Chronic dietary salt restriction in rats maintained single nephron and total kidney GFR identical to salt excess, driven by angiotensin II and prostaglandin-mediated adaptations.
Does chronic dietary salt restriction alter glomerular microcirculation compared to salt excess in rats?
Chronic dietary salt restriction in rats maintains GFR through angiotensin II-mediated efferent vasoconstriction and prostaglandin-mediated vasodilation, compensating for reduced plasma volume.
Micropuncture studies were performed in 33 Munich-Wistar rats maintained chronically either on dietary NaCl restriction (group 1) or excess (group 2). Values for single nephron (SN) and total kidney glomerular filtration rate (GFR) were identical in both groups. Nevertheless, because of preferential efferent vasoconstriction, glomerular capillary hydraulic pressure (PGC) was higher in group 1, offsetting the lower initial glomerular plasma flow rate (QA) also found in group 1. The pressor response to infusion of exogenous angiotensin II (AII) was less in group 1 than in group 2, suggesting that vascular receptors for AII may have been occupied by endogenous hormone, the latter leading to the efferent arteriolar vasoconstriction. In addition to AII, prostaglandins also appear to be involved in the adaptations of the glomerular microcirculation to chronic variations in salt intake. In group 1, indomethacin or meclofenamate infusion mimicked exogenous AII, causing declines in QA and SNGFR. These changes were lacking in group 2. Because of relative contraction of plasma volume, the vasodilatory effects of prostaglandins appear to be needed in low salt animals to sustain SNGFR and QA. In the high salt group, however, since plasma volume is not contracted, maintenance of SNGFR and QA appears to be less critically dependent on endogenous prostaglandins.
Schor et al. (Thu,) conducted a other in Dietary NaCl restriction or excess (n=33). Dietary NaCl restriction vs. Dietary NaCl excess was evaluated on Single nephron (SN) and total kidney glomerular filtration rate (GFR). Chronic dietary salt restriction in rats maintained single nephron and total kidney GFR identical to salt excess, driven by angiotensin II and prostaglandin-mediated adaptations.