Effects of angiotensin-converting enzyme inhibition and calcium channel blockade on cardiac apoptosis in rats with 2K1C (two-kidney/one-clip) renovascular hypertension

2003 ◽  
Vol 104 (1) ◽  
pp. 79 ◽  
Author(s):  
Christa THNE-REINEKE ◽  
Jan OLIVIER ◽  
Michael GODES ◽  
Rüdiger ZART ◽  
Ines GEORGE ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Calcium Channel ◽  
Renovascular Hypertension ◽  
Enzyme Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Channel Blockade ◽  
Calcium Channel Blockade ◽  
Cardiac Apoptosis ◽  
Converting Enzyme Inhibition

Effects of angiotensin-converting enzyme inhibition and calcium channel blockade on cardiac apoptosis in rats with 2K1C (two-kidney/one-clip) renovascular hypertension

2003 ◽  
Vol 104 (1) ◽  
pp. 79-85 ◽  
Author(s):  
Christa THÖNE-REINEKE ◽  
Jan OLIVIER ◽  
Michael GODES ◽  
Rüdiger ZART ◽  
Ines GEORGE ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Calcium Channel ◽  
Renovascular Hypertension ◽  
Ace Inhibition ◽  
Left Ventricular ◽  
Cardiac Remodelling ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Channel Blockade ◽  
Calcium Channel Blockade

Apoptosis plays a role in the regulation of heart mass and architecture, and might contribute to the cardiac remodelling seen in renovascular hypertension. It is not known whether the beneficial effects of angiotensin-converting enzyme (ACE) inhibition or calcium channel blockade on cardiac remodelling are linked to the modulation of apoptosis. To test this hypothesis, we established four groups of rats: (i) sham-operated controls, (ii) a group that underwent the two-kidney/one-clip (2K1C) procedure, (iii) a group with 2K1C treated for 12 weeks with quinapril (6mg·day-1·kg-1), and (iv) a group with 2K1C treated for 12 weeks with diltiazem (24mg·day-1·kg-1). Treatment started 2 weeks after clipping. Systolic blood pressure was reduced to a similar extent by quinapril and diltiazem (2K1C, 223±19mmHg; 2K1C+quinapril, 149±15mmHg; 2K1C+diltiazem, 160±40mmHg; both P<0.01 compared with 2K1C alone). Left ventricular weight, interstitial fibrosis and perivascular fibrosis were reduced significantly by both drugs. The apoptotic index (apoptotic cells/total cell number) was increased 21.6-fold (P<0.01) after quinapril treatment as compared with the 2K1C group, but was not affected by calcium channel blockade. In conclusion, our study demonstrates that ACE inhibition, in contrast with calcium channel blockade, may cause regression of cardiac hypertrophy/remodelling in 2K1C renovascular hypertensive rats through enhanced apoptosis.

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