Changes in renal prostanoid synthesis induced by potassium loading in rats.
Previous works have demonstrated changes in the urinary excretion of prostaglandins (PG) in response to changes in potassium (K) or sodium (Na) intake. In the present study, the production of PGE2, PGF2 alpha, 6-keto-PGF1 alpha and thromboxane B2 (TXB2) by isolated glomeruli, cortical homogenates, medullary and papillary slices was measured in K-loaded rats on either a normal or a low Na intake. In glomeruli, K loading increased selectively PGE2 synthesis. In Na-depleted animals, all prostanoids were elevated and K loading did not induce a further increase. In cortical and medullary preparations, PGE2 was decreased by K loading irrespective of the state of Na balance. In papilla, PGE2 decreased (in all K-loaded rats) and PGF2 alpha increased (only in rats with normal Na intake). 6-Keto-PGF1 alpha and TXB2 did not change significantly. No correlation was present between changes of PG synthesis and urinary kallikrein excretion. The results demonstrate a specific effect of K on PGE2 and PGF2 alpha, and suggest a role for these substances in K homeOstasis.
Bernheim
J
J
Department of Nephrology, Meir Hospital, Kfar Saba, Israel.
Podjarny
E
E
Kariv
N
N
Shapira
J
J
Arber
I
I
Rathaus
M
M
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D005260:Female; D006706:Homeostasis; D007668:Kidney / Q000378:metabolism*; D011188:Potassium / Q000008:administration & dosage*; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013929:Thromboxane B2 / Q000096:biosynthesis
D011453:Prostaglandins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D012964:Sodium; D015237:Dinoprost; D015232:Dinoprostone; D011188:Potassium