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Behavioral and Metabolic Research Unit (Montfort Hospital)
School of Human Kinetics
University of Ottawa, Ontario, Canada K1N 6N5
* To whom correspondence should be addressed. E-mail: fhaman{at}uottawa.ca.
Dear Editor,
The recent study by Jakulj et al. (1) provides insight into the short-term effects of dietary composition on blood pressure. Although the authors provide new data and ideas about endothelial reactivity and dietary fat, there is a potential confounder that may influence the authors' conclusions that should be addressed. The study's test meals were not matched for protein content, which was much higher in the high-fat test meal than in the high-carbohydrate test meal (31 g vs. 15 g: a 2-fold difference). Plasma protein levels modify both blood viscosity and the secretion of vasoactive hormones, which influence blood vessel diameter and blood pressure (2,3). Thus, the elevated blood pressures observed during high stress situations following the high-fat meal, when compared with the high-carbohydrate meal, may be due in part to higher protein intake, rather than simply to the higher fat content of the meal. As most of the available literature examines the long-term effects of protein intake, it is difficult to predict precisely the acute effects of not controlling for protein intake on the results of this study. However, this letter presents two means by which variations in protein intake may affect blood pressure reactivity.
First, dietary protein can affect blood viscosity. Higher viscosity requires vasoconstriction and a greater cardiac output to push blood toward the microvasculature, leading to an elevation in blood pressure (2). An increased blood viscosity and vascular resistance also applies more shear stress to the endothelial lining. This shear stress promotes the release of nitrous oxide, which has an opposing vasodilative effect; eventually, this vasodilatation plateaus and vasoconstriction exceeds vasodilatation (4). Dietary proteins are broken down into amino acids, absorbed through the endothelial lining of the gut and into the bloodstream. Free amino acids in the blood are used throughout the body in protein synthesis or as energy substrate (3). Because these amino acids are rapidly taken up, it is unclear whether the transient presence of excess amino acids in the bloodstream affects blood viscosity, endothelial reactivity, and blood pressure. Proteins such as albumin, which are produced in the body, also influence blood viscosity. Albumin is the major colloid component of plasma, affecting plasma viscosity and, hence, blood viscosity (2,3). If high protein consumption increased albumin production, blood viscosity and blood pressure would increase.
Second, dietary protein has an effect at the level of the kidneys. Glomerular filtration rate has been shown to increase by 20–30% within 1 h of consuming a high-protein meal (5). If this were to stimulate urine output, it could affect blood pressure by reducing blood volume and increasing viscosity. In this study, the reduction in blood volume could be exacerbated by the fact that the high-carbohydrate diet contained fluids, whereas the high-fat diet apparently did not. Plasma protein levels also act on the kidneys by stimulating the renin-angiotensin pathway and increasing vasoactive hormone activity (5). This pathway would be further stimulated by a low fluid intake. Angiotensin promotes vasoconstriction; aldosterone is released by the adrenals and acts on the kidneys to promote sodium and water retention (5). Combined, these actions could cause an increase in blood pressure. Similarly, angiotensin II stimulates the release of vasopressin, a vasoconstrictive agent, in response to a high plasma osmotic pressure (6).
Even though exact physiological effects of varying protein intake on acute reactive blood pressure remain uncertain, the potential impact of dietary protein on blood viscosity and renal function can not be disregarded. We believe that in the study by Jakulj et al. (1), the variations in reactive blood pressure may have been caused in part by the 2-fold difference in protein content between dietary treatments. In this context, results should be viewed with some caution, and future studies would benefit from matching diets for protein content.
Manuscript received 30 July 2007.
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LITERATURE CITED |
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 TOP LITERATURE CITED |
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1. Jakulj F, Zernicke K, Bacon SL, van Wielingen LE, Key BL, West SG, Campbell TS. A high-fat meal increases cardiovascular reactivity to psychological stress in healthy young adults. J Nutr. 2007;137:935–9.
2. Fowkes FG, Lowe GD, Rumley A, Lennie SE, Smith FB, Donnan PT. The relationship between blood viscosity and blood pressure in a random sample of the population aged 55 to 74 years. Eur Heart J. 1993;14:597–601.
3. Whitney EN, Cataldo CB, Rolfes SR. Understanding normal and clinical nutrition. Belmont (CA): Wadsworth; 2002.
4. Chandran KB, Rittgers SE, Yoganathan AP. Biofluid mechanics: The human circulation. Boca Raton (FL): CRC/Taylor and Francis; 2007.
5. Guyton AC, Hall JE. Textbook of Medical Physiology. 10th ed. Philadelphia: W.B. Saunders; 2000.
6. Daniels BS, Hostetter TH. Effects of dietary protein intake on vasoactive hormones. Am J Physiol. 1990;258:R1095–1100.[Medline]
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