scholarly journals Efektivitas Daun Sirsak (Annona muricata Linn) terhadap Penurunan Tekanan Darah Pada Hipertensi

2021 ◽  
Vol 10 (2) ◽  
pp. 413-415
Author(s):  
Niputu Swastini
Keyword(s):  
Nitric Oxide ◽  
Vitamin C ◽  
Ace Inhibitor ◽  
Annona Muricata

Pendahuluan: Hipertensi merupakan salah satu penyakit tidak menular yang sering disebut sebagai “silent killer” (pembunuh diam-diam) yang dapat didefinisikan dengan suatu kondisi dimana pembuluh darah memiliki tekanan darah tinggi (tekanan darah sistolik > 140 Daun sirsak sering digunakan sebagai pengobatan alternatif hipertensi. Kandungan daun sirsak yang diperkirakan dapat menurunkan tekanan darah adalah ion kalium. Tujuan: mengetahui efektivitas daun sirsak (Annona muricata Linn) terhadap penurunan tekanan darah pada hipertensi. Metode: Menggunakan studi literatur dari jurnal baik nasional maupun internasional dengan cara meringkas topik pembahasan dan membandingkan hasil yang disajikan dalam setiap artikel. Hasil: Ion kalium mempunyai beberapa mekanisme dalam menurunkan tekanan darah, yaitu memperlemah kontraksi miokardium, meningkatkan pengeluaran natrium dari dalam tubuh, menghambat pengeluaran renin, menyebabkan vasodilatasi, dan menghambat vasokontriksi endogen. Kadar kalium yang tinggi dapat meningkatkan eksresi natrium, sehingga dapat menurunkan volume darah dan tekanan darah. Flavonoid bekerja sebagai ACE inhibitor yang akan menghambat perubahan AI menjadi AII sehingga menurunkan sekresi hormon antidiuretik (ADH) yang membuat jumlah sekresi urin meningkat dan banyak garam (NaCl) yang dikeluarkan akhirnya mengakibatkan penurunan tekanan darah. Vitamin C juga berperan dalam menurunkan tekanan darah, karna dapat memodulasi pengeluaran nitric oxide. Kesimpulan: pemberian daun sirsak dapat menurunkan kadar tekanan darah pada hipertensi

Long-term inhibition of nitric oxide synthesis increases arterial thrombogenecity in rat carotid artery

2002 ◽  
Vol 282 (4) ◽  
pp. H1478-H1484 ◽  
Author(s):  
Mayuko Kubo-Inoue ◽  
Kensuke Egashira ◽  
Makoto Usui ◽  
Masao Takemoto ◽  
Kisho Ohtani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carotid Artery ◽  
Tissue Factor ◽  
Ace Inhibitor ◽  
Vascular Tissue ◽  
Thrombus Formation ◽  
Coronary Syndrome ◽  
Ace Activity ◽  
Reliable Marker

Reduced activity of endothelial nitric oxide (NO) may be involved in thrombus formation on atherosclerotic plaques, a major cause of acute coronary syndrome. However, mechanisms of such increase in arterial thrombogenecity have not been fully understood. We previously reported that long-term inhibition of NO synthesis by administration of N G-nitro-l-arginine methyl ester (l-NAME) causes hypertension and activates vascular tissue angiotensin-converting enzyme (ACE) activity. We used this model to investigate the mechanism by which long-term impairment of NO activity increases arterial thrombogenecity. We observed cyclic flow variations (CFVs), a reliable marker of platelet thrombi, after the production of stenosis of the carotid artery in rats treated with l-NAME for 4 wk. The thrombin antagonist argatroban suppressed the CFVs. The CFVs were detected in rats receiving l-NAME plus hydralazine but not in rats receiving l-NAME plus an ACE inhibitor (imidapril). Treatment with the ACE inhibitor imidapril, but not with hydralazine, prevented l-NAME-induced increases in carotid arterial ACE activity and attenuated tissue factor expression. These results suggest that long-term inhibition of endothelial NO synthesis may increase arterial thrombogenecity at least in part through angiotensin II-induced induction of tissue factor and the resultant thrombin generation. These data provide a new insight as to how endothelial NO exhibits antithrombogenic properties of the endothelium.

scholarly journals Effects of vitamin C on nitric oxide/L-arginine pathway in patients with atherosclerosis

2002 ◽  
Vol 39 ◽  
pp. 253
Author(s):  
Dimitris Tousoulis ◽  
Graham Davies ◽  
Costas Tentolouris ◽  
George Tousoulis ◽  
George Goumas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vitamin C

Tetrahydrobiopterin correctsEscherichia coliendotoxin-induced endothelial dysfunction

2005 ◽  
Vol 289 (4) ◽  
pp. H1752-H1757 ◽  
Author(s):  
Friedrich Mittermayer ◽  
Johannes Pleiner ◽  
Georg Schaller ◽  
Stefan Zorn ◽  
Khodadad Namiranian ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Vitamin C ◽  
Acute Inflammation ◽  
Umbilical Vein ◽  
Oxidant Stress ◽  
Double Blind ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Acute inflammation causes endothelial dysfunction, which is partly mediated by oxidant stress and inactivation of nitric oxide. The contribution of depletion of tetrahydrobiopterin (BH4), the cofactor required for nitric oxide generation, is unclear. In this randomized, double-blind, three-way crossover study, forearm blood flow (FBF) responses to ACh and glyceryltrinitrate (GTN) were measured before and 3.5 h after infusion of Escherichia coli endotoxin (LPS, 20 IU/kg iv) in eight healthy men. The effect of intra-arterial BH4(500 μg/min), placebo, or vitamin C (24 mg/min) was studied on separate days 3.5 h after LPS infusion. In addition, human umbilical vein endothelial cells were incubated for 24 h with vitamin C and LPS. ACh and GTN caused dose-dependent forearm vasodilation. The FBF response to ACh, which was decreased by 23 ± 17% ( P < 0.05) by LPS infusion, was restored to baseline reactivity by BH4and vitamin C. FBF responses to GTN were not affected by BH4or vitamin C. LPS increased leukocyte count, high-sensitivity C-reactive protein, IL-6, IL-1β, IFN-γ, monocyte chemoattractant protein-1, pulse rate, and body temperature and decreased platelet count and vitamin C concentration. Vitamin C increased forearm plasma concentration of BH4by 32% ( P < 0.02). Incubation with LPS and vitamin C, but not LPS alone, increased intracellular BH4concentration in human umbilical vein endothelial cells. Impaired endothelial function during acute inflammation can be restored by BH4or vitamin C. Vitamin C may exert some of its salutary effects by increasing BH4concentration.

The protective effect of vitamin C, vitamin E and selenium combination therapy on ethanol-induced duodenal mucosal injury

2004 ◽  
Vol 23 (8) ◽  
pp. 391-398 ◽  
Author(s):  
M Koyuturk ◽  
S Bolkent ◽  
S Ozdil ◽  
S Arbak ◽  
R Yanardag
Keyword(s):  
Nitric Oxide ◽  
Vitamin E ◽  
Nitric Oxide Synthase ◽  
Vitamin C ◽  
Protective Effect ◽  
Neuronal Nitric Oxide Synthase ◽  
Mucosal Injury ◽  
The Other ◽  
Absolute Ethanol ◽  
Oxide Synthase

In this study, the effect of a combination of vitamin C, vitamin E and selenium on ethanol-induced duodenal mucosal damage in rats was investigated morphologi-cally and biochemically. The duodenal mucosal injury was produced by oral administration of 1 mL of absolute ethanol to each rat. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg) and selenium (0.5 mg/kg) for 3 days and absolute ethanol 1 hour after last antioxidant administration and were sacrificed 1 hour after absolute ethanol. Extreme degeneration in intestinal mucosa of rats given ethanol was observed morphologically. In addition, an increase in neuronal nitric oxide synthase immunoreactive areas was observed in the rats of the group given ethanol. On the other hand, a normal morphological appearance and a decrease in neuronal nitric oxide synthase immunoreactive areas were detected in the rats given ethanol+vitamin C+vitamin E+selenium. In the group to which ethanol was administered, an increase in serum cholesterol and a decrease in serum albumin levels were determined. On the other hand, in the group to which ethanol+vitamin C+vitamin E+selenium were administered, serum cholesterol value decreased, and the serum albumin level increased. As a result, we can say that the combination of vitamin C, vitamin E and selenium has a protective effect on ethanolinduced duodenal mucosal injury.

scholarly journals Role of Oxidative Stress and Mitochondrial Dysfunction in Sepsis and Potential Therapies

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Konstantinos Mantzarlis ◽  
Vasiliki Tsolaki ◽  
Epaminondas Zakynthinos
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Intensive Care ◽  
Vitamin C ◽  
Causes Of Death ◽  
Redox Balance ◽  
Cardiac Performance ◽  
Efficiency Evaluation ◽  
Permeability Impairment

Sepsis is one of the most important causes of death in intensive care units. Despite the fact that sepsis pathogenesis remains obscure, there is increasing evidence that oxidants and antioxidants play a key role. The imbalance of the abovementioned substances in favor of oxidants is called oxidative stress, and it contributes to sepsis process. The most important consequences are vascular permeability impairment, decreased cardiac performance, and mitochondrial malfunction leading to impaired respiration. Nitric oxide is perhaps the most important and well-studied oxidant. Selenium, vitamin C, and 3N-acetylcysteine among others are potential therapies for the restoration of redox balance in sepsis. Results from recent studies are promising, but there is a need for more human studies in a clinical setting for safety and efficiency evaluation.

scholarly journals Anti-Hypertensive Drugs and Sexual Dysfunction in Men

2020 ◽  
Vol 13 (01) ◽  
pp. 1-11
Author(s):  
Noverio Tarukallo ◽  
Haerani Rasyid
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Sexual Dysfunction ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Angiotensin Receptor Blocker ◽  
Ace Inhibitor ◽  
Channel Blocker ◽  
Angiotensin Receptor ◽  
Β Blocker

Salah satu faktor yang memiliki risiko yang terkait dengan kejadian disfungsi seksual pada pria adalah obat anti-hipertensi. Obat anti-hipertensi yang memiliki efek menyebabkan disfungsi seksual pada pria termasuk; diuretik, Clonidine, dan β-blocker (kecuali nebivolol), tetapi ada beberapa obat anti-hipertensi yang memiliki efek netral, bahkan memiliki efek positif yang dalam hal ini dapat meningkatkan fungsi seksual pada pria. Obat anti-hipertensi yang memiliki efek netral pada fungsi seksual pria meliputi; Calcium Channel Blocker dan ACE-Inhibitor dan yang memiliki efek meningkatkan fungsi seksual pada pria termasuk; ARB dan β-blocker yaitu nebivolol. Penggunaan obat anti-hipertensi dapat mempengaruhi fungsi seksual pada pria melalui mekanisme yang berbeda. Obat anti-hipertensi seperti diuretik, β-blocker, dan clonidine dapat menyebabkan disfungsi seksual pada pria melalui mekanisme perubahan dalam aliran simpatis, efek pada kontraksi otot polos fisik, dan melalui pengaruh pada kadar hormon androgen. Angiotensin Receptor Blocker dan Nebivolol dapat meningkatkan fungsi seksual melalui mekanisme penghambatan pada Angiotensin II dan meningkatkan bioavailabilitas Nitric Oxide.

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