Angiotensin II antagonists and protection against subclinical cardiac and vascular damage

2006 ◽  
pp. 111-126 ◽  
Author(s):  
Enrico Agabiti-Rosei ◽  
Maria Muiesan ◽  
Damiano Rizzoni
ChemInform ◽  
2010 ◽  
Vol 25 (26) ◽  
pp. no-no
Author(s):  
R. T. WESTER ◽  
C. J. MULARSKI ◽  
G. T. MAGNUS-AYRITEY ◽  
P. DA SILVA JARDINE ◽  
J. A. LAFLAMME ◽  
...  

1994 ◽  
Vol 4 (1) ◽  
pp. 115-120 ◽  
Author(s):  
L.L. Chang ◽  
W.T. Ashton ◽  
K.L. Flanagan ◽  
E.M. Naylor ◽  
P.K. Chakravarty ◽  
...  

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Uta Erdbruegger ◽  
Christine Rudy ◽  
Joanne Lannigan ◽  
Joseph Gigliotti ◽  
Sylvia Chechova ◽  
...  

Background: Hypertension (HTN) is a leading risk factor of cardiovascular diseases. Its pathogenesis is poorly understood, but activation of the renin angiotensin system is thought to be a key event. Vascular damage is an early manifestation of HTN. There are currently no available clinical biomarkers for early detection of vascular damage. Circulating microvesicles (MVs) have gained significant attention as potential novel biomarkers for vascular injury. These vesicles are less than 1 micron in size and carry markers of the parent cell. We hypothesized that MVs of endothelial and leukocyte origin are elevated in angiotensin II (AII) induced-HTN and show a distinct phenotype depending on the duration of HTN. Methods: Mice were treated with AII (400ng/kg/min) via mini-osmotic pumps for 2 and 4 weeks (wks). Systolic blood pressure (SBP) was measured using tail-cuff manometry. Enumeration and phenotyping of MVs were determined in platelet poor plasma using imaging flow cytometry and the following surface markers: E- Selectin (CD62E), Endoglin (CD105), VE Cadherin (CD144), Annexin 5 (AV), Platelets (CD41), P-Selectin (CD62E), leukocytes (CD45). Results: Compared to untreated controls (n=5), AII treated mice (n=5) had an increase in SBP by 30mmHg (p=0.02), and significantly elevated total counts of AV negative (AV-) and positive MVs (AV+) (p=0.04 and 0.06 respectively) after 2 wks. Endothelial derived MVs were also significantly elevated after 2 wks (AV+ and AV- CD144+ (p=0.023), AV+ and AV-CD62E+ (p=0.023), AV+ and AV-CD105+ (0.023), AV+ and AV- CD144+ (p=0.04)). However, after 4 wks of AII-induced HTN, only AV-CD144+ MVs remained significantly elevated. In contrast, leukocyte derived MVs (CD45+) were significantly increased after 2 wks, and remained significantly elevated after 4 wks. Platelet derived MVs were not significantly elevated at either time point. Conclusions: Distinct populations of endothelial and leukocyte derived MVs are elevated at different time points during AII-induced HTN. The changing profiles of the MVs may reflect an evolving pathophysiologic response of the vasculature. Further studies are needed to confirm these findings, and to determine the effect of the severity and etiology of HTN on the profiles of MVs.


1977 ◽  
Vol 232 (2) ◽  
pp. H110-H113
Author(s):  
N. C. Trippodo ◽  
T. G. Coleman ◽  
A. W. Cowley ◽  
A. C. Guyton

Blood pressure effects of angiotensin II antagonists were studied in sham-operated and baroreceptor-denervated rabbits in the normal water-replete state or after 6 days of water deprivation (dehydrated). Experiments were performed in awake rabbits. Dehydrated rabbits had significantly higher plasma sodium concentrations, hematocrits, and plasma renin activities, but lower plasma potassium concentrations and body weights than water-replete rabbits. Administration of angiotensin II antagonists caused a significant decrease in mean arterial pressure in dehydrated rabbits (-16 mmHg in sham-dehydrated and -19 mmHg in denervated-dehydrated) but not in water-replete ones, whether the baroreceptor reflexes were intact or not (-1 mmHg in sham replete and -4 mmHg in denervated replete). The open-loop feedback gain of the renin-angiotensin system in blood pressure control was calculated as -1.6. The results demonstrate an important role of angiotensin II in blood pressure regulation during the high-renin, dehydrated state, but not during the normal renin, water-replete state. Abolishment of baroreceptor reflexes did not unmask an important role of normal levels of angiotensin II in blood pressure regulation.


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