Evidence in Man That Urinary Electrolyte Loss Induced by Pitressin Is a Function of Water Retention 1

Leaf, Alexander; Bartter, Frederic C.; Santos, Roberto F.; Wrong, Oliver

doi:10.1172/jci102805

Cited by 323 publications

(101 citation statements)

References 18 publications

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“…[2][3][4][5][6][7][8][9] The dose-response curve performed in this study shows that this effect occurred only for high doses (15 and 50 g/kg BW) that probably increased P AVP levels distinctly above those involved in water conservation, even after 24 h of water deprivation, as judged here by the urinary AVP data (Table 2). With lower doses (0.1 and 1 g/kg BW), likely corresponding to the range of usual osmotic stimuli, Figure 4.…”

Section: V1ar Effectsmentioning

confidence: 80%

“…In the isolated microperfused CD, V2R activation increases sodium transport, 1 an effect that should reduce sodium excretion in vivo; however, in a number of studies, AVP infusion in animals and humans has been shown to induce an increase in sodium excretion. [2][3][4][5][6][7][8][9] It is usually assumed that AVP might contribute to some forms of hypertension by its vasoconstrictive effects, but an increase in sodium excretion, if it occurred in normal life, should more likely contribute to lower BP.…”

mentioning

confidence: 99%

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Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Perucca

Bichet²,

Bardoux

et al. 2008

Journal of the American Society of Nephrology

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The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and pressor effects, via activation of V2 and V1a receptors, respectively, are relatively well understood, but the possible associated effects on sodium handling are a matter of controversy. In this study, normal conscious Wistar rats were acutely administered various doses of AVP, dDAVP (V2 agonist), furosemide, or the following selective non-peptide receptor antagonists SR121463A (V2 antagonist) or SR49059 (V1a antagonist). Urine flow and sodium excretion rates in the next 6 h were compared with basal values obtained on the previous day, after vehicle treatment, using each rat as its own control. The rate of sodium excretion decreased with V2 agonism and increased with V2 antagonism in a dose-dependent manner. However, for comparable increases in urine flow rate, the V2 antagonist induced a natriuresis 7-fold smaller than did furosemide. Vasopressin reduced sodium excretion at 1 g/kg but increased it at doses Ͼ5 g/kg, an effect that was abolished by the V1a antagonist. Combined V2 and V1a effects of endogenous vasopressin can be predicted to vary largely according to the respective levels of vasopressin in plasma, renal medulla (acting on interstitial cells), and urine (acting on V1a luminal receptors). In the usual range of regulation, antidiuretic effects of vasopressin may be associated with variable sodium retention. Although V2 antagonists are predominantly aquaretic, their possible effects on sodium excretion should not be neglected. In view of their proposed use in several human disorders, the respective influence of selective (V2) or mixed (V1a/V2) receptor antagonists on sodium handling in humans needs reevaluation. 19: 172119: -173119: , 200819: . doi: 10.1681 The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and its pressor effects are relatively well understood. On the one hand, AVP improves water conservation by increasing the permeability to water of the renal collecting duct (CD), an effect mediated by the V2 receptors (V2R) and permitted by the insertion in the luminal membrane of principal cells of preformed aquaporin 2 (AQP2) molecules. This allows more water to be reabsorbed when these ducts traverse the hyperosmotic medulla. On the other hand, AVP increases blood pressure (BP) by inducing a vasoconstriction through its binding to V1a receptors (V1aR) expressed in vascular smooth muscle cells. For these two different effects, in vivo studies are in good agreement with the expectations based on results obtained in vitro. J Am Soc NephrolIn contrast, the experiments intended to study the effects of AVP on sodium handling in vitro or in vivo provide results that are difficult to reconcile. In the isolated microperfused CD, V2R activation increases sodium transport, 1 an effect that should reduce sodium excretion in vivo; however, in a number of studies, AVP infusion in animals and humans

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Section: V1ar Effectsmentioning

confidence: 80%

mentioning

confidence: 99%

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Perucca

Bichet²,

Bardoux

et al. 2008

Journal of the American Society of Nephrology

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“…Excess natriuresis follows water retention and mainly exceeds the intake when volume expansion is relatively acute. After a few days, the Na balance is reestablished and a decline in the hydroosmotic effect of ADH is observed (vasopressin escape) (1,21).…”

Section: Urine Osmolalitymentioning

confidence: 99%

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Musch²

2008

Clinical Journal of the American Society of Nephrology

146

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Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a frequent cause of hypotonicity. Although the differential diagnosis with other causes of hypotonicity such as salt depletion is sometimes challenging, some simple and readily available biologic parameters can be helpful in the diagnosis of SIADH. In SIADH, urea is typically low; this is less specific for elderly patients, for whom lower clearance of urea accounts for higher values. Low levels of uric acid are more often seen in SIADH (70%) compared with salt-depleted patients (40%). Typically, patients with SIADH will show a lower anion gap with nearly normal total CO 2 and serum potassium, this despite dilution. In patients with hyponatremia secondary to hypocorticism, total CO 2 is usually lower than in nonendocrine SIADH despite low urea and uric acid levels. Urine biology can also be helpful in diagnosis of SIADH because patients with SIADH have high urine sodium (Na; >30 mEq/L), and most of them will have a high fractional excretion of Na (>0.5% in 70% of cases), reflecting salt intake. Conversely, low urine Na in patients with SIADH and poor alimentation is not rare. Finally, measurement of urine osmolality is useful for the diagnosis of polydipsia and reset osmostat and could further help in the choice of therapeutic strategy because patients with low urine osmolality will benefit from water restriction or urea, whereas those with high urine osmolality (>600 mOsm/kg) would be good candidates for V 2 antagonist.

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“…On a severely sodium-restricted diet, his patient continued to excrete sodium in her urine; however, despite negative sodium balance, she remained normotensive. 3,4 In 1953, Leaf et al 5 demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain. This was not "salt wasting"; it was a physiologic response to an expanded intraPublished online ahead of print.…”

mentioning

confidence: 99%

Cerebral Salt Wasting Versus SIADH

Sterns

Silver

2008

Journal of the American Society of Nephrology

123

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Evidence in Man That Urinary Electrolyte Loss Induced by Pitressin Is a Function of Water Retention 1

Cited by 323 publications

References 18 publications

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Clinical Laboratory Evaluation of the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Cerebral Salt Wasting Versus SIADH

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