2002;30(9):721–8.

18. Yorikane R. Unique cardiac effect of azelnidipine, a novel calcium antagonist [in Japanese]. Bio Clin. 2003;18(13):1210–5. 19. Palatini P, Benetos A, Julius S. Impact of increased heart rate on clinical outcomes in hypertension: implications for antihypertensive drug therapy. Drugs. 2006;66(2):133–44.PubMedCrossRef 20. Okabayashi J, Matsubayashi Autophagy inhibitor K, Sato T, et al. Effects of nifedipine and enalapril on the central nervous system in elderly hypertensive patients: power spectral analysis of heart rate variability [in Japanese]. Jpn J Geriatr. 1994;31(4):285–92.CrossRef 21. Eguchi K, Kario K, Shimada K. Differential effects of a long-acting angiotensin converting enzyme inhibitor (temocapril) and a long-acting calcium antagonist (amlodipine) on ventricular ectopic beats in older hypertensive Belnacasan cost patients. Hypertens Res. 2002;25(3):329–33.PubMedCrossRef 22. Kitai T, Yoshida Y, Kuramoto K, et al. Use-results survey of azelnidipine (Calblock®) tablet [in Japanese]. J Clin Ther Med. 2005;21:511–27. 23. UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ. 1998;317(7160):713–20.CrossRef

24. Nippon Data 80 Research Group. Impact of elevated blood pressure on mortality from all causes, cardiovascular diseases, heart disease and stroke among Japanese: 14 year follow-up of randomly selected population from Japanese-Nippon data 80. J Hum Hypertens. 2003;17(12):851–7.”
“1 Introduction Risperidone is a benzisoxazole derivate see more belonging to the class of second-generation antipsychotics. It selectively antagonizes the dopamine (D2) and serotonin (5-HT2) receptor systems in the brain and

has a lower propensity than classical neuroleptics such as haloperidol to induce extrapyramidal adverse events (AEs) at therapeutic doses [1–3]. Risperidone is effective in the treatment of schizophrenia and other psychiatric illnesses in adults and children [4, 5]. Risperidone is well absorbed (94%) after oral administration, reaching the maximum plasma concentration (Cmax) within 1–2 hours. Food does not affect the rate or the extent of absorption of risperidone. The volume of distribution is 1–2 L/kg, and the plasma protein binding of risperidone is 90% [6]. Risperidone is extensively metabolized Carteolol HCl in the liver. The main metabolic pathway is 9-hydroxylation by cytochrome P450 (CYP) 2D6, and the principal metabolite, 9-hydroxy-risperidone, has been shown to be nearly equipotent to risperidone in animal studies [7, 8]. Because CYP2D6 is subject to genetic polymorphism, the elimination half-life (t½) of risperidone has been shown to be about 3 hours in extensive metabolizers and 20 hours in poor metabolizers, while the t½ of 9-hydroxy-risperidone was about 21 hours in extensive metabolizers and 30 hours in poor metabolizers [7]. Risperidone and its metabolites are eliminated via the urine (70%) and, to a much lesser extent, via the feces [9].