CORTICAL AND MEDULLARY HEMODYNAMICS IN DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSIVE MICE

The effect of acutely increasing renal perfusion pressure or extracell ular fluid volume on renal medullary and cortical blood flow was exami ned in the low-renin deoxycorticosterone acetate (DOCA)-salt hypertens ion model in mice. A 50-mg DOCA tablet was implanted, and 1% saline wa s given as drinking water for 3 wk, Medullary and cortical blood flow were determined with laser-Doppler flowmetry, and whole-kidney blood f low was measured with a transit-time ultrasound flowprobe around the r enal artery. In control mice, total renal blood flow ranged from 6.3 a nd 7.6 ml/min per g kidney weight and in DOCA-salt mice from 4.3 and 4 .7 ml/min per g kidney weight, respectively, and was minimally affecte d as renal perfusion pressure was increased. Renal vascular resistance increased correspondingly. During stepwise increases in renal artery pressure from 90 to 140 mmHg, medullary blood flow progressively incre ased in control mice to 125% of baseline values, whereas cortical bloo d flow did not change. In DOCA-salt mice, increasing BP from 100 to 15 4 mmHg had no effect on either cortical or medullary blood flow. Urine flow and sodium excretion were lower in DOCA-salt mice than in contro ls and increased nearly to the same extent in both groups after volume expansion with isotonic saline, Total renal blood flow increased afte r saline lending, more in controls than in DOCA-salt mice. Increases i n medullary blood flow after saline loading were up to 122% of baselin e values in controls and demonstrated a significantly steeper slope th an the 110% of baseline increases in DOCA-salt mice. Cortical blood fl ow, however, was not different between the groups. Thus, medullary blo od flow is not as tightly autoregulated as cortical blood flow in norm al mice. Natriuresis with acute volume loading is facilitated by incre ased medullary blood flow. In DOCA-salt mice, the medullary blood flow reaction to renal perfusion pressure increases is abolished, whereas flow increases with extracellular volume expansion are diminished. The se results suggest that diminished pressure-natriuresis responses in D OCA-salt mice are related to perturbed medullary blood flow.