RENAL NERVES PROMOTE SODIUM-EXCRETION IN ANGIOTENSIN-INDUCED HYPERTENSION

To determine whether the sympathetic nervous system contributes to the hypertension induced by pathophysiological increments in plasma angio tensin II (Ang II) concentration, we determined the neurally induced c hanges in renal excretory function during chronic intravenous infusion of Ang II. Studies were carried out in five conscious chronically ins trumented dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separate 24 -hour urine collection from the denervated and innervated kidneys. Aft er control measurements, Ang II was infused for 5 days at a rate of 4. 8 pmol/kg per minute (5 ng/kg per minute); this was followed by a 5-da y recovery period. Twenty-four-hour control values for mean arterial p ressure (MAP) and for the ratio of denervated to innervated kidneys (D EN/INN) for urinary sodium, potassium, and creatinine excretion were 9 3+/-5 mm Hg, 1.17+/-0.09, 1.10+/-0.10, and 1.00+/-0.02, respectively. As expected, Ang II infusion caused sodium retention for several days before sodium balance was achieved at an elevated MAP (day 5=124+/-4 m m Hg). Moreover, by day 2 of Ang II-induced hypertension, there were s ignificant reductions in the DEN/INN for sodium and potassium, which p ersisted for the 5 days of Ang II infusion, on day 5, the DEN/INN valu es for sodium and potassium were 0.71+/-0.10 and 0.91+/-0.12, respecti vely. In contrast, the DEN/INN for creatinine was unchanged from contr ol levels during Ang II infusion, and measurements of renal hemodynami cs indicated comparable reductions in glomerular filtration rate (appr oximate to 13%) and renal plasma now (approximate to 25%) during Ang I I infusion. This indicates that the renal nerves promoted sodium and p otassium excretion during Ang II-induced hypertension by inhibiting tu bular reabsorption of these electrolytes. Thus, this study provides no support for the hypothesis that increased renal sympathetic nerve act ivity impairs sodium excretion and contributes to Ang II-induced hyper tension.