Figure 17

Figure 17 Vasodilatory actions of nitric oxide (NO), prostaglandin E₁ and vasoactive intestinal polypeptide (VIP) and the opposing vasoconstrictory effect of norepinephrine on intracorporeal smooth muscle cells. NO together with citrulline (cit) is produced by the enzyme nitric oxide synthase (NOS) from L-arginine (arg) and oxygen (O₂). NO acts as a neurotransmitter to stimulate the production of cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). Membrane-bound adenylate cyclase (AC) produces cyclic adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). AC activity is dependent on guanidine nucleotide binding protein (G protein). Both cAMP and cGMP lower intracellular calcium (Ca₂₊). In contrast, norepinephrine acts via the α-adrenoceptor. Activation of this G-protein-linked receptor stimulates production of inositol phosphate (IP₃) by a phospholipase C (PLC)-dependent mechanism. IP₃ acts to increase intracellular Ca²⁺ , thereby inducing contraction of intracavernosal smooth muscle cells