Vasopressin in Plasma and Cerebrospinal Fluid of Hydrated and Dehydrated Steers

Doris, Peter A.; Bell, F. R.

doi:10.1159/000123906

Cited by 34 publications

(14 citation statements)

References 34 publications

(62 reference statements)

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“…The fact that plasma AVP was suppressed and CSF AVP was hardly affected supports our earlier study of dehydration in cattle which showed that although plasma AVP and CSF AVP secretion may be activated by the same stimulus, different groups of hypothalamic neurons may be affected differently [11]. Our findings do not support the view that AVP may play a part in the genesis of salt appetite in cattle.…”

Section: Discussioncontrasting

confidence: 73%

“…The All standard (lie5 All) was the WHO standard (National Institute for Biological Standards and Control, MRC, London, UK). AVP was estimated in CSF and plasma, and PRL in plasma, as described earlier [10,11].…”

Section: Methodsmentioning

confidence: 99%

“…Prolactin (PRL) has been proposed as the causal factor in thirst and salt appetite in the rat [22] and man [21], but in cattle during both dehydration and sodium depletion plasma PRL is sup pressed [10]. During dehydration in cattle both plasma argi nine vasopressin (AVP) and cerebrospinal fluid (CSF) AVP secretion increase with rising plasma osmolality [11] as in man, dog and rat [12], Another link between thirst and salt appetite is the view that both behaviours are dependent upon angiotensin II …”

mentioning

confidence: 99%

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Relation of Endogenous Systemic and Brain Angiotensin II, Arginine Vasopressin and Prolactin with the Genesis of Salt Appetite in Cattle

1988

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Angiotensin II (AII), arginine vasopressin (AVP) and prolactin (PRL) were measured by radioimmunoassay in plasma and cerebrospinal fluid (CSF) in concurrent daily samples from conscious unrestrained steers. Packed cell volume, [Na+] and osmolality were also measured from these samples. Salt appetite was assessed during a 5-min daily session of operant conditioning. Food and water was always available. Unilateral parotid duct fistulation was effected under xylazine analgesia and halothane/Ch anaesthesia. To prevent a sodium deficit developing from loss of [Na+] in the extruded saliva, 0.3 M NaHC0₃ was available ad libitum so that each animal could ingest sufficiently to balance the salivary loss. A week later epidural cannulae were implanted in the cisternae magna using the same anaesthesia. Three days afterwards when the saliva [Na] was 78 mmol/l, the 0.3-M NaHCO3 supplement was withdrawn for 7 days so that sodium deficiency developed to a degree which evoked salt appetite. When the NaHC0₃ supplement was restored ad libitum, all aspects of [Na⁺] deficiency and salt appetite were completely ameliorated within 2–3 days. Packed cell volume increased and body weight decreased (p < 0.05) during depletion, but rapidly returned to normal on day 2 of repletion. Both plasma and CSF osmolality were reduced during depletion as were plasma [Na⁺] (p < 0.01) and CSF [Na⁺] (p < 0.001). From a basal value of 64.7 ± 9.35 fmol/ml on day 0, plasma AII increased to 229.2 ± 46.65 fmol/ml (p < 0.001) on day 3, prior to the onset of salt appetite on days 4–7. In marked contrast to plasma AII during sodium depletion, CSF AII was unchanged during salt appetite. There was no correlation between plasma and CSF AII during behavioural salt appetite. The CSF AII suggests slight plasma ‘escape’ via circumventricular organs rather than synthesis in the brain, but is not correlated with salt appetite. The effect of sodium depletion on plasma AVP and plasma PRL was to suppress plasma levels consistent with the homeostatic response arising from sodium deficiency. In cattle the perturbations of endogenous neuropeptides evoked during sodium deficit arise from physiological homeostatic responses and are not directly related to salt appetite.

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Section: Discussioncontrasting

confidence: 73%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Relation of Endogenous Systemic and Brain Angiotensin II, Arginine Vasopressin and Prolactin with the Genesis of Salt Appetite in Cattle

1988

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“…A number of investigations have demonstrated that water deprivation causes increased electrolyte excretion and a negative sodium balance in ruminants (sheep, cattle and camels) (Siebert & Mafarlane, 1975;McKinley, Denton, Nelson & Weisinger, 1983 a, b;Doris & Bell, 1984) and monogastric mammals (rats, rabbits and dogs) (McKinley et al 1983a, b;Metzler, Thrasher, Keil & Ramsay, 1986). This response appears physiologically relevant, in that it protects against further increases in plasma Na+ and osmolality.…”

Section: Dehydration-induced Natriuresis and Na+ Statusmentioning

confidence: 99%

The struggle to maintain hydration and osmoregulation in animals experiencing severe dehydration and rapid rehydration: the story of ruminants

Silanikove¹

1994

Experimental Physiology

121

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Ruminants in tropical and desert areas routinely experience cycles of severe dehydration and rapid rehydration. These animals can withstand severe dehydration (18‐40% of initial body weight), which exceeds considerably the capacity of most monogastric mammals. This capacity is related to their ability to use, during the course of dehydration, their large water reservoir in the rumen, which contributes 50‐70% of the total water loss. As rumen fluid is in approximate isotonicity with systemic fluid, the utilization of gut water during the course of dehydration involves a considerable load of sodium and potassium. Consequently, the effectiveness of utilization of rumen fluid during dehydration depends on the capacity of the kidney to ‘desalt’ the water absorbed from the gut and on maintenance of salivary flow to the rumen. Following rehydration, ruminants can imbibe their entire water deficit in one drinking and the entire amount ingested is first retained in the rumen. The rumen volume at this stage may exceed the extracellular fluid volume and the sudden drop in rumen osmolality creates a huge osmotic gradient (200‐300 mosmol kg‐1) between the rumen and systemic fluid. Ruminant animals are confronted at this stage by two opposing tasks, each of them of vital importance: (i) the need to prevent the osmotic hazard leading to water intoxication; and (ii) the need to retain the ingested water, so that it is not missing for the next dehydration cycle. The most prevalent view until recently was a theory which attributes an osmotic protective mechanism to the rumen wall. However, such a capacity has not yet been demonstrated and is challenged by contradictory observations that large amounts of water are absorbed from the rumen following rehydration. The view that is most consistent with available information is that gustatory‐alimentary and hepatoportal signals regarding the presence of large amounts of water in the rumen and the absorption of water from the gut activate a range of homeostatic responses involved in fluid and sodium restitution. The efferent elements, presumably activated by the CNS, include: a dramatic increase in secretion of hypotonic saliva and, reciprocally, a dramatic drop in urine flow. The enhanced saliva secretion recycles a considerable portion of the water absorbed from the gut back to the rumen, which allows effective retention of water while avoiding the danger of osmotic threat to the red blood cells. The enhanced saliva secretion also drains large amounts of sodium and bicarbonate from the blood. Accompanying responses are marked retention of sodium and carbonic acid in the kidney.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…It has been reported that the plasma AVP concentration increases after water deprivation in human subjects as well as animals (Doris and Bell 1984;Kirkland et al, 1984;Rockhold et al, 1984). Recently, Williams et al (1986) showed that fluid restriction for 5 days leads to a significant increase in both plasma and 24-h urinary AVP.…”

Section: Discussionmentioning

confidence: 99%

Effects of Sodium Depletion and Orthostasis on Plasma and Urinary Vasopressin in Normal Subjects.

et al. 1989

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We investigated the effects of sodium depletion and orthostasis on the plasma concentration and urinary excretion of vasopressin (AVP) in eight normal female subjects. After 4 days on a sodium controlled diet (130 mEq/ day), the subjects were placed on a low sodium diet (30 mEq/day) for 3 days and 120mg of furosemide was administered orally on the first day of the low sodium regimen.Sodium depletion in the present study reduced body weight by 1.6 kg and increased hematocrit by 3.5%.A significant (p<0.05) increase in plasma AVP and a significant (p<0.05) decrease in 24-h urinary excretion of AVP were observed during sodium depletion.One-hour ambulation significantly increased plasma AVP in both control and sodium depleted phases (p<0.01).The percent change in plasma AVP tended to correlate with that in mean blood pressure in the control phase (r= 0.69, 0.05

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Vasopressin in Plasma and Cerebrospinal Fluid of Hydrated and Dehydrated Steers

Cited by 34 publications

References 34 publications

Relation of Endogenous Systemic and Brain Angiotensin II, Arginine Vasopressin and Prolactin with the Genesis of Salt Appetite in Cattle

Relation of Endogenous Systemic and Brain Angiotensin II, Arginine Vasopressin and Prolactin with the Genesis of Salt Appetite in Cattle

The struggle to maintain hydration and osmoregulation in animals experiencing severe dehydration and rapid rehydration: the story of ruminants

Effects of Sodium Depletion and Orthostasis on Plasma and Urinary Vasopressin in Normal Subjects.

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