A low dietary sodium intake reduces neuronal noradrenaline release and the blood pressure in spontaneously hypertensive rats.

Young male spontaneously hypertensive rats were placed on a low (0.5 mmol/100 g), normal (13 mmol/100 g) or high (120 mmol/100 g) sodium diet for 6 weeks. Subsequent to the assessment of the basal blood pressure and heart rate in freely moving animals, the rats were pithed. In some of the pithed rats dose-response curves were constructed to exogenously administered noradrenaline (NA) and sympathetic nerve stimulation (SNS) through the pithing rod before and after the administration of an inhibitor of the neuronal uptake mechanism (desipramine, DMI, 0.5 mg/kg). In other pithed rats the SNS-induced (2 Hz) increase in plasma NA levels was assessed before and after the administration of clonidine (30 micrograms/kg), an agonist at the prejunctional alpha 2-adrenoceptors. We found that following the dietary intervention period the basal blood pressure and heart rate were higher in the high sodium group and lower in the low sodium group compared to values obtained in the control group. The neurogenic pressor responses clearly differed between the various diet groups. These differences could not be explained by differences in postjunctional responsiveness to exogenous NA. Rather, they were probably due to differences in the amount of transmitter at the synapse since the low sodium group was associated with decreased levels of plasma NA during SNS. Pretreatment with DMI potentiated the pressor responses, but largely to the same degree in the various diet groups, suggesting that there were no major differences in the function of the neuronal uptake mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)