sulprostone and Hydronephrosis

Evidence indicates that prostaglandin E(2) (PGE(2)) preferentially affects preglomerular renal vessels. However, whether this is limited to small-caliber arterioles or whether larger vessels farther upstream also respond to PGE(2) is currently unclear. In the present study, we first investigated the effects of PGE(2) along the preglomerular vascular tree and subsequently focused on proximal interlobular arteries (ILAs). Proximal ILAs in hydronephrotic rat kidneys as well as isolated vessels from normal kidneys constricted in response to PGE(2), both under basal conditions and after the induction of vascular tone. By contrast, smaller vessels, i.e., distal ILAs and afferent arterioles, exhibited PGE(2)-induced vasodilation. Endothelium removal and pretreatment of single, isolated proximal ILAs with an EP1 receptor blocker (SC51322, 1 micromol/l) or a thromboxane A(2) receptor blocker (SQ29548, 1 micromol/l) did not prevent vasoconstriction to PGE(2). Furthermore, in the presence of SC51322, responses of these vessels to PGE(2) and the EP1/EP3 agonist sulprostone were superimposable, indicating that PGE(2)-induced vasoconstriction is mediated by EP3 receptors on smooth muscle cells. Immunohistochemical staining of proximal ILAs confirmed the presence of EP3 receptor protein on these cells and the endothelium. Adding PGE(2) to normal isolated kidneys induced a biphasic flow response, i.e., an initial flow increase at PGE(2) concentrations

Topics: Angiotensin II; Animals; Arteries; Bridged Bicyclo Compounds, Heterocyclic; Dinoprostone; Endothelium, Vascular; Fatty Acids, Unsaturated; Hydrazines; Hydronephrosis; In Vitro Techniques; Kidney Cortex; Male; Muscle, Smooth, Vascular; Norepinephrine; Perfusion; Rats; Rats, Sprague-Dawley; Receptors, Prostaglandin E; Receptors, Prostaglandin E, EP1 Subtype; Receptors, Prostaglandin E, EP3 Subtype; Receptors, Thromboxane A2, Prostaglandin H2; Renal Circulation; Vasoconstriction; Vasoconstrictor Agents