Acid-sensing ion channels (ASICs) on the bladder lining could be behind the frequent urge to urinate, Australian researchers say.
While investigating bladder function in animals, they found that acid inside urine was an important stimulant of cells lining the bladder wall. These in turn release a chemical, ATP, which fires up nerve receptors that signal to the brain that the bladder is full. It is the first connection to be made between acid and bladder function, and raises the possibility that pH levels in urine – which is routinely acidic – can be modified to control the urge to urinate.A paper on the finding appears in the prestigious British Journal of Pharmacology.
“No-one really knows what causes overactive bladder – that’s what makes it such a difficult thing to treat,” said the paper’s lead author Professor Elizabeth Burcher, from the School of Medical Sciences in the University of New South Wales (UNSW).
Until now it’s been assumed that the release of the chemical ATP was stimulated primarily by the bladder’s ‘stretch’ as it becomes full.
“Acid is a new stimulus that we haven’t been aware of before,” Professor Burcher said.
The paper’s first author was PhD candidate Prajni Sadananda. Prajni recently submitted her thesis and has now taken up a postdoctoral position at Bristol University.
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Current treatments for overactive bladder centre on drugs that reduce the activity of neurotransmitter receptors in the bladder wall.
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“A new more cost-effective approach would be terrific. There’s no doubt it’s an area of unmet need. “
Professor Burcher said the next step would be to conduct similar investigations in humans.
“It’s always difficult to relate animal findings to human tissue, and there are species differences,” she said. “But we’ve shown that acid is a stimulus in two animals – the pig and the rat. There’s no reason to believe it wouldn’t be the case in humans too.”
The study was supported financially by the Federal Government’s National Health and Medical Research Council and by a grant from Pfizer.
Source-Medindia
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