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HYPERGLYCAEMIA ABOLISHES THE ANTIHYPERTROPHIC EFFICACY OF BRADYKININ IN RAT VENTRICULAR MYOCYTES
Author(s) -
Dusting Ac Rosenkranz, Gj,
Ritchie Rh
Publication year - 1999
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.1999.03068.x
Subject(s) - bradykinin , medicine , myocyte , endocrinology , angiotensin ii , renin–angiotensin system , biology , muscle hypertrophy , bradykinin receptor , in vitro , receptor , biochemistry , blood pressure
1. Bradykinin inhibits hypertrophy of rat ventricular myocytes, but only in the presence of endothelial cells. 2. The influence of hyperglycaemia on the ability of bradykinin to prevent hypertrophy was investigated in adult rat ventricular myocytes cocultured with bovine aortic endothelial cells (BAEC). 3. In myocytes cocultured with normal BAEC, angiotensin II (AngII; 1 μ mol/L) significantly increased [ 3 H]‐phenylalanine incorporation (an in vitro marker of hypertrophy) by 32±2%. This was abolished by bradykinin (10 μ mol/L). 4. Pretreatment of BAEC with high glucose (25 mmol/L for 24 h) prior to coculture with myocytes reduced the antihypertrophic effect of bradykinin, but did not modulate the hypertrophic effect of AngII. 5. Pretreatment of BAEC with hyperglycaemia abolishes the antihypertrophic efficacy of bradykinin in rat ventricular myocytes cocultured with BAEC. This has implications for the action of angiotensin‐converting enzyme inhibitors.