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Endothelin‐1‐induced contraction in isolated aortae from normotensive and DOCA‐salt hypertensive rats: effect of magnesium

1 The contractile responses to endothelin‐1 and the effect on these of various magnesium concentrations, were studied in isolated aortic rings from normotensive Sprague‐Dawley rats and deoxycorticosterone acetate‐salt (DOCA‐salt) hypertensive rats. 2 Contractions induced by endothelin‐1 were smaller in endothelium‐denuded aortae from DOCA‐salt hypertensive rats than in those from normotensive rats. The absence of calcium in the medium attenuated endothelin‐1‐induced contractions of aortae from both normotensive and DOCA‐salt rats, but the contraction was greater in aortae from DOCA‐salt hypertensive rats. Ryanodine (which inhibits the release of intracellular calcium) inhibited endothelin‐1‐induced contractions in aortae from DOCA‐salt hypertensive rats to a greater extent than in aortae from normotensive rats. 3 A high extracellular magnesium concentration (4.8 mM) attenuated endothelin‐1‐induced contractions in tissues from DOCA‐salt hypertensive rats but not in tissues from normotensive rats. In the absence of calcium, a high concentration of magnesium attenuated endothelin‐1‐induced contraction in aortae from both normotensive and hypertensive rats. In the presence of ryanodine, a high concentration of magnesium did not modify the contraction in preparations from either strain. 4 Absence of magnesium attenuated endothelin‐1‐induced contractions in aortae from both normotensive and DOCA‐salt hypertensive rats. In the absence of calcium, removal of magnesium totally inhibited endothelin‐1‐induced contraction in tissues from normotensive rats but had no effect in those from hypertensive rats. In the presence of ryanodine, the lack of magnesium inhibited endothelin‐1‐induced contractions in aortae from DOCA‐salt hypertensive rats but increased the sensitivity to endothelin‐1 of aortae from normotensive rats. 5 The presence of endothelium did not modify the effect of high magnesium on endothelin‐1‐induced contractions in aortae from normotensive and DOCA‐salt hypertensive rats. Conversely, the attenuating effect of magnesium removal on endothelin‐1‐induced contractions did not occur when endothelium was present. 6 In conclusion, endothelin‐1‐induced contraction was blunted in aortae from DOCA‐salt hypertensive rats. The blunted response was related to altered calcium utilization during contraction. Changes in extracellular magnesium concentration differentially alter endothelin‐1‐induced contraction in aortae from normotensive and hypertensive rats, possibly by interfering with calcium utilization during contraction. Magnesium may be required for the contractile response to endothelin‐1 and increasing magnesium may limit the vascular effects of endothelin‐1 in blood vessels from DOCA‐salt hypertensive rats.