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Guanylyl cyclase (also known as guanylate cyclase) is an enzyme that catalyzes the synthesis of cyclic guanosine 3′,5′-monophosphate (cGMP) from guanosine 5' triphosphate (GTP). Guanylyl cyclase exists in both a membrane-bound and soluble form in the cell. The membrane-bound form is a plasma membrane receptor, while soluble forms of guanylyl cyclase undergo activation by nitric oxide. Nitric oxide then functions as a primary messenger, amplifying the signal intracellularly. This review discusses guanylyl cyclase's biochemistry, function, and clinical relevance.[1]

cGMP mediates several physiologic processes in different cell types in the cardiovascular system. Dysfunctional signaling at any cascade step, including cGMP synthesis, effector activation, or cGMP breakdown, has been present in many cardiovascular diseases, such as hypertension and atherosclerosis, cardiac hypertrophy, and heart failure. [10] Guanylyl cyclase plays an important role in cardiac muscle relaxation. ANP and BNP are produced and released by cardiac muscle when there is an increase in myocardial wall stretch and/or pressure and an increase in catecholamines, arginine vasopressin, angiotensin 2, endothelin, and glucocorticoids. ANP and BNP are natriuretic peptides that bind to membrane-associated guanylyl cyclase receptors (NPRs). Of the seven mammalian membrane-associated guanylyl cyclases, the NPR-A and NPR-B participate in natriuretic peptide pathways. ANP and BNP activate NPR-A to regulate body volume homeostasis, blood pressure, and local anti-hypertrophic effects in the myocardium.[11][12] Guanylyl cyclase plays a prominent role in the process of erection during sexual arousal, at nerve terminals, and in endothelial cells in the corpus cavernosum. NO activates guanylyl cyclase, which converts GTP into cGMP, triggering a cGMP-dependent cascade of events. Smooth muscle relaxation occurs when cGMP accumulates in the corpus cavernosum to increase blood flow to the penis.[9]