Nasal heat and water exchange is not an effector mechanism for water balance regulation in grey seals.

Abstract

Phocid seals may effectively restrict respiratory heat and water loss by nasal heat and water exchange (NHE), and respiratory heat loss is, in fact, subject to thermoregulatory control. We have investigated whether phocid seals also control NHE and respiratory water loss to regulate water balance. Three resting juvenile female grey seals (Halichoerus grypus) were subjected to: (i) 5 days of food and water deprivation, (ii) intravenous infusion of 1000 ml of a hypersomotic (930 mM) solution of the diuretic mannitol, and (iii) oral injection of 1500 ml distilled water. During these experiments in air of 0 degree C, expired air temperature (T(ex)) and respiratory frequency (f) were recorded, and urine and blood samples collected. The results were compared with results from control experiments. Five days of food and water deprivation caused an average 10.5% and 20.8% increase in plasma (PO) and urine (UO) osmolality, respectively. Mannitol infusion induced excessive diuresis and caused an average 2.45% reduction of the estimated body water pool. Water loading caused an average 4.5% and 60% reduction in PO and UO, respectively, while urine production increased by 365%, on average. However, in no case did either T(ex) or f change significantly from mean control levels of 22.4 (range: 20.7-25.2) degrees C and 7.3 (range: 6.6-8.4) breaths min-1, respectively. Thus, water balance disturbances that initiate renal compensatory mechanisms fail to affect NHE in grey seals. This suggests that control of NHE is not an effector mechanism for regulation of water balance in grey seals.