Lack of blood pressure salt-sensitivity supports a preglomerular site of action of nitric oxide in type I diabetic rats

1. The relationship between sodium intake and blood pressure is affected differently by changes in angiotensin (Ang) II and preglomerular resistance, and this study measured that relationship to evaluate the link between nitric oxide and blood pressure early in diabetes. 2. Rats were chronically instrumented, placed on high-sodium (HS = 12 mEq/d) or low-sodium (LS = 0.07 mEq/d) intake diets and assigned to either vehicle- (V) or N-w-nitro-L-arginine methyl ester- (L-NAME; L) treated groups. Mean arterial pressure (MAP) was measured 18 h/day for a 6-day control and 14-day streptozotocin diabetic period in each animal. 3. The MAP of the control period averaged 95 +/- 1 and 94 +/- 1 mmHg in the LSV and HSV rats and 116 +/- 2 and 124 +/- 1 mmHg in the LSL and HSL rats, respectively (LSL vs HSL was significant at P < 0.05). Diabetes increased MAP only in the LSL and HSL rats to 141 +/- 2 mmHg and 152 +/- 2, respectively, similar to our previous reports, and those respective 25 and 28 mmHg increases were a parallel shift in the pressure natriuresis relationship. However, the apparent difference between the LSL and HSL groups when compared was a parallel of the control MAP difference. Plasma renin activity (PRA) in the control period averaged 1.5 +/- 0.5 and 8.1 +/- 1.8 ng AI/mL per h in the HSV and LSV rats, and 0.8 +/- 0.2 and 2.8 +/- 0.5 ng AI/mL per h in the HSL and LSL rats, respectively, and increased similarly by 4.6-fold in the HSL and 4.8-fold in the LSL rats during diabetes. Glomerular filtration rate (GFR) increased in the vehicle but not the L-NAME-treated groups, consistent with our previous reports. 4. Thus, the hypertension caused by the onset of diabetes in -NAME-treated rats was not salt-sensitive. The normal modulation of PRA by salt intake and the failure of GFR to increase are consistent with our hypothesis that nitric oxide may protect against hypertension early in diabetes by preventing preglomerular vasoconstriction by AngII.