In:
American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 283, No. 3 ( 2002-09-01), p. F415-F422
Abstract:
The present studies were performed to determine the contribution of EP 2 receptors to renal hemodynamics by examining afferent arteriolar responses to PGE 2 , butaprost, sulprostone, and endothelin-1 in EP 2 receptor-deficient male mice (EP 2 −/−). Afferent arteriolar diameters averaged 17.8 ± 0.8 μm in wild-type (EP 2 +/+) mice and 16.7 ± 0.7 μm in EP 2 −/− mice at a renal perfusion pressure of 100 mmHg. Vessels from both groups of mice responded to norepinephrine (0.5 μM) with similar 17–19% decreases in diameter. Diameters of norepinephrine-preconstricted afferent arterioles increased by 7 ± 2 and 20 ± 6% in EP 2 +/+ mice in response to 1 μM PGE 2 and 1 μM butaprost, respectively. In contrast, afferent arteriolar diameter of EP 2 −/− mice decreased by 13 ± 3 and 16 ± 6% in response to PGE 2 and butaprost. The afferent arteriolar vasoconstriction to butaprost in EP 2 −/− mice was eliminated by angiotensin-converting enzyme inhibition. Sulprostone, an EP 1 and EP 3 receptor ligand, decreased afferent arteriolar diameter in both groups; however, the vasoconstriction in the EP 2 −/− mice was greater than in the EP 2 +/+ mice. Endothelin-1-mediated afferent arteriolar diameter responses were enhanced in EP 2 −/− mice. Afferent arteriolar diameter decreased by 29 ± 7% in EP 2 −/− and 12 ± 7% in EP 2 +/+ mice after administration of 1 nM endothelin-1. These results demonstrate that the EP 2 receptor mediates a portion of the PGE 2 afferent arteriolar vasodilation and buffers the renal vasoconstrictor responses elicited by EP 1 and EP 3 receptor activation as well as endothelin-1.
Type of Medium:
Online Resource
ISSN:
1931-857X
,
1522-1466
DOI:
10.1152/ajprenal.00351.2001
Language:
English
Publisher:
American Physiological Society
Publication Date:
2002
detail.hit.zdb_id:
1477287-5
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