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Fig. 1 | International Journal of Retina and Vitreous

Fig. 1

From: Effects of phosphodiesterase type 5 inhibitors on choroid and ocular vasculature: a literature review

Fig. 1

Mechanism of action of phosphodiesterase type 5 (PDE5) inhibitors: 1, light rays stimulate rhodopsin with 11-cis retinal; 2, opsin separates from all-trans-retinal and activates transducin protein; 3, transducin activates PDE6; 4, PDE6 hydrolyzes cyclic guanosine monophosphate (cGMP) into 5′GMP; a, cGMP binds to Ca2+ channels, stimulating Ca2+ uptake and b, when cGMP is hydrolyzed, these channels close and the cell is hyperpolarized, starting the neurotransmission; 5, PDE inhibitor stops cGMP hydrolysis, leaving Ca2+ channels open, and there is no hyperpolarization; 6, sexual stimulation causes nitric oxide (NO) production by nerve and endothelial cells; 7, NO mediates guanylate cyclase; 8, Guanylase cyclase (GC) transforms GTP (guanosine triphosphate) into cGMP. 9, protein kinase G (PKG) is activated by cGMP; 10, this cascade hyperpolarizes the cell by inhibiting Ca2+ uptake and stimulating K+ efflux; 11, the decrease in intracellular Ca2+ results in relaxation and penis erection; and 12, PDE5 hydrolyzes cGMP into 5′-GMP to stop the cycle. The PDE5 inhibitor has the same base of the cGMP entering the PDE5 receptor

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