In rats with cardiac pressure overload, there is a tissue-specific reciprocal regulation of ACE, with upregulation in the heart and downregulation in the lungs, potentially shifting angiotensin II formation to the cardiac circulation.
No takes yet. Share an insight, caveat, or question.
Tissue-specific ACE shifts may influence local angiotensin II in overload; leaves open human relevance and therapeutic targeting.
Michael Pfeifer (1998) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: