FACTORS AFFECTING RENAL MICROVASCULAR BLOOD-FLOW IN RAT HYPERDYNAMIC BACTEREMIA

To determine whether angiotensin II and alpha-adrenergic activity cont ribute to the mechanism of impaired renal microvascular blood flow dur ing hyperdynamic live Escherichia coli (E. coli) bacteremia, we used i n vivo video microscopy in the chronic unilateral hydronephrotic kidne y of decerebrate male Sprague-Dawley rats. Intravenous infusion of E. coli caused arteriolar constriction to 83 +/- 4% of baseline (BL) in c ortical radial arteries (CRA), 82 +/- 3% of BL in afferent (AFF) arter ioles, and decreased flow to 54 +/-9% of BL. Subsequent local inhibiti on of renal prostaglandin synthesis with mefenamate increased preglome rular arteriolar constriction to 55 +/- 6% of BL in CRA and 51 +/- 6% of BL in AFF arterioles and decreased renal microvascular blood flow t o 26 +/- 8% of BL values in E. coli animals but had no effect on contr ol animals. Subsequent local renal angiotensin II receptor blockade wi th saralasin acetate increased renal microvascular blood flow in E. co li animals to 64 +/- 9% of BL by dilating CRA to 78 +/- 5% of BL and A FF arterioles to 89 +/- 5% of BL. Phentolamine caused further dilation of CRA to 104 +/- 7% BL and AFF arterioles to 116 +/- 109% and increa sed flow to 99 +/- 8% of BL. Acetylcholine increased diameters further to 110 +/- 3% of BL in CRA and 136 +/- 12% of BL in AFF arterioles. T hese data indicate that in our chronic hydronephrotic kidney model dur ing E. coli bacteremia, renal microvascular tone is due to increased a ngiotensin II and alpha-adrenergic activity and some other, as yet, un defined factor.