Effect of an acute exposure of guinea pigs to NO2 on pulmonary prostaglandin dehydrogenase and angiotensin converting enzyme

1980 ◽  
Vol 25 (1) ◽  
pp. 816-823 ◽  
Author(s):  
A. Chaudhari ◽  
S. Dutta
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Guinea Pigs ◽  
Acute Exposure ◽  
Converting Enzyme ◽  
Prostaglandin Dehydrogenase

scholarly journals Effect of angiotensin-converting enzyme inhibition on protein kinase C and SR proteins in heart failure

1999 ◽  
Vol 276 (1) ◽  
pp. H53-H62 ◽  
Author(s):  
Yasuchika Takeishi ◽  
Ajit Bhagwat ◽  
Nancy A. Ball ◽  
Darryl L. Kirkpatrick ◽  
Muthu Periasamy ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Angiotensin Converting Enzyme ◽  
Protein Expression ◽  
Guinea Pigs ◽  
Pressure Overload ◽  
Ace Inhibition ◽  
Converting Enzyme ◽  
Kinase C

We tested the hypothesis that activation of protein kinase C (PKC) isoforms in pressure-overload heart failure was prevented by angiotensin-converting enzyme (ACE) inhibition, resulting in normalization of cardiac sarcoplasmic reticulum (SR) Ca2+ATPase (SERCA) 2a and phospholamban protein levels and improvement in intracellular Ca2+ handling. Aortic-banded and control guinea pigs were given ramipril (5 mg ⋅ kg−1 ⋅ day−1) or placebo for 8 wk. Ramipril-treated banded animals had lower left ventricular (LV) and lung weight, improved survival, increased isovolumic LV mechanics, and improved cardiomyocyte Ca2+ transients compared with placebo-treated banded animals. This was associated with maintenance of SERCA2a and phospholamban protein expression. Translocation of PKC-α and -ε was increased in placebo-treated banded guinea pigs compared with controls and was attenuated significantly by treatment with ramipril. We conclude that ACE inhibition attenuates PKC translocation and prevents downregulation of Ca2+ cycling protein expression in pressure-overload hypertrophy. This represents a mechanism for the beneficial effects of this therapy on LV function and survival in heart failure.

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