Nonpressor mechanisms in CNS-induced natriuresis

Mouw, David R.; Vander, Arthur J.; Bourgoignie, Jacques J.; Kutschinski, Sandra S.; Mathias, Nancy

doi:10.1152/ajprenal.1979.237.2.f157

Cited by 13 publications

(15 citation statements)

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“…However, it has been shown that chronic infusions, as opposed to bolus injections, 4 of hypertonic sodium chloride evoke a natriuretic response with no change in blood pressure. 5 Another similarity between saline expansion and hypertonic saline natriuresis is found in the recent report of Gilmore and Nemeh, 6 in which sodium-depleted/ volume-replete dogs did not have a natriuretic response to intracarotid hypertonic saline infusions. Thus a similar conclusion could be reached as in the previously mentioned experiments on hypotonic or hyperoncotic volume expansion, namely, that the total- …”

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confidence: 68%

The natriuretic response to hydromineral imbalance.

Gruber

1987

Hypertension

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SUMMARY Many recent investigations of the mechanism of volume-expansion natriuresis fail to appreciate that the observed renal sodium excretion may not be dependent on an increase in intravascular volume, but rather on the infused sodium load or extracellular fluid volume expansion. With this in mind, the natriuresis of isotonic volume expansion, hypertonic saline infusion, and dehydration have a common basis: they present a relative or absolute sodium load. Lesions of forebrain periventricular tissue prevent the natriuretic response to these three states of body fluid imbalance. In this review we discuss the evidence for a common central nervous system-mediated natriuretic mechanism in response to disturbances of fluid and electrolyte balance. We also propose a role for pars intermedia-derived, proopiomelanocortin-derived peptides as humoral mediators of renal sodium excretion. Evidence from our laboratory, as well as others, provides data for a testable hypothesis to explain central nervous system-mediated natriuresis, as well as an explanation of how central nervous system lesions or neurochemical perturbations affect the renal response to body fluid imbalance. ume-expansion natriuresis agree that the natriuretic response is not correlated to an increase in intravascular volume, but rather to the infused sodium load or extracellular expansion. Intravascular volume-expansion with sodium-free solutions of hyperoncotic dextran, hyperosmotic glucose, hyperoncotic albumin, or hypotonic sodium chloride produces little increase in sodium excretion. '• 2 Expansion with saline or blood, however, challenges that produce an expansion of the extracellular fluid volume and present a sodium load, results in a significant increase in urinary sodium excretion.1 -2 The hemodynamic response to "pure" intravascular expansion, isotonic saline expansion, or volume expansion with blood is quite similar. These data suggest that an increase in

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confidence: 68%

The natriuretic response to hydromineral imbalance.

Gruber

1987

Hypertension

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“…It is well established that selective intraventricular or intracarotid infusion of hypertonic sodium chloride induces a significant natriuresis in a number of species including the sheep (1, 2, 4), goat (14), dog (7,12,13,18,20), cat (6,17), and rat (3). In addition, the extent of the natriuresis appears to be dependent upon dietary sodium intake.…”

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confidence: 99%

Lack of evidence for a cerebral sodium modulating mechanism in the monkey

Gilmore

1987

Basic Res Cardiol

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Summary: Experiments were carried out in seven conscious macaque monkeys undergoing a water diuresis to determine the effects of raising carotid blood sodium concentration on renal sodium excretion and free water clearance. On separate days each animal received an intracarotid infusion of hypertonic sodium chloride (90 Eq NaCl/kg. body wt./min) for 5 to 10 rain, the same hypertonic infusion intravenously, and an intracarotid infusion of isotonic NaCI. None of the infusions produced a change in sodium excretion. However, the intracarotid hypertonic infusion produced a sustained decrease in free water excretion while the other infusion did not. Creatinine clearance was not affected by any of the infusions. The results of these experimcnts support the view that while the brain of the primate contains an osmotic sensing mechanism it does not contain a mechanism which modulates sodium excretion.

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“…T h e signal route between the CNS and the kidneys is still not definitely identified. I t has been suggested that a natriuretic factor (Andersson 1977, de Wardener & MacGregor 1983) may be responsible for the enhanced sodium excretion (Mouw et al 1979, Ulfendahl et al 1986).…”

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confidence: 99%

Redistribution of glomerular filtration and renal plasma flow in CNS‐induced natriuresis

Sjöquist

Göransson

Hansell

et al. 1986

Acta Physiologica Scandinavica

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Infusion of hypertonic sodium chloride solution into the third cerebral ventricle results in a marked increase in renal sodium output, indicating an important regulator of extracellular volume homeostasis. The intrarenal events governing the enhanced excretion have not been thoroughly studied previously. In 12 anaesthetized male rats a stainless steel cannula was introduced stereotaxically into the right lateral cerebral ventricle. Urine volume and excretion rates, Na, K, and osmotically active particles were measured during control infusion of artificial cerebrospinal fluid and during stimulation of central mechanisms with I M NaCl (520 nl min-1). At the end of the stimulation period, regional renal plasma flow (86RbCl) and glomerular filtration rate (51Cr-EDTA) were measured with single injection techniques. A second group of 12 non-stimulated rats served as controls. During ICV stimulation, the urine flow rate increased from 1.8 +/- 0.19 to 6.4 +/- 1.01 microliter min-1 (P less than 0.001). The urinary concentrations of Na and K increased, leading to a rise in the excretion rates of these ions from 0.12 +/- 0.025 to 0.96 +/- 0.352 mumol min-1 (P less than 0.001) and 0.40 +/- 0.083 to 1.70 +/- 0.196 (P less than 0.001), respectively. The osmolar excretion rate was 2.9 +/- 0.35 mu Osm min-1 before stimulation and 9.6 +/- 1.09 higher (P less than 0.001) during stimulation. Simultaneously the inner medullary plasma flow rose two-fold from 0.7 +/- 0.06 to 1.4 +/- 0.12 microliter min-1 tissue (P less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

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Nonpressor mechanisms in CNS-induced natriuresis

Cited by 13 publications

References 0 publications

The natriuretic response to hydromineral imbalance.

The natriuretic response to hydromineral imbalance.

Lack of evidence for a cerebral sodium modulating mechanism in the monkey

Redistribution of glomerular filtration and renal plasma flow in CNS‐induced natriuresis

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