Figure 3: Effect of visceral fat accumulation in rabbit experimental models of increased visceral adiposity on maximal (3 μmol l − 1) acetylcholine (Ach)-induced relaxation in corpora cavernosa (CC) strips. (a) The dot plot represents the relationship between visceral fat accumulation (g) and maximal responsiveness to Ach in the following experimental groups: control (blue circles), high fat diet (HFD, green circles), HFD + chronic testosterone (T) dosing (gray circles),57 HFD + chronic obeticholic acid (OCA) dosing (yellow circles),60,65 chronic gonadotropin-releasing hormone (GnRH) analog (triptorelin pamoate) with (red circles) or without T (purple circles)58 and regular diet (blue circles).57 (b) Mean Ach-induced (3 μmol l − 1) relaxation of corpora cavernosa strips of rabbits according to different experimental groups. ***P < 0.0001 vs control; °°°P < 0.0001 vs HFD; #P < 0.05 vs GnRH analog. (c) Schematic representation of putative mechanisms of Ach-induced CC relaxation. Ach: acetylcholine; ATPase: adenosine triphosphatase; cGMP: cyclic guanosine monophosphate; GMP: guanosine monophosphate; GTP: guanosine triphosphate; IP3: inositol trisphosphate; MLC: myosin light chain; MLCK: myosin light-chain kinase; MLCP: myosin light-chain phosphatase; M3AchR: M3 muscarinic receptors; nAchR: nicotinic receptors; NANC: non-adrenergic, non-cholinergic nerves; NO: nitric oxide; PDE5: phosphodiesterase 5; PKG: cGMP-dependent protein kinase; sGC: soluble guanylate cyclase; SR: sarcoplasmic reticulum.