Impact of maternal angiotensinogen M235T polymorphism and angiotensin-converting enzyme insertion/deletion polymorphism on blood pressure, protein excretion and fetal outcome in pregnancy

2007 ◽  
Vol 25 (6) ◽  
pp. 1255-1261 ◽  
Author(s):  
Thiemo Pfab ◽  
Bulza Stirnberg ◽  
Andreas Sohn ◽  
Katrin Krause ◽  
Torsten Slowinski ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Fetal Outcome ◽  
Converting Enzyme ◽  
Deletion Polymorphism ◽  
Protein Excretion ◽  
M235t Polymorphism ◽  
In Pregnancy

scholarly journals Pharmacogenetic Association of the Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism on Blood Pressure and Cardiovascular Risk in Relation to Antihypertensive Treatment

Circulation ◽  
2005 ◽  
Vol 111 (25) ◽  
pp. 3374-3383 ◽  
Author(s):  
Donna K. Arnett ◽  
Barry R. Davis ◽  
Charles E. Ford ◽  
Eric Boerwinkle ◽  
Cathie Leiendecker-Foster ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Angiotensin Converting Enzyme ◽  
Antihypertensive Treatment ◽  
Converting Enzyme ◽  
Deletion Polymorphism

scholarly journals Evidence that an angiotensin-converting enzyme inhibitor has a different effect on glomerular injury according to the different phase of the disease at which the treatment is started.

1994 ◽  
Vol 5 (4) ◽  
pp. 1139-1146
Author(s):  
N Perico ◽  
S C Amuchastegui ◽  
V Colosio ◽  
G Sonzogni ◽  
T Bertani ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Systolic Blood Pressure ◽  
Ace Inhibitor ◽  
Diabetic Rats ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Converting Enzyme ◽  
Glomerular Injury ◽  
Protein Excretion

In rats with streptozotocin-induced diabetes, the effect of an angiotensin-converting enzyme (ACE) inhibitor on the evolution of glomerular injury according to the time at which the treatment is started with respect to the onset of the disease was studied. Three groups of animals were used, a control Group 1 and two groups of diabetic rats treated with insulin (Groups 2 and 3). The latter were monitored until urinary protein excretion reached 40 to 50 mg/24 h (on average, 23 wk after the induction of the diabetes). At this time, Group 2 continued to receive insulin alone, whereas Group 3 was also given the ACE inhibitor moexipril for 8 more wk. Untreated diabetic rats showed a moderate increase in systolic blood pressure that was normalized by moexipril administration. Urinary protein excretion progressively increased during the 8-wk follow-up in untreated diabetics that, at the end of the study, developed moderate glomerular sclerosis. Moexipril treatment lowered urinary protein excretion to a normal range and completely prevented glomerular injury. Three other groups of rats were similarly treated, except that moexipril treatment was started later on (when proteinuria reached 100 to 200 mg/24 h, on average, 32 wk after the induction of diabetes), and were monitored for another 8 wk. Untreated and treated diabetics had comparable blood glucose levels throughout. Systolic blood pressure, significantly increased in untreated diabetic rats, was effectively controlled by moexipril administration.(ABSTRACT TRUNCATED AT 250 WORDS)

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