The purpose of this study was to determine the activity of the autonomic nervous system (ANS), using spectral analysis of the heart rate variability (HRV) in the model of partial bladder outlet obstruction (PBOO) in rats treated with selected non-steroidal anti-inflammatory drugs (NSAID): piroxicam (PRX) or meloxicam (MLX), and following administration of PGF2α prostaglandin analogue (Enzaprost F5). Neither the use of PGF2α analogue nor of MLX, caused significant changes in the HRV spectrum (except for HRV spectrum total power reduction with MLX). The use of PRX caused reduction of the total power and powers of all components of the HRV spectrum (except for VLF). Moreover, increased nLF and reduced nHF were observed. The obtained results suggest that the total prostaglandin synthesis block with a non-selective cyclooxygenase inhibitor (PRX) results in reduced ANS total activity, with decreased parasympathetic activity and a relative sympathetic predominance. The preferential cyclooxygenase-2 block (MLX) caused reduction of the total ANS activity as well, however with no clear disproportion of any part of the ANS. Therefore, prostaglandin synthesis inhibition and associated decrease of parasympathetic activity may constitute an additional and favourable feature of NSAID pharmacodynamics in the treatment of BPH.Keywords: heart rate variability, autonomic nervous system, bladder, piroxicam, meloxicam, prostaglandinsBladder overactivity as a secondary condition (secondary overactive bladder; OAB) develops in course of organic illnesses. One of them is benign prostatic hyperplasia (BPH). In course of that disease, bladder overactivity is a result of compression of hypertrophic prostatic tissue on proximal section of the urethra, resulting in compromised urine outflow and progressive pressure increase in lower urinary tract. Pathophysiological description of BPH postulates the role of higher dihydrotestosterone and fibroblastic/vascular growth factors content in prostatic tissues as well as local prostatic hypoxia and inflammation that result in remodelling of prostatic tissues (8, 34). There are also reports regarding a close association between BPH development and co-existence of metabolic syndrome in the same patient. That would suggest the role of hyperinsulinaemia and insulin resistance combined with higher sympathetic activity and explained exacerbation of BPH in patients with coexistent diabetes (6).The current, classic pharmacotherapy of BPH involves the use of α-1 adrenolytics (α-1 adrenergic receptor antagonists) and 5-α reductase inhibitors as monotherapy or combined