Sequestration of urea and nonurea solutes in renal tissues of rats with hereditary hypothalamic diabetes insipidus: effect of vasopressin and dehydration on the countercurrent mechanism.

Valtin, Heinz

doi:10.1172/jci105348

Cited by 130 publications

(116 citation statements)

References 18 publications

(18 reference statements)

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“…In CDI patients, a strong drive for water reabsorption from dilute urine must exist along the CD that is surrounded by an iso-osmotic interstitium in the cortex and by a hyperosmotic interstitium in the medulla (osmotic pressure is elevated to some extent in the medulla, even in DI [36], as a result of accumulation of sodium chloride). Thus, as soon as dDAVP permeates the CD to water, a large mass of water can be reabsorbed.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Bankir

Fernandes

Bardoux

et al. 2005

Journal of the American Society of Nephrology

121

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In addition to its effect on water permeability, vasopressin, through its V2 receptors (AVPR2), stimulates Na reabsorption in the collecting duct by increasing the activity of the amiloride-sensitive sodium channel ENaC. This study evaluated whether dDAVP (a potent AVPR2 agonist) reduces sodium excretion in healthy humans (n ‫؍‬ 6) and in patients with central (C; n ‫؍‬ 2) or nephrogenic (N) diabetes insipidus (DI) as a result of mutations of either the aquaporin 2 gene (AQP2; n ‫؍‬ 3) or AVPR2 (n ‫؍‬ 10). dDAVP was infused intravenously (0.3 g/kg body wt in 20 min), and urine was collected for 60 min before (basal) and 150 min after the infusion. dDAVP markedly reduced both urine flow rate and sodium excretion in healthy individuals. A reduction in sodium excretion was also observed in CDI and NDI-AQP2 patients but not in NDI-AVPR2 patients. The magnitude of the fall in sodium excretion correlated with the rise in urine osmolality and the fall in urine output but not with the simultaneously observed fall in mean BP. These results suggest that the dDAVP-induced antinatriuresis is due to a direct V2 receptor-dependent stimulation of sodium reabsorption in the collecting duct and is not secondary to a hemodynamic effect. In conclusion, this study reveals a potent V2-dependent antinatriuretic effect of vasopressin in humans. The possibility that an inappropriate stimulation of ENaC by vasopressin might lead to significant sodium retention in chronic situations remains to be determined. 16: 192016: -192816: , 200516: . doi: 10.1681 I nappropriate retention of sodium and water by the kidney is thought to be a key factor in several forms of hypertension. Thus, it is important to identify factors that may favor excessive sodium reabsorption by the kidney. Vasopressin is known to promote water conservation by increasing the permeability to water of the collecting ducts (CD), thus allowing osmotically driven water reabsorption along these ducts when dilute distal tubular fluid enters them in the cortex and later when they traverse the hyperosmotic medulla. However, the effect of vasopressin on sodium excretion is less clear. A large number of studies have shown that vasopressin infusion increases sodium excretion in vivo in rats, dogs, and sheep (e.g., references 1-4). This natriuretic effect is difficult to reconcile with the fact that, in vitro, vasopressin stimulates sodium reabsorption in the isolated perfused CD (5,6), in the amphibian bladder (a tissue that shares a number of similarities with the mammalian CD) (7), and in several cell lines issued from these two tissues (8 -10). This effect on sodium reabsorption is inhibitable by amiloride and has been shown to result from activation of the endothelial sodium channel ENaC (11). Moreover, chronic elevation of vasopressin or infusion of its V2 agonist dDAVP (12) has been shown to increase the abundance of mRNA (13) and protein (14) of the ␤ and ␥ subunits of ENaC and to enhance markedly the subsequent functional response (water and sodium reabsorption) to exoge...

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Section: Discussionmentioning

confidence: 99%

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Bankir

Fernandes

Bardoux

et al. 2005

Journal of the American Society of Nephrology

121

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confidence: 97%

“…Explanation for the mode of action of ADH rests in part upon accurate knowledge of the changes in medullary composition effected by this hormone. Here, there is a clear conflict of evidence between those who find an increased sodium content in medulla in hydropenia and after ADH treatment [Levitin et al, 1962;Saikia, 1965;Cross and Sherrington, 1965] and the claims of Jaenike [1963] and Valtin [1966] that medullary sodium content is not affected by ADH.Thus, in order to throw further light on the rapid changes induced by ADH, the chemical composition of medulla and cortex of rats was analyzed during water diuresis interrupted by ADH. In particular, sodium, potassium, ammonium, urea and water content of six serial slices was studied.…”

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Effects of Vasopressin Upon the Composition of Rat's Kidney

Abedin

1967

Exp Physiol

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The composition of renal medulla and cortex was studied in rats during water diuresis interrupted by lysine-8-vasopressin (ADH), given as a single intravenous injection or by continuous intravenous infusion, in an attempt to mimic the effect of hydropenia.Continuous infusion of 60 ,uu./100 g./min. ADH for 2i hr. (9 mu. in all) raised the osmolality of the medulla and urine to the levels found after 24 hr. of hydropenia, but these values remained lower than values reported after prolonged hydropenia. Infusion of 30 Mu./100 g./min. ADH (4.5 mu. in all) was only slightly less effective. 10 mu./100 g. body weight of ADH given as a single intravenous injection increased the osmolality of medulla less than did continuous infusion of this hormone.Accumulation of sodium in deeper medulla and at the level of thick portion of ascending limb of loop of Henle suggests that ADH may promote transport of sodium from collecting ducts and the thick ascending limb of loop of Henle or the other structures present at these levels. The amount of potassium in the deeper medulla diminished after ADH treatment. Increased amount of water at the level of the ascending limb suggests the possibility of short-circuiting of water at this level; this would partly account for the low water content found in the deeper medulla. Accumulation of urea and ammonium in the medulla is also reported.IT is now abundantly established that elaboration of hypertonic urine is by osmotic abstraction of water from the collecting ducts into a hypertonic medulla, and that ADH is necessary for this process. Apart from this, ADH may bring about changes in the medullary composition. Explanation for the mode of action of ADH rests in part upon accurate knowledge of the changes in medullary composition effected by this hormone. Here, there is a clear conflict of evidence between those who find an increased sodium content in medulla in hydropenia and after ADH treatment [Levitin et al., 1962;Saikia, 1965;Cross and Sherrington, 1965] and the claims of Jaenike [1963] and Valtin [1966] that medullary sodium content is not affected by ADH.Thus, in order to throw further light on the rapid changes induced by ADH, the chemical composition of medulla and cortex of rats was analyzed during water diuresis interrupted by ADH. In particular, sodium, potassium, ammonium, urea and water content of six serial slices was studied. METHODSMale albino rats weighing 280-400 g. (Wistar strain bred in closed colony) were used. In 35 rats water diuresis was induced by continuous intravenous infusion of 2-5 per cent dextrose at the rate of 0 03 ml./min./100 g. into a lateral tail vein. When an amount equivalent to 4 ml./100 g. body weight had been infused, this load was maintained by infusing a volume equal to the volume of urine produced. A diuresis

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“…4 Brattleboro diabetes insipidus rats lack antidiuretic hormone. 5 These rats also have a decreased prostaglandin synthesiz-ing ability compared with the parent stock, Long Evans rats. 67 Treating diabetes insipidus rats with antidiuretic hormone restores prostaglandin production, which suggests that prostaglandin synthesis is enhanced by antidiuretic hormone.…”

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“…3 -20 Medullary plasma flow in the diabetes insipidus rat is high, and the medullary salt gradient is decreased. 5 Therefore, it is possible that the preexistent medullary washout in these animals prevents further changes in water and sodium reabsorption. As a result, pressure natriuresis becomes blunted.…”

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Blunted pressure natriuresis in the Brattleboro diabetes insipidus rat.

et al. 1989

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Antidiuretic hormone is known to stimulate the renal synthesis of prostaglandins. These autacoids, in turn, modulate the pressure natriuresis phenomenon. Accordingly, the present study was done to test the hypothesis that, in the absence of antidiuretic hormone and antidiuretic hormone-dependent prostaglandin synthesis, the pressure natriuresis response is blunted. Experiments were performed on Brattleboro diabetes insipidus rats (n=7) and Long Evans control rats (n=14). A change in perfusion pressure in the Long Evans rats from 89.3±1.0 to 108.7±l.l mm Hg (/?<0.05) was associated with significant increases in the fractional excretion of sodium ( l . l ± 0 . 2 to 2.3±0.3%) and the urinary prostaglandin excretion (32.6±6.8 to 56.6± 10.0 pg/min). In contrast, a similar change in perfusion pressure in the diabetes insipidus rat from 88.6±1.4 to 106.2±1.5 mm Hg (p<0.05) resulted in no significant increases in either sodium or prostaglandin excretions. Treatment of a third group of diabetes msipidus rats (n=9) with l-desamino-8-D-arginine vasopressin (1 /ig/day) restored the natriuretic response to increases in renal perfusion pressure. Treated diabetes insipidus and Long Evans control rats had comparable natriuretic responses to increases in renal perfusion pressure. Untreated diabetes msipidus rats, on the other hand, had blunted responses. In summary, the pressure natriuresis response in diabetes insipidus rats is blunted compared with Long Evans control rats. We conclude that antidiuretic hormone is necessary for the complete expression of the pressure natriuresis response. (Hypertension 1989; 13:322-326) I ncreases in renal perfusion pressure result in increases in urinary sodium excretion, a phenomenon known as pressure natriuresis.1 Since pressure natriuresis occurs in the absence of changes in glomerular filtration rate, renal plasma flow, or the filtered sodium load, it is likely to result from a direct inhibition of tubular sodium transport. 23Pressure natriuresis may be due, at least in part, to the renal prostaglandins. Prostaglandin synthesis inhibition blunts the effect of changes in perfusion pressure on sodium excretion.4 Brattleboro diabetes insipidus rats lack antidiuretic hormone. 5 These rats also have a decreased prostaglandin synthesiz- Received May 2, 1988; accepted November 18, 1988. ing ability compared with the parent stock, Long Evans rats. 67 Treating diabetes insipidus rats with antidiuretic hormone restores prostaglandin production, which suggests that prostaglandin synthesis is enhanced by antidiuretic hormone. 6 For the above reasons, the diabetes insipidus rat offers a unique model for studying the pressure natriuresis phenomenon in the absence of antidiuretic hormonedependent prostaglandin synthesis.Accordingly, the present study was designed to test the hypothesis that the absence of antidiuretic hormone and the resulting decreased prostaglandin synthesis lead to a blunted pressure natriuresis in the diabetes insipidus rat. Materials and MethodsExperiments were performed on male...

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Sequestration of urea and nonurea solutes in renal tissues of rats with hereditary hypothalamic diabetes insipidus: effect of vasopressin and dehydration on the countercurrent mechanism.

Cited by 130 publications

References 18 publications

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Effects of Vasopressin Upon the Composition of Rat's Kidney

Blunted pressure natriuresis in the Brattleboro diabetes insipidus rat.

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