α1-Adrenergic receptors (ARs) are involved in micturition control both centrally and peripherally. α1-AR antagonists improve not only voiding but also storage symptoms in patients with bladder outlet obstruction. We investigated the role of α1-AR mechanisms involved in detrusor overactivity induced by cold stress in conscious rats.
Continuous cystometry was performed at room temperature (RT, 28 ± 2°C) and for 40 min at cold temperature (CT, 4 ± 2°C). Voiding interval (VI), micturition volume (MV), and bladder capacity (BC) were evaluated before and after intravenous administration of KMD-3213 (selective α1A-AR antagonist), naftopidil (selective α1D-AR antagonist), tamsulosin (selective α1A/1D-AR antagonist), and prazosin (non-selective α1-AR antagonist). Blood pressure (BP), cumulative voided volume and body temperature were also evaluated.
At RT, none of the AR antagonists caused significant change in the cystometric parameters. During 40 min of cold stress cumulative voided volume and body temperature did not change, but there were significant decreases in VI, MV, and BC. Low doses of the AR antagonists had no effect on CT-induced decreases of these variables. However, high doses of KMD-3213, tamsulosin, naftopidil and prazosin significantly inhibited the CT-induced decreases in VI, MV, and BC. CT caused a significant increase in BP, and this was not affected by low doses of the AR antagonists. However, high doses of prazosin significantly lowered the CT-induced increase of BP.
Cold stress induces detrusor overactivity and increases BP in conscious rats. These effects are mediated, at least in part, by α1A-AR and α1D-AR subtypes and can be prevented/reduced by α1-AR antagonists. Neurourol. Urodynam. 28:251–256, 2009. © 2008 Wiley-Liss, Inc.