scholarly journals Metabolic costs induced by lactate in the toad Bufo marinus: new mechanism behind oxygen debt?

2003 ◽  
Vol 94 (3) ◽  
pp. 1177-1185 ◽  
Author(s):  
Ilka Pinz ◽  
Hans-O. Pörtner
Keyword(s):  
Metabolic Rate ◽  
Energy Demand ◽  
Isolated Hepatocytes ◽  
Ringer Solution ◽  
Bufo Marinus ◽  
Proton Exchange ◽  
Plasma Catecholamine ◽  
Proton Symport ◽  
Toad Bufo

The mechanism of an increase in metabolic rate induced by lactate was investigated in the toad Bufo marinus. Oxygen consumption (V˙o 2) was analyzed in fully aerobic animals under hypoxic conditions (7% O2 in air), accompanied by measurements of catecholamines in the plasma, and was measured in isolated hepatocytes in vitro under normoxia by using specific inhibitors of lactate proton symport [α-cyano-4-hydroxycinnamate (CHC)] and sodium proton exchange (EIPA). The rise in metabolic rate in vivo can be elicited by infusions of hyperosmotic (previous findings) or isosmotic sodium lactate solutions (this study). Despite previous findings of reduced metabolic stimulation under the effect of adrenergic blockers, the increase inV˙o 2 in vivo was not associated with elevated plasma catecholamine levels, suggesting local release and effect. In addition to the possible in vivo effect via catecholamines, lactate induced a rise in V˙o 2 of isolated hepatocytes, depending on the concentration present in a weakly buffered Ringer solution at pH 7.0. No increase was found at higher pH values (7.4 or 7.8) or in HEPES-buffered Ringer solution. Inhibition of the Lac−-H+ transporter with α-CHC or of the Na+/H+ exchanger with EIPA prevented the increase in metabolic rate. We conclude that increasedV˙o 2 at an elevated systemic lactate level may involve catecholamine action, but it is also caused by an increased energy demand of cellular acid-base regulation via stimulation of Na+/H+ exchange and thereby Na+-K+-ATPase. The effect depends on entry of lactic acid into the cells via lactate proton symport, which is likely favored by low cellular surface pH. We suggest that these energetic costs should also be considered in other physiological phenomena, e.g., when lactate is present during excess, postexerciseV˙o 2.

Active urea transport by the skin of Bufo viridis: amiloride- and phloretin-sensitive transport sites

1988 ◽  
Vol 255 (3) ◽  
pp. F429-F433 ◽  
Author(s):  
J. Rapoport ◽  
A. Abuful ◽  
C. Chaimovitz ◽  
Z. Noeh ◽  
R. M. Hays
Keyword(s):  
External Medium ◽  
Ringer Solution ◽  
Bufo Marinus ◽  
Urea Transport ◽  
Maximal Inhibition ◽  
Experimental Conditions ◽  
Bufo Viridis ◽  
Green Toad ◽  
Dose Response Study ◽  
Toad Bufo

Urea is actively transported inwardly (Ji) across the skin of the green toad Bufo viridis. Ji is markedly enhanced in toads adapted to hypertonic saline. We studied urea transport across the skin of Bufo viridis under a variety of experimental conditions, including treatment with amiloride and phloretin, agents that inhibit urea permeability in the bladder of Bufo marinus. Amiloride (10(-4) M) significantly inhibited Ji in both adapted and unadapted animals and was unaffected by removal of sodium from the external medium. Phloretin (10(-4) M) significantly inhibited Ji in adapted animals by 23–46%; there was also a reduction in Ji in unadapted toads at 10(-4) and 5 x 10(-4) M phloretin. A dose-response study revealed that the concentration of phloretin causing half-maximal inhibition (K1/2) was 5 x 10(-4) M for adapted animals. Ji was unaffected by the substitution of sucrose for Ringer solution or by ouabain. We conclude 1) the process of adaptation appears to involve an increase in the number of amiloride- and phloretin-inhibitable urea transport sites in the skin, with a possible increase in the affinity of the sites for phloretin; 2) the adapted skin resembles the Bufo marinus urinary bladder with respect to amiloride and phloretin-inhibitable sites; 3) we confirm earlier observations that Ji is independent of sodium transport.

Fever and metabolic rate in the toad Bufo marinus

1998 ◽  
Vol 23 (1) ◽  
pp. 49-52 ◽  
Author(s):  
Elizabeth Sherman ◽  
Antonia Stephens
Keyword(s):  
Metabolic Rate ◽  
Bufo Marinus ◽  
Toad Bufo

scholarly journals A new function for lactate in the toad Bufo marinus

1994 ◽  
Vol 76 (6) ◽  
pp. 2405-2410 ◽  
Author(s):  
H. O. Portner ◽  
L. G. Branco ◽  
G. M. Malvin ◽  
S. C. Wood
Keyword(s):  
Metabolic Rate ◽  
Bufo Marinus ◽  
Alarm Signal ◽  
Progressive Hypoxia ◽  
Critical Po2 ◽  
Adrenergic Antagonists ◽  
Lactate Formation ◽  
Lactate Levels ◽  
Toad Bufo ◽  
Elevated Lactate

In the amphibian Bufo marinus, progressive hypoxia below a critical PO2 elicits a transient 50% increase in O2 consumption that coincides with the onset of lactate formation. The present study was designed to test the hypothesis that lactate causes the observed rise in metabolic rate. Arterial bolus infusions of pH-neutral sodium lactate solutions (4 mmol/kg body wt) in toads maintained under hypoxia actually elicit a similar increase in metabolic rate. The application of adrenergic antagonists (bretylium tosylate, phentolamine, propranolol, and reserpine) inhibits this response, suggesting that catecholamines are involved. Moreover, animals injected with lactate move to a cooler environment (behavioral hypothermia), a behavioral response that is beneficial during hypoxia. We hypothesize that, in accordance with Cannon's concept of an emergency response, lactate may function as an alarm signal during hypoxia. However, the signal function of lactate is observed in animals both under hypoxia and under normoxia and should thus be considered in future studies whenever elevated lactate levels are present, e.g., during and after exercise.

Heterogeneity and lability of endogenous digitalis-like substances in the plasma of the toad, Bufo marinus

1996 ◽  
Vol 271 (2) ◽  
pp. R325-R332
Author(s):  
V. P. Butler ◽  
J. F. Morris ◽  
T. Akizawa ◽  
M. Matsukawa ◽  
P. Keating ◽  
...  
Keyword(s):  
Inhibitory Activity ◽  
Bufo Marinus ◽  
The Third ◽  
In Vitro Incubation ◽  
Low Concentrations ◽  
Atpase Inhibitors ◽  
Fresh Plasma ◽  
Toad Bufo

Three major groups of endogenous digitalis-like substances (EDLS) have been identified in the plasma of the toad, Bufo marinus. One group of compounds, present in fresh plasma, is composed of chromatographically homogeneous polar conjugates, principally bufadienolide 3-sulfates, which exhibit relatively weak Na(+)-K(+)-adenosinetriphosphatase (ATPase) inhibitory activity. A second and larger group of compounds, also found in fresh plasma, includes chromatographically heterogeneous conjugates, which are effective inhibitors of Na(+)-K(+)-ATPase; these compounds possess properties similar to those of bufotoxins. The third group of EDLS consists of free unconjugated bufadienolides, which are also effective Na(+)-K(+)-ATPase inhibitors. These unconjugated bufadienolides are present in relatively low concentrations in fresh toad plasma, but appreciable quantities are enzymatically generated from conjugates (believed to consist principally of bufotoxins) during the in vitro incubation of plasma. We suggest that the extent to which circulating polar EDLS are enzymatically deconjugated in vivo may be important in the regulation of the digitalis-sensitive Na(+)-K(+)-ATPase of toad brain, the only known digitalis-sensitive Na(+)-K(+)-ATPase in the toad.

scholarly journals CHANGES IN THE DURATION OF THE ELECTRIC RESPONSE OF SINGLE NERVE FIBERS FOLLOWING REPETITIVE STIMULATION

1956 ◽  
Vol 40 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Constantine S. Spyropoulos
Keyword(s):  
Nerve Fiber ◽  
Nerve Fibers ◽  
Repetitive Stimulation ◽  
Bufo Marinus ◽  
Electric Response ◽  
Rapid Rate ◽  
Semitendinosus Muscle ◽  
Single Nerve ◽  
Toad Bufo

Single nerve fibers were isolated from the nerve innervating the sartorius or semitendinosus muscle of the toad (Bufo marinus). Single nerve fiber responses were recorded with three arrangements of the "bridge insulator" method. During stimulation at 50 to 150 pulses per second for 20 to 140 minutes the spike duration was progressively increased. After tetanization the spike duration usually continued to increase at a more rapid rate. Within 5 to 60 minutes further prolongation stopped and within 1 to 10 hours the spike duration was normal. The duration of the response of tetanized fibers was from 2.5 to more than 10 times the spike duration of untetanized fibers. Prolongation was observed in nerve fibers isolated from nerves tetanized in vivo.

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