Long-Term Diuretic Therapy in Hypertensive Patients: Effects on Serum Homocysteine, Vitamin B6, Vitamin B12, and Red Blood Cell Folate Concentrations

Morrow, Lee E.; Grimsley, Edwin W.

doi:10.1097/00007611-199909000-00003

Cited by 37 publications

(23 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The effect profiles of coffee on folate, PLP, and riboflavin could be explained if coffee consumption, through renal mechanisms, increases vitamin excretion at high blood vitamin concentrations. Reports describing increased excretion and lower blood concentrations of micronutrients (including folate, PLP and riboflavin) and higher tHcy in patients given diuretics (32)(33)(34)(35)(36) support this hypothesis. Caffeine has been shown not to modify the glomerular filtration rate (37 ), but it affects the proximal tubules where most of the vitamins are reabsorbed (37)(38)(39).…”

Section: Possible Mechanismsmentioning

confidence: 96%

Coffee Consumption and Circulating B-Vitamins in Healthy Middle-Aged Men and Women

et al. 2008

View full text Add to dashboard Cite

Background: Coffee consumption has been associated with several risk factors for coronary heart disease, including increased cholesterol, increased blood pressure, and increased plasma total homocysteine (tHcy). tHcy is determined by several B-vitamins. However, reports about the association between coffee intake and B-vitamin status are few. Methods: We measured plasma B-vitamins and tHcy in a cohort of 10 601 healthy, middle-aged Norwegian men and women. Information about lifestyle factors, including coffee consumption, smoking, alcohol use, height, and weight, was obtained by interview. Results: Coffee consumption was dose-dependently associated with reduced plasma B-vitamin concentrations. Compared with coffee abstainers, individuals drinking ≥4 cups/day had 11.7% (P < 0.001), 14.1% (P < 0.001), and 5.5% (P = 0.01) lower plasma concentrations of folate, pyridoxal phosphate, and riboflavin, respectively, and the mean tHcy concentration was 6.8% (P < 0.001) higher. Quantile regression analysis showed essentially no difference in B-vitamin concentrations between coffee consumption categories at low vitamin concentrations but a progressive increase in the difference at higher concentrations. This pattern of differences (effect profile) was found independently of smoking status, alcohol intake, and sex. The decrease in folate explained approximately half of the increase in tHcy. Conclusions: Coffee consumption was associated with reduced circulating B-vitamin concentrations. The observed effect profiles indicated that coffee consumption preferentially affected the upper, but not the lower, part of the B-vitamin concentration distributions. We hypothesize that coffee consumption may increase the loss of surplus B-vitamins by excretion in urine.

show abstract

Section: Possible Mechanismsmentioning

confidence: 96%

Coffee Consumption and Circulating B-Vitamins in Healthy Middle-Aged Men and Women

et al. 2008

View full text Add to dashboard Cite

show abstract

“…5,[15][16][17] Recent studies have shown that the drug therapy for common medical conditions may have severe effects on plasma Hcy levels. [18][19][20][21][22] Thiazide-type diuretics are recognized as the cornerstone of antihypertensive therapy (AHT) in elderly because of their extensive track record in preventing stroke and cardiovascular events and their low cost. 23 Outcome benefits of diuretics as first-line agents have been demonstrated only at moderate doses (equivalent to X25 mg hydrochlorothiazide).…”

Section: Introductionmentioning

confidence: 99%

Effect of ACE inhibitors and β-blockers on homocysteine levels in essential hypertension

et al. 2008

View full text Add to dashboard Cite

Recent studies have shown that antihypertensive drugs like diuretics increase plasma homocysteine (Hcy) levels. However, the effect of other antihypertensive drugs on plasma Hcy levels has not been tested extensively. The aim of present study was to investigate the effect of antihypertensive therapy (AHT) on Hcy levels in essential hypertensive subjects. A case-control study of 273 patients with essential hypertension (EH) and 103 normotensive controls was undertaken. Plasma Hcy levels were measured before and after 6 weeks of AHT. The genotyping of MTHFR C677T polymorphism was performed by polymerase chain reaction-restriction fragment length polymorphism. Angiotensin-converting enzyme (ACE) inhibitors and b-blockers significantly decreased and hydrochlorothiazides significantly increased the plasma Hcy levels in hypertensive patients (Po0.05). No significant association between MTHFR C677T genotypes and changes in Hcy levels in response to antihypertensive was observed in EH patients. The decrease in Hcy induced by b-blockers and ACE inhibitors observed in our study may be due to the improvement of endothelial function along with improved renal function. Thus, our results suggest that ACE inhibitors and b-blockers may provide additional beneficial therapeutic effects to the EH patients by decreasing Hcy levels.

show abstract

“…Recent studies have shown that elevated plasma tHcys can occur before a decrease in renal function in patients with essential hypertension. 5,6,14,15 This raised a question of whether Hcys directly induces glomerular damage independent of hypertension. The present study was designed to answer this question and to test the hypothesis that elevations of plasma tHcys levels produce glomerular dysfunction and consequent sclerosis.…”

mentioning

confidence: 99%

Implications of Hyperhomocysteinemia in Glomerular Sclerosis in Hypertension

Chen

Zou

2002

Hypertension

View full text Add to dashboard Cite

Abstract-Hyperhomocysteinemia (hHcys) has been recognized as a new risk factor for cardiovascular diseases independent of plasma lipid levels or other factors. However, it remains unknown whether hHcys is implicated in the target organ damages associated with hypertension. The present study first examined the possible role of hHcys in the development of glomerulosclerosis in Dahl salt-sensitive (DS) hypertensive rats. High-performance liquid chromatography showed that plasma total homocysteine (tHcys) concentration was 7.64Ϯ0.29 mol/L in conscious DS rats on a low salt (0.4% NaCl) diet, which was higher than 5.23Ϯ0.25 mol/L in Dahl salt-resistant normotensive rats. When these rats were exposed to a high salt (4% NaCl) diet, plasma tHcys markedly increased in DS rats (14.7Ϯ1.31 mol/L) but not in Dahl salt-resistant rats (5.34Ϯ0.54 mol/L). An iron chelater, desferrioxamine (0.3 mg/kg IV per day), completely normalized high salt-induced elevations of plasma tHcys and significantly attenuated the sclerotic changes in the glomeruli in DS rats. To further determine whether hHcys has an independent effect in the development of glomerulosclerosis, Sprague-Dawley rats were fed drinking water containing methionine (1 g/kg per day) for 6 weeks to produce hHcys. In these rats, plasma tHcys increased to 12.5Ϯ1.9 mol/L (versus 6.1Ϯ2.6 mol/L in control rats), and the aorta exhibited typical sclerotic changes, but arterial pressure was not altered. Urinary protein excretion increased to 52Ϯ2 mg/24 hours (versus 17Ϯ2 mg/24 hours in control rats), and the glomerular mesangium was expanded with glomerular hypercellularity, capillary collapse, and fibrous deposition in the rats with hHcys. These results suggest that elevated plasma homocysteine may be an important pathogenic factor for glomerular damage in hypertension independent of arterial pressure.

show abstract

Long-Term Diuretic Therapy in Hypertensive Patients: Effects on Serum Homocysteine, Vitamin B6, Vitamin B12, and Red Blood Cell Folate Concentrations

Cited by 37 publications

References 0 publications

Coffee Consumption and Circulating B-Vitamins in Healthy Middle-Aged Men and Women

Coffee Consumption and Circulating B-Vitamins in Healthy Middle-Aged Men and Women

Effect of ACE inhibitors and β-blockers on homocysteine levels in essential hypertension

Implications of Hyperhomocysteinemia in Glomerular Sclerosis in Hypertension

Contact Info

Product

Resources

About