Natriuretic response of the rat to plasma concentrations of arginine vasopressin within the physiological range.

Balment, RJ; Brimble, M. J.; Forsling, Mary L.; Musabayane, C T

doi:10.1113/jphysiol.1984.sp015307

Cited by 48 publications

(43 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[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: 99%

“…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%

See 1 more Smart Citation

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Perucca

Bichet²,

Bardoux

et al. 2008

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

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

show abstract

Section: V1ar Effectsmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…Acutely hypophysectomized rats exhibit marked alteration in renal function, characterized by avid retention of sodium (Lichardus & Ponec, 1973;Balment, Brimble, Forsling & Musabayane, 1984). This has been claimed to result from the loss of posterior pituitary factors (Lichardus & Ponec, 1973) but Balment, Brimble, Forsling & Musabayane (1986) were unable to fully restore sodium excretion by administration of neurohypophysial hormone to produce plasma vasopressin and oxytocin levels within the physiological range.…”

Section: Introductionmentioning

confidence: 99%

A synergistic effect of oxytocin and vasopressin on sodium excretion in the neurohypophysectomized rat.

Balment¹,

Brimble²,

Forsling³

et al. 1986

The Journal of Physiology

Self Cite

View full text Add to dashboard Cite

SUMMARY1. Renal function and the effect of oxytocin and vasopressin replacement have been examined in anaesthetized male neurohypophysectomized rats.2. Rates of urine flow were higher but sodium excretion markedly lower in neurohypophysectomized rats than in intact animals receiving hypotonic saline infusion (33-8 + 2-3 vs. 27-0 + 0 7 ml and 472 + 84 vs. 1946 + 124 tmol respectively for the third to sixth hour of study).3. In intact animals, mean arterial blood pressure stabilized at 106 mmHg.Haematocrit (46 %) remained stable but glomerular filtration rates declined slightly over the 8 h of study to 2-5 + 0-2 ml/h. These values in neurohypophysectomized rats did not differ significantly from those in intact rats. 4. Although plasma corticosterone levels (54 + 13 ng/ml) did not differ significantly from those in intact rats, neurohypophysectomy was associated with greatly reduced aldosterone concentration (0-12 +0-03 vs. 0-76 + 0-04 ng/ml). Trace levels of vasopressin (0 17 + 0 03 /u./ml) were found in neurohypophysectomized rat plasma.5. Oxytocin administration at 15 ,u./min, which produced plasma hormone levels of 1 62 + 0 19 ,u./ml, had no detectable effect on sodium excretion but increased urine flow. Arginine vasopressin administration (12 ,u./min) inducing plasma levels of 1-24 + 0-08 ,u./ml, reduced urine flow by 80 % and produced a small increase in sodium excretion.6. Concurrent administration of oxytocin (15 #su./min) potentiated the natriuretic response to vasopressin (12 gu./min). Total sodium excretion during the 3 h combined hormone infusion (1256+149,umol) greatly exceeded that in animals receiving vasopressin alone (549 + 132,mol) and approached that observed in intact animals (1946 + 124,mol). Combined hormone administration at the lower rate of 5 #su./min oxytocin and 4,u./min vasopressin produced a similar large increment in sodium excretion.7. It is concluded that replacement of both neurohypophysial hormones, at plasma levels within the physiological range, largely reverses the renal sodium retention of neurohypophysectomized rats, oxytocin considerably potentiating the natriuretic action of vasopressin. This synergism between the two neurohypophysial R. J. BALMENT AND OTHERS peptides to promote salt excretion may be an important component of the nonsteroidal management of sodium.

show abstract

“…We have previously reported that vasopressin has a natriuretic action at physiological concentrations (Balment et al, 1984), which can be inhibited by V 1 receptor antagonism (Musabayane et al, 1997). Acute chloroquine administration under conditions of volume expansion and euvolaemia increased plasma vasopressin concentrations, as well as increasing Na ϩ excretion (Musabayane et al, 1996).…”

Section: Nitric Oxide Mediates Some Chloroquine Actions 159mentioning

confidence: 99%

The Effect of Chloroquine on Renal Function and Vasopressin Secretion: A Nitric Oxide-Dependent Effect

Ahmed

Ashton²,

Balment³

2003

J Pharmacol Exp Ther

View full text Add to dashboard Cite

We have previously reported that chloroquine administration increases plasma vasopressin concentration and urinary sodium excretion in Sprague-Dawley rats. Because chloroquine has also been shown to stimulate nitric oxide production, the aim of this study was to determine whether nitric oxide mediates chloroquine-induced changes in renal function and secretion of vasopressin. Sprague-Dawley rats (n ϭ 6 -8/group) were infused with 2.5% dextrose under Intraval anesthesia (100 mg kg Ϫ1 i.p.). After 3-h equilibration and a control hour, animals received either vehicle, chloroquine (0.04 mg h Ϫ1 ), N -nitro-Larginine methyl ester (L-NAME) (nitric-oxide synthase inhibitor, 60 g kg Ϫ1 h Ϫ1 ), or combined chloroquine and L-NAME over the next hour. L-NAME or vehicle infusion continued for a further recovery hour. Plasma was collected from a parallel group of animals for vasopressin radioimmunoassay. Chloroquine stimulated a significant increase (p Ͻ 0.05) in urine flow rate, glomerular filtration rate, and sodium excretion over the hour of infusion, in comparison with vehicle-infused rats. These effects continued after cessation of chloroquine, reaching maxima in the following recovery hour. Coadministration of L-NAME abolished these effects, returning all parameters to levels comparable with those in vehicle-infused animals. Chloroquine administration was accompanied by a significant increase (p Ͻ 0.05) in plasma vasopressin, which was also reversed by L-

show abstract

Natriuretic response of the rat to plasma concentrations of arginine vasopressin within the physiological range.

Cited by 48 publications

References 24 publications

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

A synergistic effect of oxytocin and vasopressin on sodium excretion in the neurohypophysectomized rat.

The Effect of Chloroquine on Renal Function and Vasopressin Secretion: A Nitric Oxide-Dependent Effect

Contact Info

Product

Resources

About