Antidiuretic effect of endogenous oxytocin in dehydrated Brattleboro homozygous rats

Edwards, B. R.; Larochelle, F. T.

doi:10.1152/ajprenal.1984.247.3.f453

Cited by 33 publications

(32 citation statements)

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“…71,72 It has also been shown previously that oxytocin-induced AQP2/water channel mobilization occurs, in parallel with an oxytocininduced antidiuresis in Brattleboro rats. [73][74][75] However, we were unable to detect any significant change in plasma oxytocin levels in CT-treated rats. Likewise, GFR is slightly but not significantly increased by acute CT treatment of "hormone-deprived" Brattleboro rats, 16 suggesting that changes in GFR are not responsible for the CT effect on urine concentration.…”

Section: Discussioncontrasting

confidence: 66%

Calcitonin Has a Vasopressin-like Effect on Aquaporin-2 Trafficking and Urinary Concentration

Bouley¹,

Lu²,

Nunes³

et al. 2011

Journal of the American Society of Nephrology

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The most common cause of hereditary nephrogenic diabetes insipidus is a nonfunctional vasopressin (VP) receptor type 2 (V2R). Calcitonin, another ligand of G-protein-coupled receptors, has a VP-like effect on electrolytes and water reabsorption, suggesting that it may affect AQP2 trafficking. Here, calcitonin increased intracellular cAMP and stimulated the membrane accumulation of AQP2 in LLC-PK1 cells. Pharmacologic inhibition of protein kinase A (PKA) and deficiency of a critical PKA phosphorylation site on AQP2 both prevented calcitonin-induced membrane accumulation of AQP2. Fluorescence assays showed that calcitonin led to a 70% increase in exocytosis and a 20% decrease in endocytosis of AQP2.Immunostaining of rat kidney slices demonstrated that calcitonin induced a significant redistribution of AQP2 to the apical membrane of principal cells in cortical collecting ducts and connecting segments but not in the inner stripe or inner medulla. Calcitonin-treated VP-deficient Brattleboro rats had a reduced urine flow and two-fold higher urine osmolality during the first 12 hours of treatment compared with control groups. Although this VP-like effect of calcitonin diminished over the following 72 hours, the tachyphylaxis was reversible. Taken together, these data show that calcitonin induces cAMP-dependent AQP2 trafficking in cortical collecting and connecting tubules in parallel with an increase in urine concentration. This suggests that calcitonin has a potential therapeutic use in nephrogenic diabetes insipidus.

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Section: Discussioncontrasting

confidence: 66%

Calcitonin Has a Vasopressin-like Effect on Aquaporin-2 Trafficking and Urinary Concentration

Bouley¹,

Lu²,

Nunes³

et al. 2011

Journal of the American Society of Nephrology

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“…In addition there is a linear relationship between OXY secretion and plasma osmolality in the rat, the plot of hormone concentration against osmolality being parallel to that of AVP (Forsling & Brimble, 1985). The physiological significance of these findings may lie in the reports that OXY release during dehydration in the Brattleboro rat causes a natriuresis and a weak antidiuretic response (Edwards & LaRochelle, 1984), and that OXY at physiological levels can act synergistically with exogenous AVP to reverse renal sodium retention in the neurohypophysectomized rat (Balment, Brimble, Forsling, Kelly & Musabayane, 1986b). Therefore, not only may OXY act synergistically with AVP in body fluid regulation, but these experiments confirm that they are released simultaneously and in the same relative amounts in response to elevated CSF tonicity.…”

Section: Discussionmentioning

confidence: 79%

The vasopressin response to centrally administered hypertonic solutions in the conscious rat.

Wells

Forsling

Windle

1990

The Journal of Physiology

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SUMMARY1. Intracerebroventricular (i.cv.) injections of isotonic and hypertonic solutions into the dorsal (D3V) and ventral (V3V) third ventricle were employed to examine the release of vasopressin (AVP) and the mean arterial pressure (MAP) response to elevated cerebrospinal fluid (CSF) osmolality in the conscious rat.2. The D3V injection of hypertonic sodium chloride solution was associated with a concentration-dependent, transient increase in plasma AVP concentration and MAP.3. The D3V injection of 5 Al 0-85 M-sodium chloride elicited a 7-fold increase in plasma AVP and oxytocin concentrations, but had no effect on plasma ACTH concentration. The D3V injection of I -I M-mannitol in 0 15 M-sodium chloride had no effect on plasma AVP concentration or MAP. However, the D3V injection of 0 746 M-mannitol in 0 4 M-sodium chloride elicited a significant transient increase in plasma AVP, but had no effect on MAP.4. The V3V injection of 5 Al 0f85 M-sodium chloride elicited a prolonged increase in plasma AVP concentration and a transient increase in MAP. The V3V injection of 5 1I11-M-mannitol in 0 15 M-sodium chloride elicited an equal, but transient, increase in plasma AVP concentration, but had no effect on MAP.5. The pressor effect of a D3V injection of 0-85 M-sodium chloride was unaffected by prior administration of the V1 (pressor) receptor antagonist (fl-mercapto-fl,flcyclopentamethylene propionyll, 0-Me-Tyr2, Arg8)-vasopressin. 6. These results indicate that osmotically induced AVP secretion may be mediated by both sodium receptors and osmoreceptors, although expression of the response may depend upon the maintenance of a 'permissive' concentration of sodium in the CSF.7. It appears also that the pressor effect is not due to increased plasma AVP concentration, but only results from elevation of the CSF sodium concentration.

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“…There is already evidence that such a natriuretic factor might be structurally related to, if not identical with, the posterior pituitary hormones. Oxytocin appears to be responsible for the natriuresis associated with water deprivation in the vasopressin-deficient Brattleboro rat (Edwards & La Rochelle, 1984). Cort, Rudinger, Lichardus & Hagemann (1966) reported that the natriuretic response to carotid occlusion in the cat could be inhibited by oxytocin antagonists and Sedlakova, Lichardus & Cort (1969) concluded that the natriuretic factor was a small peptide of similar size to vasopressin.…”

Section: Discussionmentioning

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

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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.

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Antidiuretic effect of endogenous oxytocin in dehydrated Brattleboro homozygous rats

Cited by 33 publications

References 0 publications

Calcitonin Has a Vasopressin-like Effect on Aquaporin-2 Trafficking and Urinary Concentration

Calcitonin Has a Vasopressin-like Effect on Aquaporin-2 Trafficking and Urinary Concentration

The vasopressin response to centrally administered hypertonic solutions in the conscious rat.

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

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