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Chronic parathyroidectomy (PTX) attenuates blood pressure and increases vascular force generation. The mechanism is not understood. We tested the hypothesis that PTX-induced changes in blood pressure and vessel contractility result from rapid changes in serum parameters induced by PTX, and the hypothesis that the endothelium-derived factors contribute to PTX-induced enhancement of force generation in the spontaneously hypertensive rat (SHR).Chronic PTX or sham surgery was performed on 5-week-old male SHR, and subacute PTX was performed on 13- to 14-week-old SHR. The following experimental parameters were measured 5—6 weeks after chronic and 2 days after subacute PTX: systolic blood pressure, serum Ca2 +, 1,25-dihydroxyvitamin D3 (vitD) and mesenteric resistance artery contractility.Results: Chronic PTX significantly reduced blood pressure, body weight and serum Ca2 + compared with sham surgery; subacute PTX reduced only serum Ca2 + and vitD. Compared with sham surgery, the mesenteric resistance artery following chronic PTX showed increased active stress responses to norepinephrine and serotonin that were not associated with changes in free intracellular Ca2 +, but were abolished by endothelial denudation. Subacute PTX did not affect the active stress response to norepinephrine or endothelin. Low-dose acetylcholine induced relaxation that was attenuated in the chronic, but not the subacute, PTX subgroup compared with the sham-operated subgroup. High-dose acetylcholine induced contraction that was significantly greater in the chronic, but not subacute, PTX rats than in sham-operated rats. Indomethacin abolished the acetylcholine-induced contraction in all groups, but did not improve the impaired relaxation response of the chronic PTX subgroup.The PTX-induced decrease in blood pressure and increase in force generation do not result from acute changes initiated by reduction of serum parathyroid hormone, vitD or Ca2 +. Moreover, the PTX-induced increase in force generation results from a decrease in the production of a non-cyclo-oxygenase endothelium-dependent relaxing factor.