Arterial pressure and exaggerated natriuresis in spontaneously hypertensive rats.

We tested the hypothesis that the exaggerated natriuretJc response of spontaneously hypertensive rats (SHR) to intragastric volume expansion may be independent of the sustained level of arterial pressure. The SHRs were treated for 10 days with guanethldine S04, 25 mg/llter, and hydralazine HO, 80 mg/liter, in drinking water. Mean arterial pressure (MAP) in conscious treated SHRs (T-SHR) was 130 ± SE 9 mm Hg vs 193 ± 3 mm Hg in untreated (U-) SHR (p < 0.001). An intragastric (i.g.) saline load (2% body weight) produced increases in absolute sodium excretion (A UN.V) by Tand U-SHR of 2.25 ± 0.85 and 2.45 ± 0.46 nEq/min, respectively (p > 0.5). However, the Increase in fractional sodium excretion (FEN>) by T-SHR (A 0.89 ± 0.33%) was significantly less than that of U-SHR (A 2.16 ± 0.40%,p < 0.005), owing to a small increase in glomerular filtration rate (GFR) by T-SHR (A 0.28 ± 0.08 ml/min, p < 0.01). The difference in FEN. between Tand U-SHR was not affected by splronolactone. Acute drug-induced normotension in other SHR abolished the natriuresis; but, when coupled with intravenous volume expansion to 5% of body weight, the response was restored. Hydrostatic pressure in surface proximal tubules and peritubular capillaries of anesthetized T-SHR was not significantly different from that in U-SHR, nor was it significantly altered after intravenous volume expansion to 2% of body weight. It is unlikely, then, that elevated arterial pressure, per se, mediated the exaggerated natriuretic response of SHR to 2% i.g. saline-loading. Additionally, the natriuretic response of T-SHR to i.g. saline-loading may have been preserved, at least in part, by expansion of extracellular fluid volume caused by the prolonged reduction of MAP.(Hypertension 3: 386-394, 1981)