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Hypertension

Hypertension is an important public health challenge in the United States because of its high prevalence and the concomitant increase in the risk of cardiovascular/renal disease. As many as 43 million Americans have hypertension, which is defined as a systolic blood pressure (SBP) 140 mm Hg and/or a diastolic BP (DBP) 90 mm Hg and/or taking antihypertensive medications. Hypertension is often portrayed as a “silent killer” because patients with mild or moderate hypertension are often asymptomatic. When symptoms appear as a result of organ damage, therapeutic options are limited. Although the symptoms produced by these organ complications (MI, HF, stroke, or chronic renal failure) are associated with decreased QoL, possible alterations in QoL in patients with mild to moderate hypertension who do not have such complications remain controversial. Declines in QoL seen in aging populations complicate the analysis of a potential relationship between “asymptomatic” hypertension and QoL in older patients.Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in the US population), stroke (the third leading cause of death), congestive heart failure, end-stage renal disease, and peripheral vascular disease.The goal of antihypertensive therapy is to abolish the risks associated with blood pressure (BP) elevation without adversely affecting quality of life. It is well established that effective blood pressure (BP) control reduces the risk of cardiovascular disease and stroke in patients with hypertension.For every 20mmHg decrease in systolic BP (SBP), there are 30 and 40% reductions in ischaemic heart disease and stroke mortality, respectively.

Age-associated increases in hypertension prevalence derive from changes in arterial structure and function accompanying aging. Large vessels become less distensible, which increases pulse wave velocity, causing late systolic blood pressure (SBP) augmentation and increasing myocardial oxygen demand. Reduction of forward flow also occurs, limiting organ perfusion. These undesirable alterations are enhanced with coronary stenosis or excessive drug-induced diastolic blood pressure (DBP) reduction. Autonomic dysregulation contributes to orthostatic hypotension (a risk factor for falls, syncope, and cardiovascular [CV] events) and orthostatic hypertension (a risk factor for left ventricular hypertrophy [LVH], coronary artery disease [CAD], and cerebrovascular disease). Progressive renal dysfunction, because of glomerulosclerosis and interstitial fibrosis with a reduction in glomerular filtration rate (GFR) and other renal homeostatic mechanisms such as membrane sodium/ potassium–adenosine triphosphatase, fosters hypertension through increased intracellular sodium, reduced sodium– calcium exchange, and volume expansion. Microvascular damage contributes to chronic kidney disease (CKD) as reduced renal tubular mass provides fewer transport pathways for potassium excretion.

Compliance to prescribed antihypertensive regimen is essential to achieve the target BP. Among many factors, the complexity and tolerability of the antihypertensive regimen are two major determinants of patient compliance. In a recent meta-analysis by Law et al of 354 randomized, double-blind trials, the mean placebo-corrected reduction in BP with monotherapy was only 9.1/5.5 mm Hg. There was little difference in this regard between a diuretic, b-blocker, angiotensinconverting enzyme (ACE) inhibitor, angiotensin receptor blocker (ARB), or calcium channel blocker (CCB). Similar results were found in the Treatment of Mild Hypertension study, in which comparable BP reduction was observed after long-term treatment with a diuretic, b-blocker, CCB, a-blocker, and ACE inhibitor.Multiple antihypertensive agents needed to achieve the target BP control in majority of the patients add to the complexity of such therapy. The combination of two antihypertensive drugs is recommended by the European Society of Hypertension (ESH)/European Society of Cardiology (ESC) in patients with blood pressure (BP) not adequately controlled with antihypertensive monotherapy or as first-line therapy in patients at high risk.Fixed-dose combinations of antihypertensive agents effectively lower BP and help simplify the therapeutic regimen and increase compliance.

In response to a rising demand for highly effective and tolerable fixed-dose combinations with amlodipine, a combination of olmesartan-amlodipine was developed that was able to reduce BP by −30.1/−19.0 mmHg in doses up to 40/10 mg in a recent study. Almost maximal BP reduction was achieved as early as four weeks after treatment initiation and was sustained throughout the eight-week study period. Tolerability was good, with a reduction of incidence of edema, known to be increased with amlodipine monotherapy at high doses. Fixed-dose combinations of antihypertensive drugs improve patient compliance which, in turn, is associated with a reduction in hospitalization and cardiovascular events. The results of the COACH (Combination of Olmesartan Medoxomil and Amlodipine Besylate in Controlling High Blood Pressure) study, a clinical trial that assessed the efficacy and safety of amlodipine besylate (dihydropyridine CCB) in combination with olmesartan medoxomil (ARB) in patients with mild-to-severe hypertension, have been published elsewhere. Here we report a prespecified subgroup analysis of the COACH study in patients with diabetes, Blacks, elderly (X65 years) patients and those who are overweight/obese with a BMIX30 kg/m 2.

Uses, Administration, Adverse Effects and Treatment ACE Inhibitors

Uses and Administration

ACE inhibitors are antihypertensive drugs that act as vasodilators and reduce peripheral resistance. They inhibit angiotensin-converting enzyme (ACE), which is involved in the conversion of angiotensin I to angiotensin II. Angiotensin II stimulates the synthesis and secretion of aldosterone and raises blood pressure via a potent direct vasoconstrictor effect. ACE is identical to bradykininase (kininase II) and ACE inhibitors also reduce the degradation of bradykinin, which is a direct vasodilator and is also involved in the generation of prostaglandins. The pharmacological actions of ACE inhibitors are thought to be primarily due to the inhibition of the renin-angiotensin-aldosterone system, but since they also effectively reduce blood pressure in patients with low renin concentrations other mechanisms are probably also involved. ACE inhibitors produce a reduction in both preload and afterload in patients with heart failure. They also reduce left ventricular remodelling, a process that sometimes follows myocardial infarction. Normally, renal blood flow is increased without a change in glomerular filtration rate. ACE inhibitors also reduce proteinuria associated with glomerular kidney disease. ACE inhibitors are used in the treatment of hypertension and heart failure and are given to improve survival after myocardial infarction and for the prophylaxis of cardiovascular events in patients with certain risk factors. They are also used in the treatment of diabetic nephropathy. They are generally given orally. In some hypertensive patients there may be a precipitous fall in blood pressure when starting therapy with an ACE inhibitor and the first dose should preferably be given at bedtime; if possible, any diuretic therapy should be stopped a few days beforehand and resumed later if necessary. In patients with heart failure taking loop diuretics, severe first-dose hypotension is common on introduction of an ACE inhibitor, but temporary withdrawal of the diuretic may cause rebound pulmonary oedema. Thus treatment should start with a low dose under close medical supervision (Sweetman).

Adverse Effects and Treatment

Many of the adverse effects of ACE inhibitors relate to their pharmacological action and all therefore have a similar spectrum of adverse effects. Some effects, such as taste disturbances and skin reactions, were at one time attributed to the presence of a sulfhydryl group (as in captopril) but have now also been reported with other ACE inhibitors; however, they may be more common with captopril. The most common adverse effects are due to the vascular effects of ACE inhibitors and include hypotension, dizziness, fatigue, headache, and nausea and other gastrointestinal disturbances. Pronounced hypotension may occur at the start of therapy with ACE inhibitors, particularly in patients with heart failure and in sodium- or volume-depleted patients (for example, those given previous diuretic therapy). Myocardial infarction and stroke have been reported and may relate to severe falls in blood pressure in patients with ischaemic heart disease or cerebrovascular disease. Other cardiovascular effects that have occurred include tachycardia, palpitations, and chest pain. Deterioration in renal function, including increasing blood concentrations of urea and creatinine, may occur, and reversible acute renal failure has been reported. Renal effects are most common in patients with existing renal or renovascular dysfunction or heart failure, in whom vasodilatation reduces renal perfusion pressure; it may be aggravated by hypovolaemia. Proteinuria has also occurred and in some patients has progressed to nephrotic syndrome. Hyperkalaemia and hyponatraemia may develop due to decreased aldosterone secretion. Other adverse effects include persistent dry cough and other upper respiratory tract symptoms, and angioedema; these may be related to effects on bradykinin or prostaglandin metabolism. Skin rashes (including erythema multiforme and toxic epidermal necrolysis) may occur; photosensitivity, alopecia, and other hypersensitivity reactions have also been reported. Blood disorders have been reported with ACE inhibitors and include neutropenia and agranulocytosis (especially in patients with renal failure and in those with collagen vascular disorders such as systemic lupus erythematosus and scleroderma), thrombocytopenia, and anaemias. Other less common adverse effects reported with ACEinhibitors include stomatitis, abdominal pain, pancreatitis, hepatocellular injury or cholestatic jaundice, muscle cramps, paraesthesias, mood and sleep disturbances, and impotence. ACE inhibitors have been associated with fetal toxicity. Most of the adverse effects of ACE inhibitors are reversible on withdrawing therapy. Symptomatic hypotension, including that after overdosage, generally responds to volume expansion with an intravenous infusion of sodium chloride 0.9%  (Sweetman).

Produksi Xilanase dari Mikroorganisme

Jenis mikroorganisme yang sudah umum menghasilkan xilanase ialah jamur dan bakteri. Contoh beberapa mikroorganisme penghasil endoxilanase disajikan pada Tabel 1. Beberapa jenis bakteri dan jamur diketahui mampu menghasilkan xilanase secara ekstraseluler. Xilanase dari Clostridium acetobuty-licum telah diteliti oleh Lee et al. (1985), yaitu dari 20 strain Clostridium sp. ternyata C. acetobutylicum NRRL B527 dan ATCC 824 menghasilkan xilanase terbanyak. Strain NRRL B527 menghasilkan xilanase pada pH 5,2, sedangkan strain ATCC 824 menghasilkan xilanase, xilopiranosidase, dan arabinofuranosidase pada kultur anaerob. Bacillus sp. penghasil xilanase bersifat alkalofilik yang telah diteliti adalah Bacillus sp. YC 335 (Park et al., 1992), Bacillus sp. 41M-1 (Nakamura et al., 1993), dan Bacillus sp. TAR-1 yang juga bersifat termofilik (Nakamura et al., 1994). Genus Bacillus diketahui sebagai penghasil xilanase yang aktif pada suhu 50 °C – 60°C, dengan pH 7 - 9, sehingga enzim dari bakteri ini diharapkan dapat diproduksi dan digunakan pada proses awal pemutihan pulp di industri pulp dan kertas.Kubata et al. (1992) telah mengisolasi Aeromonas caviae ME-1 penghasil xilanase I dari usus herbivorous insect, sedangkan Dung et al. (1993) melakukan penelitian β-1,4-xilanase 2 dan 3 dari A. caviae W-61. Irawadi (1992) berhasil memproduksi selulase dan xilanase dari Neurospora sitophila pada substrat padat limbah kelapa sawit. Richana et al. (2000) telah melakukan isolasi bakteri penghasil xilanase alkalofilik yang berasal dari tanah berkapur pH 7,9. Seleksi dilakukan berdasarkan ukuran koloni dan zona bening di sekeliling koloni yang tumbuh pada media pertumbuhan.

Winterhalter dan Liebl (1995) telah melakukan produksi xilanase thermostabil dari bakteri Thermotoga maritima MSB8, sedangkan Ruiz-Arribas et al. (1995) telah mendapatkan Streptomyces halstedii JM8 penghasil xilanase (xys I) yang diisolasi dari jerami. Lin et al., (1999), melakukan pemurnian dan karakterisasi biokimia xilanase dari fungi termofilik Thermomyces lanuginosus- SSBP.

Komposisi medium fermentasi dapat sederhana atau kompleks tergantung jenis mikroba dan kondisi fermentasinya. Baik medium sederhana maupun kompleks dapat merupakan medium sintetik atau medium kasar (crude). Medium sintetik cocok untuk skala laboratorium dan industri kecil karena mempunyai beberapa keuntungan antara lain setiap komponen dapat dengan mudah dikurangi, dihilangkan atau ditambahkan. Di samping itu, pada medium sintetik biasanya tidak membentuk buih selama proses berlangsung, dan kesalahan atau kelainan yang mungkin terjadi selama fermentasi akibat komposisi yang kurang tepat dapat dicegah. Pada industri skala besar medium sintetik tidak sesuai digunakan (Richana, 2002).

Kriteria sumber nutrisi untuk skala besar menurut Rachman (1989) adalah

1. Dapat memproduksi biomassa dengan hasil maksimal untuk tiap gram substrat yang digunakan.

2. Memungkinkan pembentukan produk fermentasi dengan laju maksimal.

3. Dapat menekan pembentukan produk yang tidak diinginkan sampai serendah mungkin.

4. Mutu konstan, murah, dan tersedia sepanjang tahun.

5. Tidak menimbulkan masalah terhadap aerasi, agitasi, ekstraksi, dan pemurnian hasil serta perlakuan limbah.

Substrat yang digunakan dalam proses fermentasi berpengaruh terhadap aktivitas dan produktivitas enzim. Adanya substrat tertentu di dalam medium produksi dapat memacu mikroorganisme untuk mensekresi metabolit selnya. Zat makanan utama bagi pertumbuhan mikroorganisme adalah sumber karbon, nitrogen, dan komponen mineral terutama fosfat. Formulasi media dalam pertumbuhan dan produksi hasil fermentasi merupakan suatu tahap penting dalam mendesain percobaan dalam skala kerja (Stanbury dan Whitaker, 1984).

Beberapa sumber karbon yangsering digunakan adalah molases, serealia, pati, glukosa, sukrosa, dan laktosa. Produksi enzim xilanase sebagai sumber karbon adalah xilan. Xilan dengan aktivitas xilanase yang dihasilkan oleh mikroorganisme akan terhidrolisis menjadi xilosa.

C5H8O4 + H2O             C5H10O5

Xilan                                Xilosa

 

Prospek Xilanase dalam Biokonversi Limbah Pertanian

Perkembangan dan kemajuan bidang pertanian dan industra pertanian di Indonesia telah

menimbulkan peningkatan limbah pertanian yang sebagian besar merupakan limbah berlignoselulosa. Limbah berlignoselulosa yang tinggi potensinya di Indonesia antara lain jerami,

onggok (ampas tapioka, garut), bonggol dan kulit jagung, sabut serta tandan kosong kelapa sawit, bagase tebu, dan lain sebagainya. Seringkali limbah yang tidak tertangani, akan menimbulkan pencemaran lingkungan. Pada dasarnya limbah tidak memiliki nilai ekonomi, bahkan mungkin bernilai negatif karena memerlukan biaya penanganan. Namun demikian, bila ditelaah lebih dalam limbah lignoselulosa sebagai bahan organik memiliki potensi besar sebagai bahan baku berbagai industri, terutama untuk pembuatan kertas. Di samping itu, fraksinasi limbah ini menjadi komponen penyusunnya akan meningkatkan pendayagunaan dalam berbagai industri. Melihat potensi bahan limbah berlignoselulosa yang melimpah maka perlu penggalian yang lebih intensif tentang pemanfaatan potensi tersebut. Bahan berlignoselulosa terdiri atas hemiselulosa, selulosa, dan lignin. Hemiselulosa dapat dimanfaatkan menjadi produk xylitol, xylosa, dan fulfural. Selulosa dapat dimanfaatkan menjadi protein sel tunggal, glukosa, fruktosa, dan sorbitol. Sedangkan lignin untuk bahan bakar, pelarut, resin, produk karbon, dan matriks adsorpsi (Paturau, 1969).

Salah satu sasaran dalam pengembangan bioteknologi adalah merintis pemanfaatan mikroorganisme dalam biokonversi limbah. Pemanfaatan limbah berlignoselulosa dengan menggunakan jasa mikroorganisme dapat menghasilkan enzim ekstraseluler yang mampu mendegradasi bahan berlignoselulosa menjadi fraksi penyusunnya. Misalkan enzim selulase yang dapat merombak bahan berlignoselulosa berupa jerami atau sampah organic menjadi kompos, atau menghidrolisis selulosa menjadi glukosa. Sedangkan xilanase dapat menghidrolisis hemiselulosa menjadi xilosa, proses ini dapat diaplikasikan ke beberapa proses dan pemanfaatannya (Richana, 2002).

Pemanfaatan Xilanase untuk Proses Pembuatan Kertas

Pada pembuatan kertas, xilanase digunakan untuk menghilangkan hemiselulosa dalam proses bleaching. Enzim ini sebagai pengganti cara kimia sehingga pencemaran racun limbah kimia akan dihindari dan lebih murah (Ruiz-Arribas et al., 1995). Bahan baku kayu pembuat kertas setelah melalui proses digester dan pencucian, sebenarnya masih dalam keadaan kotor (derajat putihnya rendah). Untuk menghasilkan kertas yang bermutu tinggi perlu dilakukan proses pemutihan. Proses pemutihan bertujuan untuk menghilangkan lignin, hemiselulosa penyebab warna coklat dan zat ekstraktif yang dikandung dari hasil pencucian dan penyaringan.

Proses pemutihan biasanya dilakukan bertahap, karena mempunyai kelebihan di antaranya adalah nilai derajat putihnya tinggi. Proses bertahap ini terdiri atas tahap khlorinasi, ekstraksi, dan penambahan khlorin dioksida. Khlorin adalah bahan beracun, sehingga khlorin sisa proses yang dibuang ke perairan sungai akan membuat polusi yang tinggi. Ternyata polusi terbesar di Negara kita adalah polusi dari pabrik kertas. Penggantian penggunaan khlorin untuk pemutihan kertas telah memberikan peluang untuk aplikasi bioteknologi. Xilanase merupakan enzim yang pertama kali dilaporkan untuk pemutihan kertas dan sekarang telah digunakan pada beberapa pabrik kertas (Richana, 2002).

Jumlah pabrik kertas yang sudah beroperasi di Indonesia saat ini lebih dari 14 perusahaan dan belum satu pun menggunakan proses enzimatis dalam proses pemutihan. Dengan demikian, untuk mendukung pelestarian lingkungan maka perlu segeradiaplikasikan proses ramah lingkungan (clean processing) di Indonesia. Untuk proses pembuatan kertas diharapkan xilanase yang digunakan adalah yang termostabil dan tahan pada pH alkali (Nakamura et al., 1993) dan jenis enzimnya adalah endoxilanase.