PDE, Phosphodiesterases

Fig. 9.1 Nitric oxide mediated inhibition of platelet activation. Abbreviations used NO, nitric oxide EDRF, endothelium-derived relaxing factor GC, guanylyl cyclase PDE, phosphodiesterase cGMP-PK, GMP-dependent protein kinase Raplb, small GTPase Raplb ...

It is a relatively selective inhibitor of cyclic GMP, cyclic AMP-PDE (phosphodiesterase) type 111 family. It causes vasodilatation with a consequent decrease in systemic vascular resistance. It increases both the force of contraction and velocity of relaxation of cardiac muscles. It is administered IV 0.75 mg/kg/min as a bolus dose followed by 5-10 pg/kg/min IV infusion and total dose not to exceed 10 mg/kg. 

Mechanism of action of nitrates, nitrites, and other substances that increase the concentration of nitric oxide (NO) in vascular smooth muscle cells. Steps leading to relaxation are shown with heavy arrows. MLCK, activated myosin light-chain kinase [see Figure 12-1]. GC, activated guanylyl cyclase PDE, phosphodiesterase eNOS, endothelial nitric oxide synthase. 

Fig. (4). Vasodilatory mechanisms of flavonoids. RWPC red wine polyphenolic compounds NO nitric made NOSe nitric oxide synthase endothelial O2 superoxide anions OONO peroxynitrites PKC protein kinase Q AC adenylate cyclase GC guanylate cyclase PDE phosphodiesterase.

FIGURE 25.1 Amrinone exerts positive inotropic and vasodilating actions. AMP = adenosine monophosphate, AC = adenlate cyclase, PDE = phosphodiesterase, Gs = stimulatory guanine nucleotide-binding regulatory protein. 

Fig. 1. Targeted lipidomics of anandamide metabolism. Postulated pathways of anandamide metabolism. Abbreviations PC, phosphatidylcholine PE, phosphatidylethanolamine NAT, JV-acyl transferase LPA, lysophosphatidic acid PA, phosphatidic acid NAPE, jV-acyl-phosphatidylethanolamine Lyso-NAPE, l-lyso,2-acyl-OT-glycero-3-phosphoethanolamine-JV-acyl ABHD-4, a//3 hydrolase-4 GP-anandamide, glycerophospho-anandamide PAEA, phospho-anandamide PLA, phospholipase A NAPE-PLD, NAPE phospholipase D PLC, phospholipase C FAAH, fatty acid amide hydrolase P, phosphatase COX, cyclooxygenase LOX, lipoxygenase CYP450, cytochrome P450 PDE, phosphodiesterase.

The biochemistry of vision, rh, RHODOPSIN Rhk, rhodopsin KINASE A, ARRESTIN GC, GUANYLATE CYCLASE T, TRANSDUCIN PDE, PHOSPHODIESTERASE. 

Fig. 24.5 Management of chronic cardiac faiiure (N = no,Y = yes, Rx = treatment, PDE = phosphodiesterase). Reproduced with permission from Lancet.

Figure 5-4. Outline of postulated steps leading to prostaglandin-induced physiological events. AMP = adenosine monophosphate GMP = guanosine monophosphate PDE = phosphodiesterase.

ATP, adenosine triphosphate cAMP, cyclic adenosine monophosphate PDE, phosphodiesterase ... 

NOs NO synthase PDEs phosphodiesterases sCC soluble gunnylatc cyclase SOCC store-operated calcium channel IOCC voltage-opernled calcium channel ( ) activation (-) inhibition. 

Figure 13-1. Subgroups of drugs discussed in this chapter. PDE, phosphodiesterase.

Figure 20-3. Possible mechanisms of beta agonists, muscarinic antagonists, theophylline, and leukotriene antagonists in altering bronchial tone in asthma. AC, adenylyl cyclase PDE, phosphodiesterase.

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