Systolic and diastolic blood pressure responses to norepinephrine (NE; 0.125, 0.25, 0.5, 1, 2, and 4 μg/kg, i.v.) were significantly potentiated in anesthetized rats treated with i.v. lysine acetylsalicylate (LASA; 200 mg/kg) or indomethacin (IND; 8 mg/kg). In arterial specimens taken out from these rats, the prostacyclin-like substance production was completely inhibited. Also, the PGI2 infusion (15 ng/kg/min, i.v.) counteracted the LASA or IND induced potentiation of the systolic and diastolic blood pressure responses to NE. These results clearly indicate PGI2, and not PGE2, as the prostaglandin mainly involved in the modulation of systemic vascular reactivity to noradrenergic stimulation.
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