Macrophage depletion in hypertensive rats accelerates development of cardiomyopathy

Harmen R. Zandbergen, Umesh C. Sharma, Sudhir Gupta, Johan W.H. Verjans, Susanne Van Den Borne, Saraswati Pokharel, Thomas Van Brakel, Adriaan Duijvestijn, Nico Van Rooijen, Jos G. Maessen, Chris Reutelingsperger, Yigal M. Pinto, Jagat Narula, Leo Hofstra

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


Inflammation contributes to the process of ventricular remodeling after acute myocardial injury. To investigate the role of macrophages in the chronic process of cardiac remodeling, they were selectively depleted by intravenous administration of liposomal clodronate in heart failure-prone hypertensive Ren-2 rats from the age of 7 until 13 weeks. Plain liposomes were used for comparison. Liposomal clodronate treatment reduced the number of blood monocytes and decreased the number of macrophages in the myocardium. Compared to plain liposomes, liposomal clodronate treatment rapidly worsened left ventricular ejection function in hypertensive rats. Liposomal clodronate- treated Ren-2 rat hearts showed areas of myocyte loss with abundant inflammatory cell infiltration, predominantly comprising CD4 positive T lymphocytes. The current study showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats. Modulation of macrophage function may be of value in the evolution of cardiomyopathy.

Original languageEnglish
Pages (from-to)68-75
Number of pages8
JournalJournal of Cardiovascular Pharmacology and Therapeutics
Issue number1
StatePublished - Mar 2009
Externally publishedYes


  • Heart failure
  • Hypertension
  • Inflammation
  • Ventricular remodeling


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