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Houpt, K. A., Northrup, N., Wheatley, T., & Houpt, T. R. (1991). Thirst and salt appetite in horses treated with furosemide. J Appl Physiol, 71(6), 2380–2386.
Abstract: When a preliminary experiment in sodium-replete ponies revealed an increase, but not a significant increase, in salt consumption after furosemide treatment, the experiment was repeated using sodium-deficient horses in which aldosterone levels might be expected to be elevated to test the hypothesis that a background of aldosterone is necessary for salt appetite. Ten Standardbred mares were injected intravenously with furosemide or an equivalent volume of 0.9% sodium chloride as a control to test the effect of furosemide on their salt appetite and blood constituents. Sodium intake and sodium loss in urine, as well as water intake and urine output, were measured and compared to determine accuracy of compensation for natriuresis and diuresis. Plasma protein and packed cell volume showed significant increases in response to furosemide treatment (F = 29.31, P less than 0.001 and F = 11.20, P less than 0.001, respectively). There were no significant changes in plasma sodium concentration or osmolality in response to the treatment (P greater than 0.05). The furosemide-treated horses consumed 126 +/- 14.8 g salt, significantly more than when they were given the control injection (94.5 +/- 9.8 g; t = 2.22, P = 0.05). In response to furosemide, horses lost 962 +/- 79.7 and consumed 2,170 +/- 5 meq sodium; however, compared with control, they lost 955 meq more sodium and ingested only 570 meq more sodium, so they were undercompensating for natriuresis. The furosemide-treated horses drank 9.6 +/- 0.8 kg of water, significantly more than when they received the control injection (6.4 +/- 0.8 kg; t = 6.9, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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Houpt, K. A., Thornton, S. N., & Allen, W. R. (1989). Vasopressin in dehydrated and rehydrated ponies. Physiol. Behav., 45(3), 659–661.
Abstract: Six pony mares deprived of water for 24 hours showed significant increases in plasma vasopressin (2.8 pg/ml) and osmolality (9 mosmol/kg). When water was made available the ponies drank rapidly (5 of 6 drank to satiety within 90 seconds) and corrected their fluid deficits precisely. Vasopressin did not return to predehydration levels until osmolality did after 15 minutes of access to water. The horse differs from rodents and humans, but is similar to pigs in that vasopressin levels do not fall before osmolality returns to normal. Oropharyngeal factors, therefore, may not be as important in vasopressin release in horses as in other species.
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