Low
sodium intake is the most widely used nonpharmacological approach to the treatment of
hypertension. Although nonpharmacological treatment is by definition regarded as safe, the suggestion has been made that low
sodium intake is not totally devoid of inconveniences, and animal data have shown it to be accompanied by an impairment of reflex blood pressure control and homeostasis. However, no data exist on this issue in humans. In mild essential hypertensive patients (age, 34.1+/-3.3 years [mean+/-SEM]), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation, induced by stepwise
intravenous infusions of
phenylephrine and
nitroprusside, respectively. Measurements were performed at the end of three dietary periods, ie, after 8 days of regular
sodium intake (210 mmol NaCl/d), low
sodium intake (20 mmol NaCl/d) with unchanged
potassium intake, and again regular
sodium intake. Compared with the initial regular
sodium diet, low sodium intake reduced urinary
sodium excretion, whereas urinary
potassium excretion was unchanged. Systolic blood pressure was significantly (P<.05), although slightly, reduced, whereas diastolic blood pressure was unaffected. Muscle sympathetic nerve activity was increased by 23.1+/-5.2% (P<.05). The increase was accompanied by a clear-cut impairment of the baroreceptor ability to modulate muscle sympathetic nerve activity, ie, by a 43.9+/-5.7% (P<.01) reduction in the sensitivity of the baroreceptor-muscle sympathetic nerve activity reflex compared with the control condition. Baroreceptor modulation of heart rate was also impaired, although to a smaller and less consistent extent. When regular
sodium intake was restored, all the above-mentioned parameters and baroreflex responses returned to the values observed at the initial regular
sodium diet. These data raise evidence that in humans
sodium restriction may impair the arterial baroreflex. This may be responsible for the sympathetic activation occurring in this condition and for the impairment of blood pressure homeostasis.