Control of breathing in African lungfish (Protopterus dolloi): a comparison of aquatic and cocooned (terrestrialized) animals.

African lungfish, Protopterus dolloi exhibited constant rates of O(2) consumption before (0.95+/-0.07 mmol kg(-1) h(-1)), during (1.21+/-0.32 mmol kg(-1) h(-1)) and after (1.14+/-0.14 mmol kg(-1) h(-1)) extended periods (1-2 months) of terrestrialization while cocooned. Although a breathing event in terrestrialized fish consisted of multiple bouts of inspiration and expiration in rapid succession, the mean frequency of pulmonary breathing events was unaltered in the terrestrialized fish (16.7+/-1.4 h(-1)versus 20.1+/-4.9 h(-1) in the aquatic and terrestrialized fish, respectively). Hypoxia (approximately 20 mmHg) increased the frequency of breathing events by 16 and 23 h(-1) in the aquatic and terrestrialized fish, respectively. Hyperoxia (approximately 550 mmHg) decreased breathing event frequency by 10 and 15 h(-1) in the aquatic and terrestrialized animals. Aquatic hypercapnia (approximately 37.5 mmHg) increased pulmonary breathing frequency (from 15.3+/-2.3 to 28.7+/-5.4 h(-1)) in free swimming lungfish, whereas aerial hypercapnia was without effect in aquatic or terrestrialized fish.

Mechanisms of acid-base regulation in the African lungfish Protopterus annectens.

African lungfish Protopterus annectens utilized both respiratory and metabolic compensation to restore arterial pH to control levels following the imposition of a metabolic acidosis or alkalosis. Acid infusion (3 mmol kg(-1) NH(4)Cl) to lower arterial pH by 0.24 units increased both pulmonary (by 1.8-fold) and branchial (by 1.7-fold) ventilation frequencies significantly, contributing to 4.8-fold and 1.9-fold increases in, respectively, aerial and aquatic CO(2) excretion. This respiratory compensation appeared to be the main mechanism behind the restoration of arterial pH, because even though net acid excretion (J(net)H(+)) increased following acid infusion in 7 of 11 fish, the mean increase in net acid excretion, 184.5+/-118.5 micromol H(+) kg(-1) h(-1) (mean +/- s.e.m., N=11), was not significantly different from zero. Base infusion (3 mmol kg(-1) NaHCO(3)) to increase arterial pH by 0.29 units halved branchial ventilation frequency, although pulmonary ventilation frequency was unaffected. Correspondingly, aquatic CO(2) excretion also fell significantly (by 3.7-fold) while aerial CO(2) excretion was unaffected. Metabolic compensation consisting of negative net acid excretion (net base excretion) accompanied this respiratory compensation, with J(net)H(+) decreasing from 88.5+/-75.6 to -337.9+/-199.4 micromol H(+) kg(-1) h(-1) (N=8). Partitioning of net acid excretion into renal and extra-renal (assumed to be branchial and/or cutaneous) components revealed that under control conditions, net acid excretion occurred primarily by extra-renal routes. Finally, several genes that are involved in the exchange of acid-base equivalents between the animal and its environment (carbonic anhydrase, V-type H(+)-ATPase and Na(+)/HCO (-)(3) cotransporter) were cloned, and their branchial and renal mRNA expressions were examined prior to and following acid or base infusion. In no case was mRNA expression significantly altered by metabolic acid-base disturbance. These findings suggest that lungfish, like tetrapods, alter ventilation to compensate for metabolic acid-base disturbances, a mechanism that is not employed by water-breathing fish. Like fish and amphibians, however, extra-renal routes play a key role in metabolic compensation.