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What is hypertension?

Hypertension (HTN or HT), also known as high blood pressure or arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is persistently elevated. Blood pressure is expressed by two measurements, the systolic and diastolic pressures, which are the maximum and minimum pressures, respectively, in the arterial system. The systolic pressure occurs when the left ventricle is most contracted; the diastolic pressure occurs when the left ventricle is most relaxed prior to the next contraction. Normal blood pressure at rest is within the range of 100–140 millimeters mercury (mmHg) systolic and 60–90 mmHg diastolic. Hypertension is present if the blood pressure is persistently at or above 140/90 mmHg for most adults; different numbers apply to children.

Hypertension usually does not cause symptoms initially, but sustained hypertension over time is a major risk factor for hypertensive heart disease, coronary artery disease, stroke, aortic aneurysm, peripheral artery disease, and chronic kidney disease.

Antihypertensive can be categorized into the following eight mechanisms:

1, Help the kidneys eliminate excess salt and water from the body's tissues and the blood. This helps reduce the swelling caused by fluid buildup in the tissues. The reduction of fluid dilates the walls of arteries and lowers blood pressure.

2, Block the entry of calcium into muscle cells in artery walls. Muscle cells need calcium to constrict, so reducing their calcium keeps them more relaxed and lowers blood pressure.

3, Act on the nervous system to slow the heart rate and reduce the force of the heart's contraction. Centrally acting agonists also act on the nervous system to relax arteries and slow the heart rate.

4,Activate GABA receptors. γ-Aminobutyric acid (GABA), one of the major inhibitory neurotransmitters in the central nervous system and is also found in many peripheral tissues. GABA has been shown to play an important role in the modulation of cardiovascular function by acting not only within the central nervous system but also within peripheral tissues.

5, Act on the Renin-angiotensin-aldosterone system(RAAS). ACE (Angiotensin converting enzyme) inhibitors block the production of substances that constrict blood vessels. They also help reduce the build-up of water and salt in the tissues. AngII is a potent vasoconstrictor which reduces renal blood flow;The reduction of AngII is beneficial for blood pressure.

6, Lower Ameliorate ED (Endothelial dysfunction), lower SVR (systematic vascular resistance) , and BP is reduced. Homocysteine is known to cause endothelial cell damage and dysfunction.

7, Act directly on arteries to relax their walls by Vasodilators, so blood can move more easily through them. They lower blood pressure rapidly and are injected in hypertensive emergencies when patients have dangerously high blood pressure.

8, Promote the release of NO. NO has the effect that reduce pulmonary artery pressure.

What can be used to treat hypertension?

Vitamin B6 (Pyridoxine)

Mechanisms: 1, 2, 3, 4

Low serum vitamin B6 levels are associated with hypertension in human beings. Vitamin B6 is a readily metabolized and excreted water-soluble vitamin. The participation of vitamin B6 in neurotransmitter and hormone biosynthesis and amino acid reactions with kynureninase, cystathionine synthetase, cystathionase, and membrane L-type Ca channels may account for much of its antihypertensive effects.

The proposed mechanisms of hypertension in vitamin B6:

1. Acting on central nervous system, brain stem, depletion of neurotransmitters such as NE(Norepinephrine), serotonin, and GABA, which leads to an increase in sympathetic outflow.

2. Increased peripheral SNS (Sympathetic nervous system) activity.

3. Increased VSMC (vascular smooth muscle cells) Ca uptake and increased intracellular Ca release.

4. Increased end-organ responsiveness to glucocorticoids and mineralocorticoids (aldosterone).

One human study that high-dose vitamin B6 significantly lowered BP. This study compared 9 normotensive men and women with 20 hypertensive subjects, all of whom had significantly higher BP, plasma NE, and HR compared with control normotensive subjects. Subjects received 5 mg/(kg. d) of vitamin B6 for 4 weeks. The SBP fell from 167± 13 to 153 ± 15 mm Hg, an 8.4% reduction ( P < .01), and the DBP fell from 108± 8.2 to 98± 8.8 mm Hg, a 9.3% reduction ( P< .005). Plasma NE was reduced from 1.80 ±0.21 to 1.48 ±0.32 nmol/L (18% reduction; P < .005); plasma epinephrine fell from 330± 64 to 276± 67 pmol/L (16% reduction; P < .05). There was no significant change in HR (heart rate).

In summary, vitamin B6 has multiple antihypertensive effects that resemble those of central a agonists (ie, clonidine), CCBs (ie, DHP-CCB such as amlodipine), and diuretics. Finally, changes in insulin sensitivity and carbohydrate metabolism may lower BP in selected hypertensive individuals with the metabolic syndrome of insulin resistance.

Chronic intake of vitamin B6 at 200 mg/d is safe and has no adverse effects. Even doses up to 500 mg/d are probably safe.

Folic acid (FA)

Mechanisms: 5, 8

Folic acid (FA) treatment normalized plasma Hcy (homocysteine) levels in Ang II mice, and partially mitigated high blood pressure. These changes were associated with an increase in vascular density and normalization of renal cortical blood flow. In addition, FA supplementation mitigated the effect of ADMA on NO synthesis and also increased VEGF (vascular endothelial growth factor) expression and reduced anti-angiogenic factors endostatin and angiostatin.

Renal cortical blood flow and vascular density is improved in Ang II hypertension with FA supplementation

Nitric oxide production is improved with FA treatment in Ang II hypertension.

The production of NO is vital to maintaining vascular homeostasis and its reduction is an early sign of endothelial dysfunction.

FA treatment normalized these factors partially suggesting that Hcy was, in part, responsible for some of these effects. In addition, VEGF is a permeability factor which increases cellular permeability. Thus, it is also possible that the diminished VEGF in renal tissue inhibited vascular permeability, and decreased vascular fenestration required for vessel growth; whereas, FA treatment increased VEGF expression and normalized tissue vascularity.

Vitamin E

Mechanisms: 6, 8

The relationship of vitamin E and BP has been studied in vitro, extensively in animals, but limited studies have been done in human beings. a-Tocopherol inhibits thrombin-induced endothelin secretion in vitro at least partially through PKC (protein kinase C) inhibition. Reduced PKC levels reduce vascular smooth muscle proliferation through inhibition of activated protein-1 and NF-KB (nuclear factorκ-β). In turn, ED is improved, SVR is lowered, and BP is reduced.One study showed that gave α-tocotrienol 15 mg/kg to SHRs(spontaneously hypertensive rats) and found significant reductions in lipid peroxides in plasma and in vascular walls, increased SOD (Superoxide dismutase) activity, increased total antioxidant status, and lowered BP( P<.001). In a similar study, gave 34 mg/kg of a-tocopherol to SHRs, Lipid peroxide levels were decreased in plasma and in vascular walls, plasma SOD activity increased, total antioxidant status increased, and BP fell ( P<.001). Another study administered a-tocopherol to SHRs in doses of 17, 34, or 170 mg/kg. Nitric oxide synthase increased significantly ( P < .01) only at the 34 mg/kg dose and BP fell the most also at the same dose ( P < .001).

One human study performed a double-blind, placebo-controlled study on the effects of dlα-tocopherol nicotinate in 94 hypertensive subjects with cerebral atherosclerosis. Subjects received 3000 mg of the study vitamin for 4 to 6 weeks. In subjects with hypertension, the SBP declined from 151.0 F 22.1 to 139.2 F 16.8 mm Hg ( P b .05), but DBP did not change.

Human studies of vitamin E in doses of 400 to 1000 IU/d, although limited, have shown beneficial effects on improving insulin sensitivity, lowering serum glucose, increasing serum glutathione levels, reducing ED and vascular resistance.


Mechanisms: 7, 8

NO and ROS play important roles in blood pressure regulation via the modulation of the autonomic nervous system, particularly in the central nervous system (CNS). An imbalance between NO bioavailability and ROS generation in the CNS activates the sympathetic nervous system and this mechanism is involved in the pathogenesis of neurogenic aspects of hypertension.

CoQ10 levels have been shown to be lower in older adults known to have a greater prevalence of hypertension. CoQ10 may reduce mitochondrial superoxide production by increasing the efficiency of electron transfer from Complexes I and II down the mitochondrial electron transport chain. CoQ10 may also expert an antioxidant effect by scavenging free radicals and reducing lipid peroxidation at the level of the plasma membrane.

CoQ10 attenuates the oxLDL (Oxidized low density lipoprotein)-mediated down-regulation of eNOS and up-regulation of inducible nitric oxide synthase (iNOS). CoQ10 reduces peripheral resistance by preserving NO. In some forms of hypertension, superoxide radicals that inactivate NO are overproduced; CoQ10, with its antioxidant effects, may prevent the inactivation of NO by these free radicals.

CoQ10 may boost the production of the prostaglandin prostacyclin (PGI2), a potent vasodilator, or it may enhance the sensitivity of arterial smooth muscle to PGI2.


Mechanisms: 2 ,3, 4

Taurine plays an important role in the modulation of cardiovascular function by acting not only within the brain but also within peripheral tissues. Taurine has been shown to regulate the intracellular calcium homeostasis. Within the context of cardiac and smooth muscle physiology, calcium ions are very important in the regulation the contractility of these muscle cells and thus regulate both peripheral resistance and cardiac output. Taurine also has been shown to be a potent agonist of GABA receptors and activation of these receptors has been shown to affect cardiovascular function and peripheral resistance.

Through modulation of the nervous control of the cardiovascular function. The effect of taurine on peripheral resistance after acute injection was not gender-specific. Both males and females responded by a drop in blood pressure.


Mechanisms: 8

Arginine is the primary precursor for the production of NO, which has numerous cardiovascular effects, mediated through conversion of L-arginine to NO by eNOS(Endothelial nitric oxide synthase) to increase cyclic GMP levels in vascular smooth muscle, improve ED, and reduce vascular tone and BP. Administration of L-arginine in human beings at doses of 10 g/d will increase coronary artery blood flow, reduce angina, and improve peripheral blood flow and peripheral vascular disease symptoms.

Responses of MBP during L-arginine infusion at four different doses of 15, 50, 150, and 500 mg/kg, and nicardipine infusion at 0.4 ug/kg.

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