Effect of sodium intake on prostacyclin generation in rabbit mesenteric artery.
Effect of sodium intake on prostacyclin (PGI2) generation in response to angiotensin II (A II) or noradrenaline (NA) stimulation was studied using the rabbit mesenteric artery (RMA) perfusion system. 6-oxo-PGF1 alpha, a stable metabolite of PGI2, was continuously released into the effluent at a rate of 10.7 +/- 2.2 ng/min for the initial 60 min. Perfusion pressure and 6-oxo-PGF1 alpha promptly increased in response to A II and NA. Chronic sodium loading caused a significantly (p less than 0.05) smaller PGI2 production following the A II stimulation. Vasoconstrictive responses induced by these stimuli were greater in the high sodium group. Acute changes in potassium concentration at a range between 1.2 and 5.4 mEq/L failed to affect basal PGI2 production, but an augmented response of PGI2 release by A II and NA was observed at the lowest potassium concentration. These results may suggest that vascular prostaglandins may participate in the mechanism of an altered vascular responsiveness during an altered sodium or potassium homeostasis.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D004039:Diet, Sodium-Restricted; D011464:Epoprostenol / Q000096:biosynthesis*; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D012964:Sodium / Q000494:pharmacology*
D000804:Angiotensin II; D015121:6-Ketoprostaglandin F1 alpha; D012964:Sodium; D011464:Epoprostenol; D011188:Potassium; D009638:Norepinephrine