A method for the assay of very small amounts of antidiuretic activity with a note on the antidiuretic titre of rats' blood

Dicker, S. E.

doi:10.1113/jphysiol.1953.sp004986

Cited by 138 publications

(70 citation statements)

References 11 publications

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“…After centrifugation the supernatant fluid was assayed for its antidiuretic activity, by intravenous injection into rats in ethanol anaesthesia, with a constant water load (Dicker, 1953). Each assay consisted of four injections, two doses of the standard and two of the unknown, the ratio, high to low dose, being the same for standard and unknown solutions.…”

Section: Methodsmentioning

confidence: 99%

The degree of inactivation of the antidiuretic activity of vasopressin by the kidneys and the liver of rats

Dicker¹,

Greenbaum²

1954

The Journal of Physiology

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Heller (1937) Heller's (1937) conclusions that 'as the amount of hormone injected is increased the proportion of the hormone which is excreted in the urine decreases'. This would suggest that glomerular filtration might be a contributory factor, as the filtration rate of rabbits would be very small after large doses.More recently it has been found that in rats infused with amounts of vasopressin ranging from 300 to 1500 ,uU/100 g, the antidiuretic activity of the urine was equivalent to 8.1 + 1-23 % of the dose administered (Dicker, 1954).The antidiuretic activity present in the urine was unaffected by the height of the water load, and hence by changes in glomerular filtration or by the rate of urine flow. In hypophysectomized dogs, O'Connor (1951) showed that the rate of excretion of antidiuretic activity in the urine was equivalent to 12 % of the rate at which vasopressin was infused, and was, as in rats, independent of the volume of urine excreted. Finally, in man, the antidiuretic activity of the urine was found to be equivalent to 12-8 % of the amount of vasopressin infused (Noble & Taylor, 1953). There can thus be little doubt that the antidiuretic activity found in the urine could account for only 10 % of the activity of the vasopressin administered. Therefore vasopressin antidiuretic activity is largely destroyed in the body. This paper is concerned with the nature of this inactivation process, and incidentally demonstrates that the small amount of

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Section: Methodsmentioning

confidence: 99%

The degree of inactivation of the antidiuretic activity of vasopressin by the kidneys and the liver of rats

Dicker¹,

Greenbaum²

1954

The Journal of Physiology

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“…Measurement of urine outflow and urine osmotic pressure: Urine outflow was measured by the method of Dicker (21), with some modifications (8-10). The rats were starved overnight for approx.…”

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confidence: 99%

Antidiuretic Effects of Methionine-Enkephalin and 2-D-Alanine-5-Methionine-Enkephalinamide Microinjected into the Hypothalamic Supraoptic and Paraventricular Nuclei in a Water-Loaded and Ethanol-Anesthetized Rat

Tsushima

Mori

Matsuda

1986

Japanese Journal of Pharmacology

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Abstract-Effects of methionine-enkephalin (ME) and 2-D-alanine-5-methionine enkephalinamide (DAMEA) microinjected into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, which contain neurons synthesizing and releasing antidiuretic hormone, upon the outflow and the osmotic pressure of urine and the other visceral functions were studied in a rat which was loaded with water and anesthetized with ethanol. These opioid peptides when microinjected into the SON or PVN induced potent antidiuretic effects in dose-dependent and time dependent manners with no significant effects on the other visceral functions. The approx. ED50 values for DAMEA were 1.3 (in the SON) and 0.7 (in the PVN) nmol, and the values for ME were 110 (in the SON) and 60 (in the PVN) nmol. The antidiuretic effects showed slow onset and long duration, with a minimal urine outflow at approx. 0.5 hr after microinjection and an approx. 2 hr-duration. The effects induced by the opioid peptides were inhibited by pretreatment with naloxone or atropine, without effects of pretreatment with alpha or beta-adrenoceptor antagonists, suggesting that the antidiuretic effects were mediated through an opioid receptor having low sensitivity to naloxone and also possibly mediated through a muscarinic receptor which was stimulated probably by the ACh released by the opioid peptides.

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“…This method of extraction was found to give a recovery of 80% ADH in controls and results were modified accordingly. The ADH in the eluate was estimated by the antidiuretic assay method in rats (Dicker, 1953). Arginine-vasopressin (Pitressin, Parke-Davis) was used as a standard in the bioassay.…”

Section: Methodsmentioning

confidence: 99%

Central Mechanism of Vasopressin‐induced Changes in Antidiuretic Hormone Release

Bhargava

Kulshrestha

Srivastava

1977

British J Pharmacology

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A method for the assay of very small amounts of antidiuretic activity with a note on the antidiuretic titre of rats' blood

Cited by 138 publications

References 11 publications

The degree of inactivation of the antidiuretic activity of vasopressin by the kidneys and the liver of rats

The degree of inactivation of the antidiuretic activity of vasopressin by the kidneys and the liver of rats

Antidiuretic Effects of Methionine-Enkephalin and 2-D-Alanine-5-Methionine-Enkephalinamide Microinjected into the Hypothalamic Supraoptic and Paraventricular Nuclei in a Water-Loaded and Ethanol-Anesthetized Rat

Central Mechanism of Vasopressin‐induced Changes in Antidiuretic Hormone Release

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