Effects of 30 min intense hay‐feeding on acid/base and sodium homeostasis were studied in semi‐starved goats during hyper‐ and euhydration. Parallel analyses of carotid and jugular blood samples revealed that feeding induced metabolic acidosis, which to some extent was subjected to respiratory compensation. The acidosis was accompanied by renal sodium retention and urinary acidification persisting for 2–3 h. The sodium retention was succeeded by an increase in renal Na excretion above the initial level. This natriuresis was most accentuated during hyperhydration. Blood samples taken for hormone assays during euhydration revealed a 15% increase in haematocrit and a significant rise in plasma aldosterone at termination of feeding. Inhibition of the water diuresis in hyperhydrated animals, and moderate increases in renal arginine vasopressin (AVP) excretion and plasma AVP were inconsistent effects of feeding. It is concluded, that simply jugular vein blood provides reliable information on the acid/base status of goats, but that the feeding schedule has to be considered in all experiments where small ruminants are used to investigate the integrated control of acid/base and sodium homeostasis.

Hyperhydrated goats were exposed to an environmental temperature of 45 degrees C (relative humidity 70%) for 120 min. After 90 min, rectal temperature and respiratory frequency reached plateau levels of 40.5 degrees C and 280 respirations min-1, respectively. Measurements of arterial and venous blood acid-base parameters revealed that respiratory alkalosis had started to develop after 60 min, and had become obvious at the end of the heat exposure period. Renal compensation (evidenced by gradual increases in urinary pH and renal Na excretion) developed in parallel with the respiratory alkalosis. The heat exposure elicited a moderate, temporary inhibition of the water diuresis, but no obvious increase in the renal excretion of arginine vasopressin (antidiuretic hormone, ADH). Preliminary determinations of plasma aldosterone did not show any change during the actual heat exposure period, but a 50% temporary decrease in plasma aldosterone 30 min thereafter. The study confirms the susceptibility of goats to develop respiratory alkalosis during thermoregulatory panting, and shows that this is not to any appreciable extent diminished during hyperhydration. It can further be concluded that a heat-induced rise in body temperature to 40.5 degrees C is no powerful stimulus for vasopressin release in the hyperhydrated goat. The determinations of plasma aldosterone suggest that reduced liberation of the hormone does not contribute to the immediate renal compensation of respiratory alkalosis, but that respiratory alkalosis reaching a certain intensity inhibits aldosterone secretion.