These studies were aimed at investigating whether chronic hypertension in pregnancy causes changes both in salt excretion (Na(E)) and in glomerular hemodynamics. Metabolic and renal micropuncture studies were performed in pregnant (P) and Virgin (V) Munich-Wistar rats with normal blood pressure (N) and two-kidney Goldblatt hypertension (H). Mean Na(E) was higher in PN than VN (2.7 vs. 1.7 meq/day, P <0.01). Hypertension raised Na(E) both in P and V rats; in P and V rats with 'benign' hypertension (blood pressure <180 mmHg) Na(E) averaged 3.2 and 2.6 meq/day, respectively (P <0.05); mean Na(E) was 5.9 and 3.8 meq/day, respectively (P <0.01), in P and V rats with 'malignant' hypertension (blood pressure ≥ 180 mmHg). Afferent arteriole resistance (R(a)) averaged 1.73 and 3.50 10 dyn · s-1 · cm5 in PN and VN, respectively (P <0.01). Hypertension raised R(a) in V, but not in P rats (4.47 vs. 2.14 10 dyn · s-1 · cm5, P <0.01). Thus glomerular plasma flow, glomerular capillary hydrostatic pressure, and single-nephron glomerular filtration rate were markedly higher in PH than VH rats: in PH rats single-nephron filtration fraction was significantly lower than in VH. These results show that in PH rats a marked rise in Na(E) is associated with glomerular vasodilation.
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Publication status||Published - 1989|
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