Abstract

Angiotensin II (ANG II) is one of the most powerful sodium-retaining hormones in the body, in which it can be induced by low dietary sodium intake. Although ANG II alters sodium re-absorption through multiple intra-renal and extra-renal effects, ANG II can contribute to increased tubular re-absorption by reducing peritubular capillary hydrostatic pressure and renal blood flow. Recent evidence suggests that ANG II can stimulate the release of vascular endothelial growth factor (VEGF) from human vascular tissue. In the present study, we seek to determine whether low dietary sodium intake can induce VEGF mRNA expression in kidney of normal-tensive rats (WKY). Male WKY (∼250g) rats were placed in the metabolic cages and treated with normal sodium rodent diet (0.5% Na) (control) or low sodium rodent diet (0.02% Na) for 8 weeks. The urinary sodium excretion (μEq/d) was 176±136 and 1537±292 in low sodium diet group and control group, respectively (P<0.01). Water intake (ml/d) was 59±18 and 38±4 in low sodium group and control group, respectively (P<0.01). Mean arterial pressure (MAP) was determined under conscious condition through the carotid artery catheter in the end of experiment. MAP was 149±3 and 142±2 mmHg in low sodium group and control group, respectively (P=0.105). Northern blot analysis indicated that VEGF mRNA expression in whole kidney tissue increased by 2.2-fold in low sodium group, compared to the control group (P<0.05). These results support the speculation that low dietary sodium intake may induce angiogenesis in kidney, in which it may promote tubular re-absorption. (supported by HL-51971)