The transport of Na+, K+ and Cl- across the isolated epithelium of the eel intestine was studied using a combination of four experimental strategies: short-circuiting, measurements of intracellular potentials and ion concentrations, application of a variety of transport inhibitors and measurement of unidirectional fluxes with radioactive tracers. When short-circuited, the system performs a net transport of Cl- and Na+ towards the blood side, with a stoichiometry approaching 2, and a much smaller net transport of K+ towards the lumen. The system is totally driven by the sodium pump located in the basolateral barrier and the main coupling between the fluxes of the three ions is through the operation of a furosemide-sensitive transporter in the apical barrier, probably a 2Cl-/Na+/K+ symporter. The inhibitory effect of DIDS and picrylsulphonic acid on the short-circuit current, when added to the serosal side, suggests the presence of a sodium-dependent anionic shuttle located in the basolateral membrane. The short-circuit current is inhibited by H25, a non-specific inhibitor of the K+/Cl- symport, added to the serosal side. This effect occurs after a delay of at least 5 min and may result from the diffusion of the drug to the apical barrier, where it blocks the 2Cl-/Na+/K+ symport with much higher affinity.

Isolated, saline-perfused gastrocnemius muscles of Xenopus laevis were used to assess the relationships between aerobic and anaerobic metabolism during conditions of rest, isotonic contraction and recovery. The major part (85%) of the energy used during 25 min of isotonic contractions in the saline-perfused muscles was from anaerobic rather than aerobic sources. However, the small contribution made by oxidative metabolism during activity can be attributed, in part at least, to limitations imposed by the rate of perfusion and the low O2 capacity of the perfusate. The respiratory exchange ratio (R = VCO2/VO2) of saline-perfused gastrocnemius muscles of Xenopus was 0.82 at rest, increasing to values well above 1.0 during activity. The elevated R value is consistent with liberation of CO2 by metabolic acid titration of the bicarbonate buffer system of the saline perfusate. Recovery from exercise was characterized as a period of net CO2 retention (R values of 0.4) presumably reflecting a replenishment of depleted CO2 stores. Depending on the acid-base status of the venous outflow from the isotonically contracting muscles, hydrogen ions were found to be released at either a greater rate (alkalosis) or slower rate (acidosis) than that of lactate.

1. The elimination of CO 2 through the lungs and skin of Xenopus laevis and its distribution between plasma and erythrocytes were determined during breathing and submergence periods. 2. CO 2 output does not decrease during submergence, as lack of lung ventilation is compensated by an increase in cutaneous exchange. The total CO 2 carried in the blood decreases after a 30 min dive, but the fraction carried in red blood cells increases substantially, due to an increase in the haematocrit values. This increase is related to a decrease in plasma volume during diving. 3. During short dives the blood shows changes characteristic of respiratory acidosis but longer dives result in a combination of respiratory and metabolic acidosis.

1. Unrestrained Xenopus with access to air had an oxygen consumption, as measured at 20 °C by manometric and electrode techniques, of approximately 4.5 ml O 2 100 g -1 h -1 of which 1.1 ml was taken in through the skin. 2. Measurements of body volume showed that the rate of oxygen uptake from the lungs was high when the animal was at the surface but fell rapidly during the first few minutes of a dive. 3. Oxygen tensions in systemic (80 mmHg) and pulmocutaneous (60 mmHg) vessels provided evidence for separation of blood flows in the ventricle of the animal when breathing air. The tensions fell in all parts of the circulation throughout a dive. 4. The above data, together with a conventionally determined oxygen dissociation curve, show that both blood and lungs are used to a limited extent as oxygen stores during a dive, the blood being more important. The stores do not permit tissue consumption to go on at a uniform rate throughout a normal breathing-diving cycle.

1. A series of breathing movements which are effective in ventilating the lungs are accompanied by a marked increase in pulmonary blood flow and a decrease in pulmocutaneous arterial pressure. This reaction must involve considerable vasodilation of the pulmonary vascular bed. 2. Similar vasodilation is produced by artificial inflation of the lungs via an implanted cannula. Nitrogen is not so effective as air in producing the vasodilation, whereas oxygen is more effective. It is suggested that both stretch receptors in the lungs and chemical receptors in lungs or blood are involved in the reaction. 3. The level of anaesthesia is important in determining the degree of vasodilation response to the different stimuli. It is concluded that the central nervous system is the site where interaction occurs between signals from stretch receptors and chemical receptors and from the breathing movements themselves. Experiments with atropine suggest that the efferent pathway is in the vagus nerve. 4. Recordings from free-swimming, unanaesthetized toads show that the vasodilation response occurs as part of normal diving-emergence behaviour.