Reduced sympathetic inhibition in salt-sensitive Japanese young adults.

The purpose of our study was to investigate the sympathetic response to excess salt loading of 54 normotensive young adults with and without a family history of hypertension. We examined muscle sympathetic nerve activity, plasma concentration and urinary excretion of catecholamines, and ambulatory blood pressures during low (4 g NaCl) and high (16 g NaCl) salt diet intake. Ambulatory blood pressure and urinary excretion of catecholamines are known to be reduced during sleep. These parameters were therefore calculated during waking and sleeping periods. The subject was defined as salt-sensitive when mean ambulatory systolic pressure during the waking period was > or =3 mm Hg higher during high salt intake than during low salt intake (n = 26: 21.4+/-0.3 years old). When mean systolic pressure was either lower or equal during high salt intake than during low salt intake, the subject was defined as salt-resistant (n = 24: 21.3+/-0.3 years old). Muscle sympathetic nerve activity, plasma concentration and urinary excretion of norepinephrine in salt-resistant subjects were significantly reduced (P<.05) by salt intake, whereas plasma concentration of epinephrine was unchanged and urinary excretion of epinephrine was reduced. In contrast, urinary excretion of epinephrine in salt-sensitive subjects was significantly elevated (P<.05) during high salt intake, whereas muscle sympathetic nerve activity and urinary excretion of norepinephrine remained unchanged despite a significant increase (P<.01) of ambulatory blood pressure. Of the salt-sensitive subjects, 73% (19 of 26) had a positive family history of hypertension, whereas only 5 of 24 salt-resistant subjects had a positive family history. These data indicate that the inhibition of sympathetic activity during a high salt intake did not occur in salt-sensitive young adults, and this may be linked with a hereditary predisposition to hypertension.