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Effect of dinitrophenol on bladder metabolism and contraction
Author(s) -
Levin Robert M.,
van Arsdalen Keith,
Thomas Theresa,
Wein Alan J.
Publication year - 1985
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.1930040109
Subject(s) - bethanechol , intracellular , contraction (grammar) , stimulation , adenine nucleotide , 2,4 dinitrophenol , muscle contraction , mitochondrion , nucleotide , endocrinology , medicine , chemistry , biochemistry , biology , receptor , muscarinic acetylcholine receptor , gene
Urinary bladder function is dependent on the utilization of intracellular metabolic energy. Although preformed ATP is generally regarded to be the major source of metabolic energy for smooth muscle contraction, recent evidence suggests that other sources of metabolic energy may be involved in bladder function. In order to study the relationship between bladder contraction and intracellular ATP, we characterized the effect of 2,4 dinitrophenol (DNP) on rabbit urinary bladder adenine nucleotide metabolsim, intracellular ATP concentration, and isolated bladder strip contraction. DNP specifically inhibits mitochondrial formation of ATP by “uncoupling” mitochondrial oxidation from the phosphorylation of adenine nucleotides. The results can be summarized as follows: (1) DNP produced a dose‐dependent inhibition of ATP synthesis. (2) DNP (250 μM) produced a similar gradual decrease (with respect to time) in both contractile response to field stimulation and intracellular ATP concentration. (3) DNP (30‐2,000 μM) produced a similar graded dose‐dependent decrease in both contractile response to field stimulation and intracellular concentration of ATP. The effect of DNP on bethanechol stimulation of bladder strip contraction was similar to its effect on field stimulation. The inhibitory effect of DNP on the contractile response to both electrical stimulation and bethanechol appears to be directly related to the progressive decline in the contraction of intercellular adenine nucleotides and the decline of adenine nucleotide synthesis.