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

Abstract

SUMMARY1. 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 1-1) 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.

Natriuresis in conscious dogs caused by increased carotid [Na+] during angiotensin II and aldosterone blockade

“…Over the years a number of experimental results have suggested that the concentration of Na+ presented to the central nervous system (CNS) either from the blood or from the cerebrospinal fluid may participate in the regulation of renal Na+ excretion (Andersson et , Chodobski & McKinley 1989, Emmeluth et al 1992. However, it is still a Correspondence : Claw Emmeluth, Department of Medical Physiology, University of Copenhagen, 3 Blegdamsvej, DK-2200 Copenhagen N, Denmark.…”

Influence of ruminal water‐loading on renal sodium excretion and water intake following feeding in sheep

“…1992). Preventing CSF sodium concentration from increasing during intravenous infusion of hypertonic saline infusion, or postprandially, also blocks the natriuretic responses following intravenous hypertonic saline or feeding (Chodobski & McKinley 1989, McKinley et al . 1994).…”

Natriuresis after a water load in humans under different sodium body content

“…Urinary Na retention ensued body fluid dilution by means of rehydration in a dehydrated animal (21). A hypertonic NaCI intravenous load resulted in a compensating natriuresis (8). A severe antinatriuretic response was produced by a water load ( 14,15).…”

“…In other studies, the ventriculocisternal perfusion with isosmotic low-sodium solution or hyposmotic low-sodium solution produced a notable decrease of the renal Na output (25), an increase in plasmatic Na concentration, and excessive loss of water (8). Furthermore, the natriuresis induced by an intravenous hypertonic NaC1 load could be blocked by lowering the cerebrospinal fluid Na concentration (8). Finally, the natriuresis observed in normal sheep after water deprivation (22) or after intravenous infusion of hypertonic saline (19) was blocked by ablation of the anterior third ventricle.…”

“…Additionally, in some of these same studies, intracerebroventricular injection of equally hypertonic solutions of other solutes, such as glucose (1,12) or NH4C1 (1), were ineffective in that regard. In other studies, the ventriculocisternal perfusion with isosmotic low-sodium solution or hyposmotic low-sodium solution produced a notable decrease of the renal Na output (25), an increase in plasmatic Na concentration, and excessive loss of water (8). Furthermore, the natriuresis induced by an intravenous hypertonic NaC1 load could be blocked by lowering the cerebrospinal fluid Na concentration (8).…”