Reduction in extracellular Ca2+ attenuates endothelium-dependent relaxation more than nitroprusside-induced relaxation.

AIM

To quantitatively assess the effect of lowering external Ca(2+) (Ca(2+)) on both endothelium-dependent and -independent relaxations in rabbit aorta.

METHODS

Isometric contractions and relaxations of isolated aortae were recorded. When assessing the effect of reduced Ca(2+) on relaxations, the normal Ca(2+) solution was substituted with one of the reduced Ca(2+) solutions for one aorta, while a paired aorta was replenished with normal Ca(2+) solution.

RESULTS

The extent of acetylcholine (ACh)-induced relaxation, which is dependent on an intact endothelium, is time-dependent, and inversely related to Ca(2+) in a range of 0.02-2 mmol/L. ACh-induced relaxations were not significantly altered by the magnitude of the precontraction induced by PGF(2alpha). Nitroprusside-induced relaxations, which are independent of the endothelium, are also attenuated by reduced Ca(2+). Relaxant responses to ACh were significantly more susceptible to reduced Ca(2+) than nitroprusside-induced relaxations. A maximally effective relaxing concentration of D600, an L-type Ca channel blocker methoxyverapamil, (10(-5) mol/L) attenuated ACh-induced relaxations, whereas nitroprusside-induced relaxations were unaffected by D600.

CONCLUSION

Thus, endothelium-dependent relaxation is more dependent on Ca(2+) than endothelium-independent relaxation, and it seems likely that Ca(2+) plays an important role not only in contractile processes, but also in relaxant processes as well.