Key result
Amiloride analogues cause endothelium-dependent relaxation in dog coronary arteries, implicating Na+/Ca2+ exchange in EDRF release.
Amiloride analogues induce endothelium-dependent relaxation in canine coronary arteries, suggesting a role for Na+/Ca2+ exchange in EDRF release.
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Findings remain preclinical; extends mechanistic evidence for Na+/Ca2+ exchange in EDRF release but leaves open human relevance.
A number of amiloride analogues were used to test the proposal that Na+/Ca2+ exchange may play a role in the secretion of endothelium-derived relaxing factor (EDRF). The analogues used were those substituted on either the 5-amino group or the terminal guanidino nitrogen atom. The former block both Na+/Ca2+ and Na+/H+ exchange whilst the latter block the Na+ channel and the Na+/Ca2+ exchange. 2. Both series of compounds caused relaxation in isolated rings of dog coronary artery (EC50 values, 1-10 microM) presumably due to release of EDRF since removal of endothelium greatly attenuated the response. 3. Amiloride (1-100 microM) had little effect on either endothelium-intact or denuded arteries. 4. The guanidino substituted analogues also appeared to block selectively the relaxation response to acetylcholine in the coronary artery, independently of their EDRF-releasing activity. 5. It is proposed that endothelial cells have an active Na+/Ca2+ exchange operating in the forward mode to extrude Ca2+. This mechanism may be important in the control of EDRF release.
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Cocks et al. (1988) studied this question. Amiloride analogues was evaluated on Relaxation in isolated rings of dog coronary artery. Amiloride analogues caused endothelium-dependent relaxation in isolated dog coronary arteries (EC50 1-10 microM), suggesting a role for Na+/Ca2+ exchange in EDRF release.
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