Which neurotransmitter systems interact with the mechanism of action of Tadalista?

Tadalista, also known as Tadalafil, is a medication primarily used to treat erectile dysfunction (ED) and symptoms of benign prostatic hyperplasia (BPH). Its mechanism of action primarily involves the inhibition of an enzyme called phosphodiesterase type 5 (PDE5), which leads to increased levels of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of the penis. However, Tadalista is interaction with neurotransmitter systems is not direct. Instead, its primary mode of action involves the enhancement of the nitric oxide-cGMP pathway, which is involved in smooth muscle relaxation and vasodilation in the penis. Nitric oxide (NO) is released from nerve endings and endothelial cells during sexual stimulation, and it activates the enzyme guanylate cyclase, which increases levels of cGMP. This, in turn, relaxes smooth muscles in the corpus cavernosum of the penis, leading to increased blood flow and thus facilitating an erection. So, while Tadalafil indirectly affects neurotransmitter systems involved in the release of NO, its primary mechanism of action is related to the regulation of cyclic nucleotide levels rather than direct interaction with neurotransmitters.