Chun‑Kai Hsua, Hsi‑Hsien Changa, Stephen Shei‑Dei Yanga,b*
aDivision of Urology, Department of Surgery, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei, Taiwan, bSchool of Medicine, Tzu Chi University, Hualien, Taiwan
Open Access funded by Buddhist Compassion Relief Tzu Chi Foundation
Abstract
Objective: We have demonstrated that phenylephrine (PE) activates the capsaicin‑sensitive nerves, and then activates capsaicin‑sensitive nerves to release an unknown substance that facilitates the release of norepinephrine (NE) from adrenergic nerves. Subsequently, NE stimulates β‑ARs in the detrusor muscle in mice, leading to neurogenic relaxation of the urinary bladder (UB). Materials and Methods: We examined if there existed sensory‑motor dysfunction in UB of aging mice. To investigate the change of PE‑induced detrusor relaxation in aging male‑C57BL/6 mice (12‑ vs. 24‑month‑old mice), UB strips from mice were isolated, cut into strips, and mounted in the organ bath. Results: The UB strip contractility responding to various agents was estimated using tissue bath wire myography. Acetylcholine (ACh) and KCl‑induced UB strips contraction was not significantly different between 24‑ and 12‑month mice. NE‑induced UB strips relaxation was significantly lower in 24‑month than 12‑month mice. Denuded bladder strips showed similar decreased relaxation response to NE. This NE‑induced relaxation was inhibited by silodosin and lidocaine. PE did not induce contraction in UB strips of aging mice. In contrast, PE‑induced relaxation was weaker in 24‑month than 12‑month mice. Conclusion: Our results suggested that the PE‑induced relaxation was age related. Aging seemed to lead the sensory‑motor dysfunction. More animal and human studies are required to prove this concept and its clinical usefulness in the future.
Keywords: Adrenergic receptor, Aging, Bladder, Lower urinary tract dysfunction, Sensory‑motor interaction
