Low Urin Tract Symptoms
January 2018
Objectives: To clarify the role of bradykinin in urogenital pain, we investigated bradykinin involvement in rat models of testicular pain.
Methods: Bradykinin (0.1, 0.
Objectives: To clarify the pathophysiological factor underlying neural crosstalk among pelvic organs, we investigated the possible role of nerve growth factor (NGF) in the neural crosstalk between the testes and urinary bladder.
Methods: Nerve growth factor (10, 30, and 100 µg/mL) or saline was injected into the testes of male Wistar rats. The change in bladder capacity via cystometry and duration of spontaneous scratching behavior induced by NGF in conscious rats was measured.
Introduction: The urethrogenital reflex (UGR) is used as a physiological animal model of the autonomic and somatic activity that accompanies ejaculatory-like reflexes (ELRs). Serotonin (5-HT) plays an important role in regulating ejaculation.
Aim: To examine the effects of intraurethral 5-HT on ELRs and to examine the effects of various 5-HT receptor subtypes on the 5-HT-induced changes in the ELRs.
Objectives: To develop an animal model of testicular pain to examine the hypothesis that neural crosstalk between testicular nociceptors and bladder reflex pathways may underlie bladder overactivity. In chronic pelvic pain disorders, neural crosstalk is thought to underlie referred pain and functional interaction in pelvic organs, and patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) suffer from pain in multiple organs, including the testes and perineum, as well as increased urinary frequency.
Methods: In male Wistar rats, acetic acid was injected into the testes, and behaviors and bladder functions with conscious cystometry were examined.
Voltage-dependent L-type Ca2+ channels are modulated by the binding of Ca2+ channel antagonists and agonists to the pore-forming alpha1c subunit (CaV 1.2). We recently identified Ser1115 in IIIS5-S6 linker of alpha1C subunit as a critical determinant of the action of 1,4-dihydropyridine agonists.
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