Urine output and blood ADH in rats under different grades of hypoxia

Subramanian, Raju; Bhatia, B.; SlDDIQUI, H.H.

doi:10.1016/b978-0-08-021210-4.50055-1

Cited by 2 publications

(5 citation statements)

References 15 publications

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“…More severe hypoxia, 11-1% 02, lowered the concentration of ADH in seven out of the eight subjects, but the mean reduction was not as great and the effect was not statistically significant. These results suggest a possible dose-dependent effect of hypoxia on the release of ADH, which is similar to the observa¬ tions of Subramanian et al (1975) on rats exposed to mild and severe hypoxia for 6 h as a result of hypobaria. In their experiments, the severity of hypoxia was extended to about Percentage of oxygen in gas mixture Fig.…”

Section: Resultssupporting

confidence: 73%

“…introduction It has been suggested that the diuresis which develops during mild hypoxia is a result of a reduced concentration of antidiuretic hormone (ADH) in the plasma which is due to an increase in the volume of blood in the thorax arising from hyperventilation induced by hypoxia (Singh, Malhotra, Khanna, Nanda, Purshottam, Upadhyay, Radhakrishnan & Brahmachari, 1974). A reduction in the concentration of ADH in the plasma response to mild hypoxia has been recently demonstrated in rats (Subramanian, Bhatia & Siddiqui, 1975); other work, however, would suggest that the release of ADH was stimulated by hypoxia. For instance, in artificially ventilated, anaesthetized dogs (Forsling & Ullman, 1974) and in foetal sheep (Alexander, Forsling, Martin, Nixon, Ratcliffe, Redstone & Turnbridge, 1972), hypoxia stimulates the release of ADH, probably by stimulation of chemoreceptors (Share & Levy, 1966).…”

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confidence: 99%

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Response of Antidiuretic Hormone to Acute Exposure to Mild and Severe Hypoxia in Man

Claybaugh¹,

Hansen²,

Woźniak³

1978

Journal of Endocrinology

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Eight men, 19-35 years of age, breathed 20.9% (normal oxygen), 13.9% (mild hypoxia) or 11.1% (severe hypoxia) oxygen in nitrogen gas mixtures during three 20 min periods, which were separated by 1 h recovery periods. The order in which the gas mixtures were breathed was random. The partial pressure of oxygen decreased from a mean of 93.5 during exposure to normal oxygen to 53.9 and 36.7 mmHg during mild and severe hypoxia respectively. There were corresponding decreases in haemoglobin saturation. The partial pressure of carbon dioxide was lower and the pH higher during severe hypoxia than during exposure to normal oxygen. There were no changes in the plasma osmolality or in the concentrations of sodium or potassium in the plasma. There was a tendency for both the renin activity and the concentration of aldosterone in the plasma to decrease progressively as the percentage of oxygen breathed decreased. Unlike severe hypoxia, mild hypoxia suppressed the concentration of antidiuretic hormone (ADH) in the plasma of all subjects by about 59%; during severe hypoxia the reduction was not significant, being only about 33%. These data are consistent with the suggestion that the effect of hypoxia on the release of ADH is dependent on the level of hypoxia.

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Section: Resultssupporting

confidence: 73%

mentioning

confidence: 99%

Response of Antidiuretic Hormone to Acute Exposure to Mild and Severe Hypoxia in Man

Claybaugh¹,

Hansen²,

Woźniak³

1978

Journal of Endocrinology

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“…Variations in the results could also be accounted for in terms of the different methods of inducing hypoxia as well as differing basal neurohypophysial activity. Using a bioassay technique Subramanian et al (1975) noted a basal value of 6·7+0·2µ ./ 1 vasopressin, considerably higher than the resting values in the present study. No details of electrolyte concentrations in urine and plasma were given.…”

Section: Discussioncontrasting

confidence: 72%

“…Subramanian et al (1975) concluded that in the normally hydrated rat moderate hypoxia led to a reduction in plasma vasopressin concentrations and a diuresis whereas severe hypoxia (lowering atmospheric pressure to below 307 mmHg, equivalent to 8-5% oxygen) led to increased plasma vasopressin concentrations. It is difficult to compare the two studies as Subramanian et al (1975) made no measurements of blood gas tensions. Variations in the results could also be accounted for in terms of the different methods of inducing hypoxia as well as differing basal neurohypophysial activity.…”

Section: Discussionmentioning

confidence: 98%

“…Many studies on the effect of hypoxia have yielded conflicting results. Such results appear to depend on whether direct estimates of vasopressin have been made rather than measurements of urine flow, the degree of hypoxia (Stickney, Northup & Van Liere, 1946;Subramanian, Bhatia & Siddiqui, 1975), whether conscious or anaesthetized animals were employed and the nature of the anaesthetic (Forsling, Ingram & Stanier, 1980). In general, hypoxia has little effect on vasopressin release in man (Baylis, Stockley & Heath, 1977;Forsling & Milledge, 1977: Claybaugh, Hansen & Wozniak, 1978), but appears to stimulate release in other animals (Share & Levy, 1966;Anderson, Pluss, Berns, Jackson, Arnold, Schrier & McDonald, 1978).…”

Section: Introductionmentioning

confidence: 88%

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Release of vasopressin in response to hypoxia and the effect of aminergic and opioid antagonists

Forsling¹,

Aziz²

1983

Journal of Endocrinology

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Plasma vasopressin, arterial blood gas tensions, pH, arterial blood pressure, heart rate and respiration were monitored in conscious rats breathing room air or exposed to varying degrees of hypoxia. A similar series of observations was made in a group of anaesthetized rats and in rats treated with alpha- and beta-adrenergic and dopaminergic blocking agents. The effect of two opioid antagonists on the vasopressin response was also noted. Hypoxia produced an increase in circulating vasopressin concentrations in both conscious and anaesthetized rats. In the conscious animals the increase reached statistical significance when the animals were exposed to 12% oxygen in nitrogen, which produced a fall in arterial PaO2 of 44.7 +/- 5.0%. Guanethidine, phentolamine and propranolol all produced a significant fall in the basal concentrations of vasopressin, while guanethidine, phenoxybenzamine and propranolol blocked the increase seen on breathing 12% oxygen in nitrogen. Naloxone and levallorphan also reduced the vasopressin response to hypoxia. Thus it appears that aminergic pathways play a role in the maintenance of circulating concentrations of vasopressin and in the response to hypoxia. Endogenous opioids also appear to be involved in the hypoxic response.

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Urine output and blood ADH in rats under different grades of hypoxia

Cited by 2 publications

References 15 publications

Response of Antidiuretic Hormone to Acute Exposure to Mild and Severe Hypoxia in Man

Response of Antidiuretic Hormone to Acute Exposure to Mild and Severe Hypoxia in Man

Release of vasopressin in response to hypoxia and the effect of aminergic and opioid antagonists

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