Very-low-dose combination of perindopril and indapamide: efficacy on blood pressure and target-organ damage

2003 ◽  
Vol 21 ◽  
pp. S11-S18 ◽  
Author(s):  
Stéphane Laurent
Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Nadine Haase ◽  
Stefan Hupfer ◽  
Michaela Golic ◽  
Florian Herse ◽  
Fatimunnisa Qadri ◽  
...  

We investigated whether or not Relaxin ameliorates the hypertension induced damage to heart and kidney. We used double transgenic rats harboring both human renin and angiotensinogen genes (dTGRs). These rats develop moderately severe Hypertension but die of end-organ cardiac and renal damage by week 7. Untreated dTGRs had an around 50% mortality rate at 7 weeks. The heart shows necrosis and fibrosis, whereas the kidneys esemble the hemolytic-uremic syndrome vasculopathy. We started Relaxin-treatment on four weeks old dTGR in low (26 μg/kg/d) and high dose (240 μg/kg/d) and age-matched SD rats. Blood-pressure- and albuminuria-measurements were monitored during the treatment period (three weeks). Seven weeks old animals were killed, hearts and kidneys were isolated and used for histochemical and quantitative TaqMan RT-PCR analysis. Systolic blood pressure increased progressively in untreated dTGRs from 161.6 ± 3.02 mmHg in week 5 to 225.3 ± 4.48 mmHg in week 7. Relaxin treatment had no significant influence on blood pressure (low dose 208.0 ± 5.51 mmHg and high dose 222.2 ± 5.60 mmHg at week 7 ) whereas SD rats were normotensive (106.3 ± 1.15 mmHg). Untreated (5.38 ± 0.13 mg/g) and Relaxin treated dTGRs (low dose 5.20 ± 0.18 mg/g and high dose 5.33 ± 0.29 mg/g) had similar cardiac hypertrophy indices (heart-to-body weight ratio), which were significantly higher compared with nontransgenic SD rats (2.90 ± 0.08 mg/g). BNP and CTFG mRNA expression in the hearts was significant higher in untreated dTGRs compared to SD rats. There were no differences in BNP and CTFG expression between untreated and Relaxin treated dTGRs. Relaxin treatment (low dose 78502 ± 16848 μg/day and high dose 43642 ± 10852 μg/day at week 7) did not ameliorate albuminuria compared with untreated dTGRs (57937 ± 6122 μg/day at week 7). Furthermore the treatment with Relaxin did not prevent matrix deposition in the heart and kidney of d TGRs. Finally, Relaxin treatment did not reduce mortality. Although survival was 52 %, in untreated dTGRs 36 % in low dose and 54 % high dose Relaxin treated dTGRs at week 7. These data demonstrate that Relaxin did not improve angiotensin II-induced target organ damage.


Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Gregory A Harshfield ◽  
Gregory A Harshfield ◽  
Jennifer Pollock ◽  
David Pollock

The overall goal of this study was to determine race/ethnic differences in the associations between renal ET-1 and indices of blood pressure-related target organ damage in healthy adolescents. The subjects ranged in age between 15-19 years, had no history of any disease, and were not on any prescription medications. The 92 subjects consisted of 48 Caucasians (CA) and 44 African-Americans (AA). The two groups were similar with respect to height, weight, body mass index, blood pressure, ET-1), albumin excretion rate (AER), and left ventricular mass). Results: The CA’s were slightly older 17±1 v 16±1 (p=.02). The protocol was preceded by a 3 day self-selected sodium controlled diet of 250 mEq/day day which the subject picked up each day. The test day began with an echocardiogram for the assessment of left ventricular mass. Next, the subjects were seated for 60 minutes of rest during which the subjects consumed 200 ml of water. This was followed by the collection of a urine sample for the measurement of ET-1 and AER. Overall, ET-1 excretion was correlated with AER (r=.278), LV mass/ht 2.7 (r=.341), and systolic blood pressure (SBP; r=.365; p=.01 for each). The significant overall correlations were the result of significant correlations in AAs for AER (r=.344; p=.05), LV mass/ht 2.7 (r=.520; p=.01), and SBP (r=.645; p=.01) which were not apparent in CA’s. These findings suggest urinary ET-1 contributes to the development of BP-related target organ damage in AA youths prior to the development of increases in blood pressure.


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