Is there relationship between the A1166C polymorphism of the angiotensin II receptor AT1 and plasma renin activity, insulin resistance and reduction of blood pressure after angiotensin‑converting enzyme inhibitor therapy?

2008 ◽  
Vol 118 (4) ◽  
pp. 194-200
Author(s):  
Jerzy Głuszek ◽  
Karolina Jankowska
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Converting Enzyme ◽  
Angiotensin Ii Receptor ◽  
A1166c Polymorphism

Effect of Angiotensin II and Converting Enzyme Inhibitor (Captopril) on Blood Pressure, Plasma Renin Activity and Aldosterone in Primary Aldosteronism

1981 ◽  
Vol 61 (s7) ◽  
pp. 289s-293s ◽  
Author(s):  
F. Mantero ◽  
F. Fallo ◽  
G. Opocher ◽  
D. Armanini ◽  
M. Boscaro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Idiopathic Hyperaldosteronism

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma and urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

scholarly journals Ventricular and Vascular Remodelling – Effects of the Angiotensin II Receptor Blocker Telmisartan and/or the Angiotensin-Converting Enzyme Inhibitor Ramipril in Hypertensive Patients

2005 ◽  
Vol 33 (1_suppl) ◽  
pp. 39A-49A ◽  
Author(s):  
J Petrovic ◽  
D Petrovic ◽  
N Vukovic ◽  
B Zivanovic ◽  
J Dragicevic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitor ◽  
Left Ventricular ◽  
Angiotensin Ii Receptor Blocker ◽  
Converting Enzyme ◽  
Vascular Remodelling ◽  
Angiotensin Ii Receptor ◽  
Once Daily

Angiotensin II induces inflammatory activation of vascular smooth muscle cells and can cause left ventricular hypertrophy (LVH). Telmisartan is an angiotensin II receptor blocker with demonstrated beneficial effects on cardiac and vascular structure and function in animal models. The angiotensin-converting enzyme inhibitor ramipril also reduces ventricular and vascular remodelling. The open-label study observed 75 treatment-naïve, moderately or severely hypertensive (systolic blood pressure 160-190 mmHg, diastolic blood pressure 90-110 mmHg) patients (age range, 42-58 years) treated with once-daily telmisartan 40 mg force-titrated to 80 mg after 1 month (n = 25), once-daily ramipril 2.5 mg force-titrated to 5 mg after 1 month (n = 25), or once-daily telmisartan 40 mg plus ramipril 2.5 mg (n = 25); the total duration of treatment was 6 months. At baseline, blood pressure, left ventricular mass index (LVMI), carotid intima-media thickness (IMT) and carotid cross-sectional intima-media area (CSA) were measured. Measurements were repeated 1, 3 and 6 months after initiation of treatment. After 6 months, comparable blood pressure reductions were achieved with the three treatments. Reductions in LVMI after 6 months' treatment were 11.4%, 9.9% and 15.6% with telmisartan, ramipril, and telmisartan plus ramipril, respectively. Respective reductions in IMT were 14.6%, 12.0% and 18.2%, and for CSA were 7.8%, 4.3% and 11.5%. In conclusion, treatment with telmisartan or ramipril for 6 months resulted in regression of LVH and vascular remodelling. When a combination of telmisartan and ramipril was administered, additional regression and remodelling occurred.

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