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It has been reported that storage of norepinephrine by the sympathetic nervous system was decreased in rats made hypertensive by the administration of desoxycorticosterone trimethylacetate (DOCA) and sodium chloride. The present investigation indicated that the storage of norepinephrine was impaired at an early stage of treatment with DOCA and NaCl (1 week), and preceded the appearance of hypertension. The role of sodium and sympathetic activity, the two major factors suspected of contributing to the development of the abnormality in storage of norepinephrine, was studied in normotensive and hypertensive rats. The withdrawal of sodium from the diet of hypertensive rats for 2 weeks lowered the blood pressure to normotensive levels and simultaneously restored to normal the storage and binding capacity as well as the endogenous norepinephrine content of the sympathetic storage granules in the heart. Sodium restriction or depletion in normotensive rats caused a slight decrease in blood pressure and the retention of norepinephrine in the storage granules was increased. These findings suggested that the capacity of the sympathetic granules to bind and store norepinephrine was influenced by the state of sodium balance and showed that the capacity of storage could be correlated with the level of blood pressure. The finding that treatment with a long-acting ganglionic blocker could restore the blood pressure and the norepinephrine storage capacity in hypertensive animals to normal suggested a neurogenic component in the development of this form of hypertension.

Relationship between Sodium Intake and Norepinephrine Storage during the Development of Experimental Hypertension