Arterial pressure and exaggerated natriuresis in spontaneously hypertensive rats.

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Abstract
The hypothesis was tested that the exaggerated natriuretic response of spontaneously hypertensive rats (SHR) to intragastric volume expansion may be independent of the sustained level of arterial pressure. The SHR were treated for 10 days with guanethidine SO4, 25 mg/l, and hydralazine HCl, 80 mg/liter, in drinking water. Mean arterial pressure (MAP) in conscious treated SHR (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 Na excretion (.DELTA. UNa V) by T- and U-SHR of 2.25 .+-. 0.85 and 2.45 .+-. 0.46 meq/min, respectively (P > 0.5). The increase in fractional Na excretion (FENa) by T-SHR (.DELTA. 0.89 .+-. 0.33%) was significantly less than that of U-SHR (.DELTA. 2.16 .+-. 0.40%, P < 0.005), owing to a small increase in glomerular filtration rate (GFR) by T-SHR (.DELTA. 0.28 .+-. 0.08 ml/min, P < 0.01). The difference in FENa between T- and U-SHR was unaffected by spironolactone. Acute drug-induced normotension in other SHR abolished the natriuresis; when coupled with i.v. 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 i.v. volume expansion to 2% of body weight. It is unlikely that elevated arterial presure, per se, mediated the exaggerated natriuretic response of SHR to 2% i.g. saline-loading. The natriuretic response of T-SHR to i.g. saline-loading may preserved by expansion of extracellular fluid volume caused by the prolonged reduction of MAP.