ATTENUATED CA2-CELLS FROM AORTA OF ALDOSTERONE-SALT HYPERTENSIVE RATS( RESPONSE TO ACETYLCHOLINE IN ENDOTHELIAL)

Ca2+ is essential for endothelial production of vasorelaxing factors. We determined whether the impaired endothelium-dependent relaxation in aldosterone-salt hypertensive rats (AHR) is associated with a decreas ed free Ca2+ ([Ca2+](i)) response in endothelial cells. In isolated ao rta, the EC(50) for the acetylcholine-induced endothelium-dependent re laxations did not differ between AHR and the age-matched control-salt rats (CSR). However, maximal relaxation was significantly reduced by 4 7% in AHR (P < .05). In contrast, the endothelium-independent relaxati on to sodium nitroprusside was not impaired in aorta from AHR. The [Ca 2+](i) was measured with fura-2 microfluorometry in endothelial cells freshly dispersed from aorta. Although the basal [Ca2+](i) was not dif ferent between CSR and AHR, the peak [Ca2+](i) response to acetylcholi ne was significantly reduced in cells from AHR compared with CSR (P <. 05). These results suggest that depressed endothelial [Ca2+](i) respon ses to acetylcholine may be involved in the impaired endothelium-depen dent relaxation in aorta from AHR.