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

Abstract

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.

The effect of hypohydration severity on the physiological, psychological and renal hormonal responses to hypoxic exercise

“…This response to exercise is consistent with other normoxic work, whereby exercise of [60% _ VO 2max is thought to induce renal hormone release through adrenocorticotrophic elevation (Viru 1992). However, hypoxia is thought to suppress ADH (Claybaugh et al 1978) and aldosterone (Bouissou et al 1987) release irrespective of exercise (Zaccaria et al 1998). Plasma osmolality did not significantly alter with exercise, even though it is widely thought plasma osmolality stimulates the release of renal hormones (Takamata et al 2000).…”

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

“…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). In most studies anaesthetized animals and a relatively narrow range of oxygen tensions have been employed.…”

High Altitude Ills: A Malady of Water, Electrolyte, and Hormone Imbalance?

“…Renal water excretion is under the control of arginine vasopressin (AVP), and short-term hypoxia has generally resulted in no change in plasma AVP levels. 1,5,8 However, in two of these studies, some subjects had an increase in plasma AVP levels. 1,5 Only one study has reported the changes in plasma AVP levels during hypoxic exposure in which subjects experienced the spectrum of urine flow responses seen at altitude.…”