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[the recent] news from the New England Journal of Medicine suggesting that mild asthmatics should be treated as needed with steroids and short-acting betaagonists? NICK HANANIA, MD: It's an interesting paper. Obviously, the group that did this study is highly respected, the Asthma Clinical Research Network or ACRN. Nonetheless, within the study conclusion, the authors themselves are only cautiously optimistic about their findings. To generalize from the results of such studies does a disfavor to all the asthmatic patients whom we're treating now. Most studies on the anti-inflammatory effects of inhaled steroids show that continuous treatment is needed. As to why the results are different in this study, I cannot explain it. Yet it is worth mentioning that daily inhaled corticosteroid therapy was superior to intermittent steroids in most of the secondary endpoints in this study. It is taking us much time to convince primary care physicians to start antiinflammatory therapy early. I would not generalize the results of this paper to my practice until I see more studies. I showed you data from the START trial where inhaled steroids were used once daily instead of twice daily and showing some effect compared to placebo. This, however, is the first study demonstrating that intermittent use of inhaled steroids might work. SEAN D. SULLIVAN, RPH, PHD: I agree that the ACRN is an accomplished group of investigators. They posed an extremely interesting question regarding 1-year outcomes of various monotherapy treatments in very mild persistent asthma. The study concludes that patients who use their inhaled steroids less than daily are not harmed in terms of lung function during 1 year. The caveat, however, is that this was a 1-year study, not a 3- or a 5-year study. Also, it showed that patients on inhaled corticosteroid [ICS] therapy had improvements in symptom-free days at the exact same magnitude as what we found in the START [Inhaled Steroid as Regular Therapy in Early Asthma]. This is only one study, but it will probably get repeated, as it's raised interest in the clinical and research community. HANANIA: The new asthma guidelines will focus on asthma control rather than severity based on FEV1 [forced expiratory volume in one second]. Obviously FEV1 is important, but mild, persistent asthmatics. Magnesium pemoline can be given once a day as a regular or a chewable tablet, for instance, tadalafil hypertension.

Ignarro LJ 2002 ; Nitric oxide as a unique signaling molecule in the vascular system: a historical overview. J Physiol Pharmacol 53: 503514. Kloner RA, Hutter AM, Emmick JT, Mitchell MI, Denne J, and Jackson G 2003 ; Time course of the interaction between tadalafil and nitrates. J Coll Cardiol 42: 18551860. Kruuse C, Rybalkin SD, Khurana TS, Jansen-Olesen I, Olesen J, and Edvinsson L 2001 ; The role of cGMP hydrolysing phosphodiesterases 1 and 5 in cerebral artery dilatation. Eur J Pharmacol 420: 55 65. Kuriyama H, Kitamura K, and Nabata H 1995 ; Pharmacological and physiological significance of ion channels and factors that modulate them in vascular tissues. Pharmacol Rev 47: 387573. Lucas KA, Pitari GM, Kazerounian S, Ruiz-Stewart I, Park J, Schulz S, Chepenik KP, and Waldman SA 2000 ; Guanylyl cyclases and signaling by cyclic GMP. Pharmacol Rev 52: 375 414. Maurice DH, Palmer D, Tilley DG, Dunkerley HA, Netherton SJ, Raymond DR, Elbatarny HS, and Jimmo SL 2003 ; Cyclic nucleotide phosphodiesterase activity, expression and targeting in cells of the cardiovascular system. Mol Pharmacol 64: 533546. Mochida H, Inoue H, Takagi M, Noto T, Yano K, and Kikkawa K 2002 ; Sildenafil and T-1032, phosphodiesterase type 5 inhibitors, showed a different vasorelaxant property in the isolated rat aorta. Eur J Pharmacol 440: 4552. Montorsi F, Briganti A, Salonia A, Montorsi P, and Rigatti P 2004 ; The use of phosphodiesterase type 5 inhibitors for erectile dysfunction. Curr Opin Urol 14: 357359. Moreno L, Losada B, Cogolludo A, Lodi F, Lugnier C, Villamor E, Moro M, Tamargo J, and Perez-Vizcaino F 2004 ; Postnatal maturation of phosphodiesterase 5 PDE5 ; in piglet pulmonary arteries: activity, expression, effects of PDE5 inhibitors and role of the nitric oxide cyclic GMP pathway. Pediatr Res 56: 563570. Munzel T, Feil R, Mulsch A, Lohmann SM, Hofmann F, and Walter U 2003 ; Physiology and pathophysiology of vascular signaling controlled by guanosine 3 , 5 -cyclic monophosphate-dependent protein kinase. Circulation 108: 21722183. Pauvert O, Bonnet S, Rousseau E, Marthan R, and Savineau JP 2004 ; Sildenafil alters calcium signaling and vascular tone in pulmonary arteries from chronically hypoxic rats. J Physiol 287: L577L583. Pauvert O, Lugnier C, Keravis T, Marthan R, Rousseau E, and Savineau JP 2003 ; Effect of sildenafil on cyclic nucleotide phosphodiesterase activity, vascular tone and calcium signaling in rat pulmonary artery. Br J Pharmacol 139: 513522. Rosen RC and Kostis JB 2003 ; Overview of phosphodiesterase 5 inhibition in erectile dysfunction. J Cardiol 92: 9M18M. Rybalkin SD, Yan C, Bornfeldt KE, and Beavo JA 2003 ; Cyclic GMP phosphodiesterases and regulation of smooth muscle function. Circ Res 93: 280 291. Saenz de Tejada I, Angulo J, Cuevas P, Fernandez A, Moncada I, Allona A, Lledo E, Korschen HG, Niewohner U, Haning H, et al. 2001 ; The phosphodiesterase inhibitory selectivity and the in vitro and in vivo potency of the new PDE5 inhibitor vardenafil. Int J Impot Res 13: 282290. Sakuma I, Akaishi Y, Tomioka H, Sato A, Kitabatake A, and Hattori Y 2002 ; Interactions of sildenafil with various coronary vasodilators in isolated porcine coronary artery. Eur J Pharmacol 437: 155163. Sampson LJ, Hinton JM, and Garland CJ 2001 ; Evidence for expression and function of phosphodiesterase type 5 PDE-V ; in rat resistance arteries. Br J Pharmacol 132: 1317. Sussman DO 2004 ; Pharmacokinetics, pharmacodynamics and efficacy of phosphodiesterase type 5 inhibitors. J Osteopath Assoc 104: S11S15. Thebaud B, Michelakis E, Wu XC, Harry G, Hashimoto K, and Archer SL 2002 ; Sildenafil reverses O2 constriction of the rabbit ductus arteriosus by inhibiting type 5 phosphodiesterase and activating BKCa channels. Pediatr Res 52: 19 24. Ungvari Z and Koller A 2001 ; Selected contribution: NO released to flow reduces myogenic tone of skeletal muscle arterioles by decreasing smooth muscle Ca2 sensitivity. J Appl Physiol 91: 522527. Wallis RM, Corbin JD, Francis SH, and Ellis P 1999 ; Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function and the contractile responses of trabeculae carneae and aortic rings in vitro. J Cardiol 83: 3C12C. Webb DJ, Muirhead GJ, Wulff M, Sutton JA, Levi R, and Dinsmore WW 2000 ; Sildenafil citrate potentiates the hypotensive effects of nitric oxide donor drugs in male patients with stable angina. J Coll Cardiol 36: 2531. Wedel B, Harteneck C, Foerster J, Friebe A, Schultz G, and Koesling D 1995 ; Functional domains of soluble guanylyl cyclase. J Biol Chem 270: 2487124875. Zhao Y, Brandish PE, DiValentin M, Schelvis JP, Babcock GT, and Marletta MA 2000 ; Inhibition of soluble guanylate cyclase by ODQ. Biochemistry 39: 10848 10854.

Inhibitors, there is no evidence that one drug presents a higher risk than another. Sildenafil has been used by more than 23 million men worldwide, tadalafil by more than 4.5 million, and vardenafil by more than 1.8 million. The difference in the number of NAION cases among all three PDE5 inhibitors reflects the quantities of each drug used worldwide rather than real differences in risk among drugs. There have also been multiple clinical studies on the effects of PDE5 inhibitors on the ocular circulation. None of those studies indicated that PDE5-inhibitor treatment causes a decrease in optic nerve head or choroidal blood flow; on the contrary, some studies actually suggested that the drug causes small increases in ocular blood flow. A review of 103 clinical trials of sildenafil involving 13, 000 patients found no reports of NAION. NAION has been reported rarely through postmarketing surveillance with short- and long-acting PDE5 inhibitors. These cases have, for the most part, been in patients who had underlying anatomic or vascular risk factors for the development of NAION. Birth-control pills slightly increase your risk of strokes, blood clots, high blood pressure, heart attacks, gallbladder disease, vision problems, and liver tumors and tagamet. INTRODUCTION Cyclic nucleotide phosphodiesterases PDEs ; constitute a large superfamily with at least 11 different gene families, i.e., PDE1 to PDE11 ; of structurally related, functionally distinct, and highly regulated enzymes 1 ; . Most PDE families comprise more than one gene ; 20 PDE genes ; , which generate multiple protein products .50 PDE proteins ; via alternative mRNA splicing or use of different promoters transcription initiation sites 2 ; . PDEs regulate physiological processes by degrading intracellular second messengers, cyclic adenosine 39, 59-monophosphate cAMP ; and cyclic guanosine 39, 59-monophosphate cGMP ; , through PDEcatalyzed hydrolysis 312 ; . PDE4, PDE7, and PDE8 are highly specific for cAMP, whereas PDE5, PDE6, and PDE9 are highly specific for cGMP. PDE1, PDE2, PDE3, PDE10, and PDE11 exhibit dual specificity with greater or lesser preference for cAMP or cGMP 3 ; . Thus, PDEs are clinical targets for such biological disorders as retinal degeneration, congestive heart failure, depression, asthma, erectile dysfunction, and inflammation 5, 1318 ; . Selective inhibitors of PDEs have already been shown or are expected to exert beneficial effects in a number of therapeutic areas, including stimulation of myocardial contractility, inhibition of mediator release, inhibition of platelet aggregation, cancer chemotherapy, analgesia, and treatment of depression, Parkinson's disease, and learning and memory disorders 14, 16, 1941 ; . For example, selective inhibitors of PDE4 may be used as new antidepressants, memory-enhancing drugs, and novel antiasthmatic and antiinflammatory agents for the treatment of chronic obstructive pulmonary disease COPD ; , asthma, and other respiratory diseases 42 ; . Selective inhibitors of PDE5, such as the well-known sildenafil Viagra ; , vardenafil Levitra ; , and tadalafil Cialis ; , have been used to treat male erectile dysfunction ED ; 4349 ; . Understanding the protein structures, particularly the active site structures, and catalytic mechanism will provide a solid basis for rational design of novel, more potent inhibitors of PDEs for therapeutic treatment of a number of human diseases. PDE families share a similar active site structure. In particular, a conserved carboxyl-terminal catalytic domain contains a histidine-rich motif [HD X2 ; H X ; 4N] and two divalent metal ion-binding sites 3, 50, 51 ; . A divergent amino-terminal domain confers isoform-specific regulatory properties. Xu et al. 52 ; first reported a three-dimensional 3D ; x-ray crystal structure of the catalytic domain of human phosphodiesterase 4B2B PDE4 ; . In the reported x-ray crystal structure, the active site contains a cluster of two divalent metal ions, denoted by Me1 and Me2. Me1 should be a Zn21 ion based on the observed geometry of the metal-coordinating ligands, the anomalous x-ray diffraction behavior, the existing biochemical evidence, and the known high affinity of PDE4 for zinc. Me2 is most likely Mg21 53, 54 ; , but the possibility of Me2 Mn21 or Zn21 cannot be ruled out 52 ; . According to the 3D x-ray crystal structure reported by Xu et al. 52 ; , in the PDE4.

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