Effect of low sodium intake and β-blockade on renin synthesis and secretion in mice with unilateral ureteral ligation

Abstract

We previously reported that sodium depletion increased renin secretion from the normal kidney in mice. We postulated that the combined procedures of sodium depletion and β-adrenoceptor blockade would affect the activity of the renin-angiotensin system. To test this hypothesis, we investigated the interaction of low sodium intake (LSI) and propranolol (PRO) on renin synthesis and secretion. To prevent the influence of tubule flow on renin secretion, mice with a left hydronephrotic kidney were used. LSI increased plasma renin concentration (PRC) 5.6-fold in the right renal vein (P<0.01). There was no net increase of PRC in the left renal vein. Tissue renin concentration (TRC) was elevated 3.6-fold and 1.3-fold in the right and left kidneys (P<0.01), respectively. After administration of PRO, PRC decreased by 34% in the right renal vein and 47% in the aorta (P<0.05); TRC was reduced by 37.5% in the right and 29.3% in the hydronephrotic kidneys (P<0.05). The combination of LSI and PRO increased PRC 3.4-fold and 1.8-fold in the right (P<0.01) and left renal veins (P<0.05), respectively. TRC increased 3.4-fold in the right (P<0.01) but only 61% in the left kidneys (P<0.05). The pattern in change of renin mRNA levels was similar to TRC but the absolute amount was smaller. There were correlations between PRC and renin mRNA, and between TRC and renin mRNA in both kidneys (P<0.001). Thus, LSI increased renin synthesis in both kidneys. However, there was no apparent renin secretion in the hydronephrotic kidney. PRO treatment suppressed renin synthesis and renin secretion, irrespective of hydronephrosis and LSI. The macula densa is critical for renin secretion under all of the circumstances studied.