IV Vitamin C improves endothelial vasodilation in essential hypertension. The Vitamin C reduces the oxygen free radicals which allowed eNOS to increase NO production. Two take homes: oxygen free radicals may be responsible for the endothelial dysfunction that leads to essential hypertension and vitamin C, particularly IV, can be used to counter this process. Other studies have shown IV vitamin C to be anti-hypertensive in its action.
Among postmenopausal women, serum T was elevated in hypertensive participants [9, 11, 12], and total T, free T, and DHEA were positively correlated with SBP
T and DHEA were attenuated by adjustment for BMI, reflecting either a confounding or a mediating effect of obesity
SHBG concentration was inversely associated with risk of hypertension and longitudinal rise of BP over time
SHBG has been postulated as a marker for insulin resistance
In vitro studies showed that insulin inhibits SHBG production from hepatoma cells
In intervention studies, successful weight loss and weight maintenance increased SHBG in men with obesity
E2 may also induce insulin resistance and thereafter tend to raise BP.
strong association between E2 and measures of insulin resistance in postmenopausal women, independent of adiposity
In postmenopausal women that received hormone replacement therapy, estrogen therapy increased mononuclear cell secretion of tumor necrosis factor alpha (TNF-α)
estrone levels were positively associated with inflammatory markers in postmenopausal women
higher baseline concentrations of endogenous E2, total and bioavailable T, and DHEA and lower concentration of SHBG were associated with a higher incidence of hypertension and a greater increase in BP during follow-up
Data from MESA study finds that increasing endogenous Estradiol, Total and free Testosterone, DHEA, and lower SHBG were associated with hypertension in postmenopausal women.
IV vitamin C therapy shown to improved the response of blood pressure to acetylcholine and nitroprusside in those patients with essential hypertension. This effect was not found in NAC. Vitamin C acts as a superoxide scavenger and glutathione recycler.
Animal model found that low Hg decreased NO availability. The result is vasoconstriction induced by ROS and hypertension. The hypertension is the result of an activation of the renin angiotensin system. The importance here is that low Hg levels induced this change.
animal study finds vitamin C improves hypertension via renovascular source and oxidative stress. The dosage was 150 mg/kg/day. This would be equivalent to 10,800 grams daily for a 72 human. But what about a 200 lb male or female? That would be 13,650 grams of vitamin C daily.
Asian study finds Testosterone is inversely associated with increased central obesity, increased dyslipidemia, and metabolic syndrome in me with new diagnosis of type II diabetes and hypertension. Men with metabolic syndrome, type II diabetes, and CVD must have appropriate hormone evaluation.
Tetrahydrobiopterin is a critical cofactor for the NO synthases
at hypertension produces a cascade involving production of ROSs from the NADPH oxidase leading to oxidation of tetrahydrobiopterin and uncoupling of endothelial NO synthase (eNOS). This decreases NO production and increases ROS production from eNOS
Tetrahydrobiopterin oxidation may represent an important abnormality in hypertension
Treatment strategies that increase tetrahydrobiopterin or prevent its oxidation may prove useful in preventing vascular complications of this common disease.