IMPACT OF CYCLOOXYGENASE BLOCKADE ON JUXTAMEDULLARY MICROVASCULAR RESPONSES TO ANGIOTENSIN-II IN RAT-KIDNEY

1. Experiments were designed to evaluate the hypothesis that cyclo-oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat-treated rats. 2. The in vitro blood-perfused juxtamedullary nephron technique was utilized to provide access to afferent arterioles, efferent arterioles and descending vasa recta located in the outer stripe of the outer medulla. 3. Baseline afferent arteriolar diameter was 20.8+/-1.9 mu m in kidneys subjected to cyclo-oxygenase blockade (1 mu mol/L piroxicam), a value significantly lower than that observed in untreated kidneys (26.1+/-1.0 mu m) Baseline diameters of efferent arterioles and outer medullary descending vasa recta did not differ between untreated and piroxicam-treated groups. 4. Topical application of 1 nmol/L AII reduced blood now through outer medullary descending vasa recta by 22+/-6% in untreated kidneys and by 24+/-7% in piroxicam-treated kidneys. 5. In untreated kidneys, AII (0.01-100 nmol/L) produced concentration-dependent afferent and efferent arteriolar constrictor responses of similar magnitudes. Neither afferent nor efferent arteriolar An responsiveness was significantly altered in piroxicam-treated kidneys, although afferent responses exceeded efferent responses at An concentrations greater than or equal to 10 nmol/L. 6. We conclude that endogenous cyclo-oxygenase products exert a vasodilator influence on juxtamedullary afferent arterioles under baseline conditions. Although cyclo-oxygenase inhibition had little effect on juxtamedullary microvascular responses to AII, the response to high AII concentrations may be modulated by cyclo-oxygenase products in a manner which delicately alters the relative influence of the peptide on pre- vs postglomerular resistances.