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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Cerebral regulation of renal sodium excretion in sheep infused intravenously with hypertonic NaCl.

1. The natriuretic response to intravenous infusion of 2 M-NaCl was investigated in six conscious sheep. This hypertonic NaCl load resulted in relatively small, physiological (2-3 mmol l-1) increases in plasma Na+ concentration and was followed by a natriuresis with a maximum mean urinary sodium excretion 5 times higher than pre-infusion values. 2. Intravenous infusion of isotonic NaCl, delivering the same Na+ load as hypertonic NaCl infusion, did not induce natriuresis. This suggested, therefore, that with the hypertonic sodium load administered in the present study, the rise in plasma Na+ and/or tonicity rather than increase in blood volume is important in evoking the natriuretic response. 3. Intracerebroventricular infusion of low-Na+ artificial cerebrospinal fluid (CSF) reduced CSF Na+ concentration, decreased plasma vasopressin ( AVP) levels and caused a copious water diuresis. This was associated with excessive loss of water and large increases in plasma Na+ concentration and osmolality. 4. The natriuresis induced by intravenous hypertonic NaCl load could be blocked by lowering CSF Na+ concentration in situations where water diuresis was either prevented or reduced by intravenous infusion of AVP or by delayed intracerebroventricular infusion of low-Na+ CSF, respectively. 5. The results of the present study provide further evidence that renal sodium excretion can be controlled by the central nervous system.[1]


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