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Blood pressure,baroreflex sensitivity,and end organ damage in hybrid offspring of spontaneously hypertensive rats and Spraque-Dawlev rats

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Acta Pharmacologica Sinica 2005年第9期26卷 1049-1056页

作者： He-hui XIE~2 Fu-ming SHEN~2 Chao-yu MIAO Ding-feng SU~3 Department of Pharmacology,Second Military Medical University,Shanghai 200433,China Department of Pharmacology Second Military Medical University Shanghai China

Aim:To investigate the blood pressure(BP),baroreflex sensitivity(BRS),andorgan damage in hybrids of spontaneously hypertensive rats and ***:Spontaneously hypertensive rats and Sprague-Dawley rats werecrossbred,and the F1hybrids were inbred randomly to produce an *** the age of 52 weeks,the F1and F2hybrids were tested to determine BP and BRSin a conscious *** examinations were carried out after BPrecording and BRS ***:BP and BRS were not different in F1and *** was inversely related to systolic BP(SBP)in male,female,or wholepopulations of ***,BRS values were one-third determined bySBP level(the determinant coefficient was 0.326).The indexes for left ventricularhypertrophy,aortic hypertrophy,and renal damage were all positively related toBP,and negatively related to *** multiple-regression analysis,left ventricularand aortic hypertrophy and glomerulosclerosis score were all most significantlyassociated with lower BRS and higher systolic *** contribution of BRS to leftventricular and aortic hypertrophy and glomerulosclerosis was greater than thatof ***:The present work with hybrid rats demonstrated quantita-tively that the BRS value was one-third determined by SBP *** BP leveland BRS value contributed greatly to the hypertensive organ ***,the contribution of BRS to the hypertensive organ damage was greater than thatof BP level in these rats.

关键词： baroreflex blood pressure end organ damage hypertension genetic hybridization

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end-organ protection in hypertension by the novel and selective Rho-kinase inhibitor, SAR407899

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World Journal of Cardiology 2015年第1期7卷 31-42页

作者： Matthias Lohn Oliver Plettenburg Aimo Kannt Markus Kohlmann Armin Hofmeister Dieter Kadereit Peter Monecke Alexander Schiffer Anke Schulte Hartmut Ruetten Yuri Ivashchenko Translational Medicine Sanofi-AventisIndustriepark Hoechst65926 Frankfurt am MainGermany

AIM: To compare the therapeutic efficacy of SAR407899 with the current standard treatment for hypertension [an angiotensin converting enzyme(ACE)-inhibitor and a calcium channel blocker] and compare the frequency and severity of the hypertension-related end-organ damage. METHODS: Long-term pharmacological characterization of SAR407899 has been performed in two animal models of hypertension, of which one is sensitive to ACE-inhibition and the other is insensitive [deoxycorticosterone acetate(DOCA)]. SAR407899 efficiently lowered high blood pressure and significantly reduced late-stage end organ damage as indicated by improved heart, kidney and endothelial function and reduced heart and kidney fibrosis in both models of chronic hypertension. RESULTS: Long term treatment with SAR407899 has been well tolerated and dose-dependently reduced elevated blood pressure in both models with no signs of tachyphylaxia. Blood pressure lowering effects and protective effects on hypertension related end organ damage of SAR407899 were superior to ramipril and amlodipine in the DOCA rat. Typical end-organ damage was significantly reduced in the SAR407899-treated animals. Chronic administration of SAR407899 significantly reduced albuminuria in both models. The beneficial effect of SAR407899 was associated with a reduction in leukocyte/macrophage tissue infiltration. The overall protective effect of SAR407899 was superior or comparable to that of ACE-inhibition or calciumchannel blockade. Chronic application of SAR407899 protects against hypertension and hypertension-induced end organ damage, regardless of the pathophysiological mechanism of hypertension. CONCLUSION: Rho-kinases-inhibition by the SAR407899 represents a new therapeutic option for the treatment of hypertension and its complications.

关键词： Hypertension end organ damage Rhokinase Angiotensin converting enzyme-inhibition

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