Excessive salt intake is a risk factor for hypertension. The most reliable method for estimating daily salt intake is measurement of 24-h urinary sodium excretion, while it is inconvenient. Sodium-to-potassium ratio (Na/K) of a urine sample is another index of salt loading. We previously reported that a simple measure of spot urine Na/K might be a representative of salt loading in a cross-sectional setting. Here, we conducted a longitudinal study aiming to clarify a prognostic significance of spot urine Na/K for increasing blood pressure (BP) levels. Study subjects consists of 9,769 general individuals. Among them, individuals whose baseline Na/K was available (n=9,328), who were normotensive at baseline (n=6,392), and who participated in the follow-up measurement (n=5,209) were included in this analysis (51.8±12.9 years old, male: 29.2%). Mean follow-up duration was 5.0±0.5 years. Mean Na/K at baseline was 3.1±1.7, and showed step-wise increase with BP levels (optimal: 3.0±1.6, normal: 3.3±1.8, high normal: 3.4±1.8, P<0.001). Other major factors that were significantly associated with Na/K was fasting time (r=-0.220, P<0.001), and CKD (CKD (n=694): 2.7±1.6, control: 3.2±1.7, P<0.001). Mean SBP was significantly increased during follow-up period (baseline: 116±12, follow-up: 119±15 mmHg), and 805 individuals (15.5%) were newly diagnosed as hypertension (HT). These individuals were significantly older (HT: 60.3±9.9, NT: 50.3±12.8 years), were frequently male (36.4%, 27.9%), and had higher SBP (127±9, 115±11 mmHg) at baseline (P<0.001). In contrast, baseline spot urine Na/K was slightly lower in individuals who developed HT (3.0±1.6, 3.1±1.8, P=0.013), while that measured at follow-up investigation was oppositely higher in hypertensives (3.1±1.8, 2.8±1.5, P<0.001). Multiple linear regression analysis adjusted for the covariates identified baseline Na/K (β=0.108, P<0.001) and changes in Na/K during follow-up period (β=0.222, P<0.001) as independent determinants for future SBP levels. Higher spot urine Na/K, as well as increases in the Na/K levels, was significant determinant for future BP levels. The apparently lower baseline Na/K levels in individuals who developed HT might be due to reverse causality.