Abstract
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 μmol/L) significantly increased [3H]-phenylalanine incorporation (an in vitro marker of hypertrophy) by 32±2%. This was abolished by bradykinin (10 μmol/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.
Original language | English |
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Pages (from-to) | 519-521 |
Number of pages | 3 |
Journal | Clinical and Experimental Pharmacology and Physiology |
Volume | 26 |
Issue number | 7 |
DOIs | |
Publication status | Published - 14 Jul 1999 |
Externally published | Yes |
Keywords
- Angiotensin II
- Bradykinin
- Endothelial function
- Hyperglycaemia
- Hypertrophy
- Ventricular myocytes