockade may be effective for CKD in hypertensive patients, especially those with excessive salt intake.

Ingrid Klöting - One of the best experts on this subject based on the ideXlab platform.

  • Metabolic features of newly established congenic diabetes-prone BB.SHR rat strains.
    Life sciences, 1998
    Co-Authors: Ingrid Klöting, Birger Voigt, Peter Kovács
    Abstract:

    Abstract The well-known association of Hypertension and diabetes mellitus and the lack of suitable animal models to study Diabetic Hypertension prompted us to transfer 4 chromosomal regions with quantitative trait loci (QTLs) for blood pressure of the spontaneously hypertensive SHR rat onto the genetic background of the diabetes-prone and normotensive BB/OK rat. Four congenic strains developed are named as BB.Sa (Chr. 1), BB.Bp2 (Chr. 18), BB.1K (Chr.20) and BB.Xs (Chr.X). Because the systolic blood pressure is significantly elevated in all congenics, renal related traits were investigated in serum and urine. Comparing BB/OK and their congenic derivatives, significant differences were found in all serum and in 7 out of 8 urine constituents studied. Most significant differences were found between BB/OK and BB.Bp2 rats. Significant differences were also found between the different congenic strains indicating that each congenic strain has its own phenotype and that each chromosomal region contains most probably further QTLs for some of the traits studied.

  • Alleles of the Spontaneously Hypertensive Rat Decrease Blood Pressure at Loci on Chromosomes 4 and 13
    Biochemical and biophysical research communications, 1997
    Co-Authors: Peter Kovács, Birger Voigt, Ingrid Klöting
    Abstract:

    In this study the spontaneously hypertensive rat (SHR/Mol) and the spontaneously Diabetic BB/OK rat were crossed, and the F1 hybrids were backcrossed onto the BB/OK rat in order to search for cosegregation between blood pressure and loci on chromosomes 4 and 13. Cosegregation of microsatellites on chromosomes 4 (Spr, Npy, D4mit6, Il-6) and 13 (Atp1a2, D13Mit1, D13Uwm1) with blood pressure was evaluated using one-way analysis of variance. On chromosome 4 linkage of the Npy and D4Mit6 markers to systolic blood pressure was observed. A blood pressure QTL was also found on chromosome 13 within the renin locus. Surprisingly, alleles of the SHR strain at loci showing linkage to blood pressure on chromosome 4 and 13 promote lower blood pressure than the same alleles from the BB/OK strain. The transfer of D4Mit6 and renin locus from the SHR rat onto the genetic background of BB/OK rat will probably not lead to a model of Diabetic Hypertension, but the thorough characterisation of such congenics could contribute to the explanation of genetics and pathophysiology of Hypertension in the SHR rat.