Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension.

Abstract

Recent studies showed that taurine, a sulphonic amino acid, could decrease blood pressure and increase sympathoadrenal tone in DoCA-salt-treated hypertensive rats. To determine whether taurine exerts its antihypertensive action in man in a similar fashion, we studied the effect of oral administration of taurine (6 g for 7 days) on blood pressure and plasma catecholamines in 19 young patients with borderline hypertension in a double-blind, placebo-controlled fashion. Systolic blood pressure in the 10 patients who were treated with taurine decreased by 9.0 ± 2.9 mm Hg (mean ± SE; p < .05 by paired t test), compared with a 2.7 + 2.3 mm Hg decrease (NS) in the nine patients treated with placebo and diastolic blood pressure in the taurine-treated patients decreased by 4.1 + 1.7 mm Hg (p < .05) compared with 1.2 ± 3.0 mm Hg (NS) in the placebo-treated subjects. In the patients receiving taurine plasma epinephrine (E) decreased significantly, with a negligible decrease in plasma norepinephrine (NE). The effect of taurine on plasma catecholamines and the response of plasma E after the stimulation with glucagon was also studied in 12 borderline hypertensive and nine agematched normotensive subjects. Basal plasma E was significantly higher in borderline hypertensive than in normal subjects, but basal plasma NE did not differ in the two groups. The intravenous bolus injection of glucagon (1 mg) caused a rapid and transient increase in plasma E in each subject studied; plasma E reached a peak concentration 2 to 5 min after the injection of glucagon and thereafter declined rapidly to the baseline level. The overall response of plasma E to glucagon stimulation was significantly (p < .01) greater in the borderline hypertensive than in the normotensive subjects. Taurine not only reduced mean blood pressure and basal plasma E, but also attenuated the increased response to glucagon in the borderline hypertensive subjects. In the normotensive subjects, however, the administration of taurine did not significantly change blood pressure, basal plasma catecholamines, or the response of plasma E to glucagon. Overall, there was a direct correlation (r = .670, p < .01) between the decrements in mean blood pressure and those in plasma E after taurine in the 22 borderline hypertensive subjects. Evidence presented suggests, therefore, that sympathoadrenal tone is increased in young borderline hypertensive individuals, and that oral administration of taurine attenuates increased tone, leading to the reduction of blood pressure. Circulation 75, No. 3, 525-532, 1987. YOUNG PATIENTS with borderline hypertension are at least three times more likely to develop established essential hypertension than age-matched normotensive subjects.1'2 Thus, young patients with borderline hypertension have been of particular interest to investigators because they may provide insight into the pathogenesis of essential hypertension. The majority of studies have reported increased average circulating norepinephrine levels in borderline hypertensive sub-

The role of nutrition and nutraceutical supplements in the treatment of hypertension

“…In cardiomyocytes, it represents about 50% of the free amino acids and has a role of an osmoregulator, inotropic factor and antihypertensive agent [155] . Human studies have noted that essential hypertensive subjects have reduced urinary taurine as well as other sulfur amino acids [1,154,155] .…”

“…In cardiomyocytes, it represents about 50% of the free amino acids and has a role of an osmoregulator, inotropic factor and antihypertensive agent [155] . Human studies have noted that essential hypertensive subjects have reduced urinary taurine as well as other sulfur amino acids [1,154,155] . Taurine lowers BP, SVR and HR, decreases arrhythmias, CHF symptoms and SNS activity, increases urinary sodium and water excretion, increases atrial natriuretic factor, improves insulin resistance, increases NO and improves endothelial function.…”

“…Taurine lowers BP, SVR and HR, decreases arrhythmias, CHF symptoms and SNS activity, increases urinary sodium and water excretion, increases atrial natriuretic factor, improves insulin resistance, increases NO and improves endothelial function. Taurine also decreases A-Ⅱ, PRA, aldosterone, SNS activity, plasma norepinephrine, plasma and urinary epinephrine, lowers homocysteine, improves insulin sensitivity, kinins and acetyl choline responsiveness, decreases intracellular calcium and sodium, lowers response to beta receptors and has antioxidant, anti-atherosclerotic and anti-inflammatory activities, decreases IMT and arterial stiffness and may protect from risk of CHD [1,[154][155][156][157][158][159][160] . A lower urinary taurine is associated with increased risk of hypertension and CVD [160,161] .…”

“…The BP reduction of 14.8/6.6 mmHg was proportional to increases in serum taurine and reductions in plasma norepinephrine [162] . Fujita et al [155] demonstrated a reduction in BP of 9/4.1 mmHg (p < 0.05) in 19 hypertension subjects given 6 g of taurine for 7 d. Taurine has numerous beneficial effects on the cardiovascular system and BP [156] . The recommended dose of taurine is 2 to 3 g/d at which no adverse effects are noted, but higher doses up to 6 g/d may be needed to reduce BP significantly [1,70,71,[154][155][156][157][158][159][160][161][162] .…”

Plasma taurine and cysteine levels following an oral methionine load: relationship with coronary heart disease

“…This may reflect a direct effect of taurine, since supplementation with pharmacological doses of taurine has been shown to improve a number of processes including endothelial-dependent arterial dilatation (Fennessy et al, 1998) and neutrophil activation and endothelial adhesion (McCarty, 1999), and to have a potential role in the control of hypertension (Fujita et al, 1987) and hypercholesterolaemia . On the other hand, it may be an artefact arising from a relationship between vitamin B 6 status and CHD, since taurine can be produced endogenously by a series of reactions, several of which involve vitamin B 6 (pyridoxal phosphate, PLP) as a cofactor (see Figure 1).…”