Sodium Nitroprusside Potentiates Capsaicin‐Activated TRPV1‐mediated Relaxation of Goat Detrusor Smooth Muscle

ABSTRACT Aim Although TRPV1 is present in detrusor smooth muscle (DSM), interstitial cells of Cajal, and urothelium, its physiological role remains unclear. The present study demonstrated the presence of TRPV1 mRNA in goat DSM, including the physiological effects of the TRPV1 channel and its modulation by nitric oxide. Methods Species identity was confirmed by amplification of the mitochondrial 16S rRNA gene from the genomic DNA of the goat ( Capra hircus ) DSM, and the samples were subjected to RT‐PCR for TRPV1 gene expression. For functional studies, DSM strips (2–3 × 4–5 mm) from freshly slaughtered male goats (6–8 months) were mounted in organ baths. Capsaicin (1 nM–10 µM) was applied cumulatively to DSM precontracted with carbachol (CCh, 10 µM) or high K⁺ solution (30 mM), in the absence or presence of BCTC (1 µM), yohimbine (1 µM), glibenclamide (10 µM), sodium nitroprusside (SNP, 10 µM), l ‐NAME (10 µM), or ODQ (1 µM). Results RT‐PCR confirmed TRPV1 mRNA expression. Capsaicin produced maximal relaxation (Rmax) of 45.5% (95% CI = 41.9–49.1) and 42.8 (95% CI = 37.1–48.5) in CCh‐ and high K⁺‐ contracted DSM, respectively. R max was reduced to 0% and 3.9% (95% CI = 1.4–6.4) by BCTC; 6.8% (95% CI = 2.7–10.9) and 27.3% (95% CI = 10.1–44.5) by yohimbine, 4.7% (95% CI = 1.8–7.6) and 28.5% (95% CI = 9.7–47.3) by glibenclamide in CCh‐ and K⁺30‐PSS ‐ contracted DSM, respectively. SNP enhanced the capsaicin‐evoked R max to 76.3 (95% CI = 55–97.6) and 85.2% (95% CI = 50.2–120.2), whereas l ‐NAME decreased it to 26.7% (95% CI = 11.1–42.3) and 11.8% (95% CI 4.8–18.8), and ODQ to 12.4% (95% CI = 4.8–20.0) and 7.7 (95% CI = 3.2–12.2) in CCh‐contracted and high K⁺‐depolarized DSM, respectively. Conclusion The present study demonstrates that goat DSM expresses functional TRPV1 channels and capsaicin elicits relaxation by activating these channels. The NO donor SNP further potentiates the capsaicin‐induced relaxation through a NO‐cGMP signalling pathway.