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1 Vascular Biology Center, Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912; and Departments of 2 Medicine (Nephrology) and Molecular Biology and Biophysics and of 3 Medicine (Nephrology) and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
The present studies were performed
to determine the contribution of EP2 receptors to renal
hemodynamics by examining afferent arteriolar responses to
PGE2, butaprost, sulprostone, and endothelin-1 in
EP2 receptor-deficient male mice (EP2
/).
Afferent arteriolar diameters averaged 17.8 ± 0.8 µm in
wild-type (EP2+/+) mice and 16.7 ± 0.7 µm in
EP2/ 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 EP2+/+ mice in response to 1 µM PGE2 and 1 µM butaprost, respectively. In contrast,
afferent arteriolar diameter of EP2/ mice decreased by
13 ± 3 and 16 ± 6% in response to PGE2 and
butaprost. The afferent arteriolar vasoconstriction to butaprost in
EP2/ mice was eliminated by angiotensin-converting enzyme inhibition. Sulprostone, an EP1 and EP3
receptor ligand, decreased afferent arteriolar diameter in both groups;
however, the vasoconstriction in the EP2/ mice was
greater than in the EP2+/+ mice. Endothelin-1-mediated
afferent arteriolar diameter responses were enhanced in
EP2/ mice. Afferent arteriolar diameter decreased by
29 ± 7% in EP2/ and 12 ± 7% in
EP2+/+ mice after administration of 1 nM endothelin-1.
These results demonstrate that the EP2 receptor mediates a
portion of the PGE2 afferent arteriolar vasodilation and
buffers the renal vasoconstrictor responses elicited by EP1
and EP3 receptor activation as well as endothelin-1.
prostaglandins; endothelin; kidney; microcirculation
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