The Value of Rats With Hereditary Hypothalamic Diabetes Insipidus for the Bioassay of Vasopressin

Jones, Janet; Lee, J.

doi:10.1677/joe.0.0370335

Cited by 25 publications

(13 citation statements)

References 12 publications

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“…The ADA of the pituitaries of DI rats is of the order that would be expected from the pituitary oxytocin content (Jones & Lee, 1967) except in one rat (L55 4TR). The antidiuretic response to pituitary extracts 4 On the basis of the pituitary antidiuretic activity, it is considered that this rat was wrongly classified (see Discussion).…”

Section: Resultsmentioning

confidence: 83%

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The effect of vasopressin (Pitressin) administration and dehydration on the concentration of solutes in renal fluids of rats with and without hereditary hypothalamic diabetes insipidus

Lee¹,

Williams²

1972

The Journal of Physiology

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SUMMARY1. The method of sequential centrifugation has been used to obtain fluid samples from both the renal papilla and inner medulla of the rat.2. Experiments were carried out on Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI; homozygous recessive), and on their (heterozygous) litter-mates with normal quantities of neurohypophysial vasopressin. Initial classification of the animals by measurement of urine volume and osmolality was confirmed by post-mortem bio-assay of the pituitary glands, in thirty-five out of forty-seven animals.3. In rats with DI, urine osmolalities comparable to those of heterozygous rats were obtained after four daily injections of 1 u. Pitressin Tannate in Oil (PTO). Under these conditions, when dehydration was superimposed for 72 hr, urine osmolality did not increase markedly. In heterozygous rats dehydrated for the same period of time, urine osmolality increased by some twofold.4. In rats with DI, the administration of PTO induced a rise of both sodium and urea concentrations in renal fluids and in urine. Dehydration during PTO administration caused a further rise of urea concentrations only. Dehydration per se significantly raised urinary and renal fluid urea concentrations, but sodium concentrations did not rise.5. In heterozygous rats dehydration per se increased both urea and sodium concentrations in renal fluids and urine.6. The evidence is discussed that the action of vasopressin involves factors apart from increasing the permeability of the distal nephron to water and urea. t M.R.C. Scholar.

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Section: Resultsmentioning

confidence: 83%

“…The glands were treated with acetic acid to release neurohypophysial peptides; the extracts were assayed for vasopressin using a modification of the ethanol-anaesthetized rat preparation. These procedures have been described by Jones & Lee (1967) and Forsling, Jones & Lee (1968). Statistics.…”

Section: Methodsmentioning

confidence: 99%

The effect of vasopressin (Pitressin) administration and dehydration on the concentration of solutes in renal fluids of rats with and without hereditary hypothalamic diabetes insipidus

Lee¹,

Williams²

1972

The Journal of Physiology

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“…6 shows, however, even 28 days of treatment failed to raise this go down an osmotic gradient from the papillary tip toward the medulla in order to obtain enough tissue for analysis. This methodological error must have been minimized when papillary osmolality was determined after 3 days of treatment, for the interstitial osmotic gradient is much less steep when less concentrated urine is formed (22 (24)(25)(26). Furthermore, contrary to the expectation if enzyme adaptation were involved, the sensitivity of the bioassay cannot be enhanced by prior prolonged treatment with exogenous vasopressin (25).…”

Section: Resultsmentioning

confidence: 99%

Impaired urinary concentration after vasopressin and its gradual correction in hypothalamic diabetes insipidus

Harrington¹,

Valtin²

1968

J. Clin. Invest.

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A B S T R A C T This study utilized rates with hereditary hypothalamic diabetes insipidus (D.I.) in order to explore possible mechanisms which prevent full urinary concentration after acute administration of vasopressin in hypothalamic D.I. and which correct this concentrating defect with prolonged therapy.It was found: (a) that the concentrating defect persisted even when the urinary osmolal excretion of D. I. rats was reduced to that of normal animals; (b) that the defect was not corrected more rapidly if larger doses of vasopressin were given; (c) that it persisted even when the D.I. rats were deprived of drinking water after vasopressin was given; (d) that there was osmotic equilibration between urine and renal papilla at a time when the concentrating defect was still evident; and (e) that the correction of the defect was associated with progressive and significant rise of the papillary osmolality.These studies appear to rule out osmotic diuresis, accumulation of exogenous vasopressin, persistent primary polydipsia, or delay in the induction of membrane permeability as causes for the concentrating defect. Rather, subnormal osmolality of the renal papilla, which can be corrected only gradually, accounts for the initial concentrating Dr. Harrington's present address is

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“…However, the results of chronic experiments such as these are obviously not directly comparable with those of the present investigation in which the period studied after haemorrhage was of relatively short duration. The mean prehaemorrhage plasma vasopressin concentration in the Long Evans rats was relatively high, presumably because of anaesthesia and the stress of surgery (Bonjour & Malvin, 1970 (Valtin, Sawyer & Sokol, 1965;Jones & Lee, 1967;Lee & Williams, 1972), and since oxytocin has measurable antidiuretic activity if released in sufficient quantity (Bisset & Lewis, 1962), the present finding supports the view that haemorrhage stimulates the independent release of vasopressin (Chaudhury & Walker, 1958;Ginsburg & Smith, 1959;Beleslin et al 1967;Schrier, Verroust, Jones, Fabian, Lee & de Wardener, 1968).…”

Section: Discussionmentioning

confidence: 99%

The role of vasopressin in blood pressure regulation immediately following acute haemorrhage in the rat

Laycock¹,

Penn²,

Shirley³

et al. 1979

The Journal of Physiology

112

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SUMMARY1. The possible pressor effect of vasopressin immediately after acute haemorrhage has been studied using anaesthetized Brattleboro rats with diabetes insipidus and rats of the Long Evans parent strain.2. A blood loss of 0.5 % of the body weight caused a significant decrease in mean arterial blood pressure, measured 10 min later, in Brattleboro rats, whereas this degree of haemorrhage was non-hypotensive in the control Long Evans rats.Following subsequent blood losses (each of 0-5 % of the body weight), mean arterial blood pressure in Brattleboro rats was always significantly lower than in Long Evans rats.3. While no antidiuretic activity was at any time found in the plasma of Brattleboro rats, haemorrhages greater than 1 % of the body weight were associated with marked increases in plasma arginine vasopressin (AVP) of Long Evans rats. 4. When Brattleboro and Long Evans rats were subjected to a single haemorrhage of 2 % of the body weight, the immediate decrease in arterial blood pressure was similar in the two groups. However, 5 and 10 min after the haemorrhage the arterial blood pressure was significantly higher in the Long Evans rats. When vasopressin was infused into Brattleboro rats so that plasma levels of the hormone approached those found in Long Evans rats, the mean arterial blood pressure 0, 5 and 10 min after haemorrhage was similar to that in the Long Evans animals. 5. It is concluded that in the anaesthetized rat, vasopressin plays an important role in the regulation of arterial blood pressure during the period immediately following acute haemorrhage.

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The Value of Rats With Hereditary Hypothalamic Diabetes Insipidus for the Bioassay of Vasopressin

Cited by 25 publications

References 12 publications

The effect of vasopressin (Pitressin) administration and dehydration on the concentration of solutes in renal fluids of rats with and without hereditary hypothalamic diabetes insipidus

The effect of vasopressin (Pitressin) administration and dehydration on the concentration of solutes in renal fluids of rats with and without hereditary hypothalamic diabetes insipidus

Impaired urinary concentration after vasopressin and its gradual correction in hypothalamic diabetes insipidus

The role of vasopressin in blood pressure regulation immediately following acute haemorrhage in the rat

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