A Study of 48-Hour Faecal and Urinary Electrolyte Excretion in Normotensive Black and White South African Males

Barlow, R.J.; Connell, M. A.; Milne, F. J.

doi:10.1097/00004872-198604000-00009

Cited by 27 publications

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“…Moreover, we assessed 24-hour urinary excretion rates only once, and this is subject to inaccuracies in urine collection and does not account for daily variations in salt intake. However, the mean 24-hour urine volumes noted in the present study are higher than those reported on in 23 of 52 sites of the Intersalt Study, 40 and the electrolyte excretion rates in the present study are the same as that reported on in an alternative study conducted in the same population group and region in South Africa (South West Township, Johannesburg) 44 as the present study and in other "salt-sensitive" populations. 45 Moreover, assuming there was a degree of inaccuracy of urine collection, under these circumstances we are likely to have underestimated the impact of salt intake on PP independent of MAP.…”

Section: Discussionsupporting

confidence: 69%

Relationship Between Urinary Salt Excretion and Pulse Pressure and Central Aortic Hemodynamics Independent of Steady State Pressure in the General Population

et al. 2010

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Abstract-Although central pulse pressure (PPc) is strongly related to central mean arterial pressure (MAPc), PPc predicts cardiovascular outcomes beyond MAPc. Whether modifiable risk factors for hypertension contribute to PPc and its determinants, independent of MAPc, is uncertain. In 635 randomly recruited participants, we assessed the independent relationship between 24-hour urinary sodium (Na ϩ ) or potassium (K ϩ ) excretion and brachial artery PP (in office or 24-hour; nϭ487), PPc, the forward (P1) and augmented (Paug) pressure wave components of PPc, central augmentation index, and determinants of central pressure waves, including aortic pulse wave velocity, effective reflecting distance, and reflective wave transit time. Central dynamics were determined using applanation tonometry of the carotid, femoral, and radial arteries. With adjustments for potential confounders, urinary Na ϩ /K ϩ was independently associated with in-office, central, and 24-hour PP, as well as Paug, P1, and central augmentation index (PϽ0.05 to PϽ0.005). With further adjustments for MAPc (or diastolic BP), urinary Na ϩ /K ϩ was independently associated with PPc, 24-hour PP, Paug, P1, and central augmentation index (PϽ0.05 to Pϭ0.005) but not with in-office PP, pulse wave velocity, effective reflecting distance, or reflective wave transit time. In conclusion, in a population of African ancestry, urinary salt excretion is independently related to central and 24-hour PP independent of MAPc or diastolic BP, effects that are attributed to increases in both P1 and Paug but not to pulse wave velocity. Hence, modifying salt intake could influence cardiovascular risk through effects on 24-hour and central PPs, as well as P1 and Paug, independent of steady-state pressure (MAP or diastolic BP) or pulse wave velocity. (Hypertension. 2010;56:584-590.) Key Words: pulse pressure Ⅲ arterial stiffness Ⅲ central blood pressure Ⅲ salt intake P ulse pressure (PP) predicts cardiovascular outcomes beyond other measures of blood pressure (BP), including measures of steady-state pressure, such as mean arterial pressure (MAP). [1][2][3][4][5][6][7][8][9][10][11][12][13][14] Moreover, central PP may be more closely associated with cardiovascular outcomes than peripheral PP. [15][16][17][18][19] Thus, contemporary notions of the adverse actions of BP are viewed in terms of steady-state effects, indexed by MAP, and dynamic or pulsatile effects, indexed by PP, with central PP receiving the most attention. The effects of PP independent of MAP on cardiovascular outcomes 1-14 are particularly impressive considering the close relationship between MAP and PP. Developing strategies that decrease PP, particularly central PP, without necessarily influencing MAP, is, therefore, of considerable interest, and in this regard understanding the mechanisms responsible for these changes is of importance. Although aging has been identified as the major determinant of PP, with increases in both the augmented and the forward pressure wave contributing to central PP, 20 -23 the im...

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Section: Discussionsupporting

confidence: 69%

Relationship Between Urinary Salt Excretion and Pulse Pressure and Central Aortic Hemodynamics Independent of Steady State Pressure in the General Population

et al. 2010

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“…In two small studies (one in South Africa and one in the United States), urinary and stool K excretion were both higher in white than in black individuals on uncontrolled diets, but the ratio of fecal to urinary K was higher in black than in white individuals. 18,22 The exact mechanism of this is not understood. In our study, fecal and sweat K were not collected.…”

Section: Discussionmentioning

confidence: 99%

Racial Differences in Urinary Potassium Excretion

Turban

Miller

Ange

et al. 2008

Journal of the American Society of Nephrology

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Racial differences in potassium (K) intake and urinary K excretion may contribute to the higher BP observed in black compared with white individuals. Although black individuals typically consume less dietary K than white individuals, the lower urinary K excretion observed in black individuals may reflect more than differences in intake. In this study, data from the Dietary Approaches to Stop Hypertension (DASH) trial (413 white and black participants) were used to evaluate urinary K excretion in black and white individuals with similar K intake. At screening, mean urinary K excretion was higher in white than black individuals (mean ⌬ ϭ 645 mg/d for white minus black individuals, adjusted for age, gender, and weight; P Ͻ 0.001). After a 3-wk run-in period during which all participants received a low-K control diet, a significant racial difference remained (mean ⌬ ϭ 201 mg/d, adjusted for age, gender, and caloric intake; P Ͻ 0.001). Participants were then randomly assigned to continue the control diet or switch to a high-K diet (either a high fruit/vegetable diet or the DASH diet) for 8 wk. At the end of intervention, the mean difference in urinary K in white compared with black individuals after adjustment for age, gender, and caloric intake was Ϫ6 mg/d (P ϭ 0.95) in the control group, 163 mg/d in the fruits/vegetables group (P ϭ 0.39), and 903 mg/d in the DASH group (P Ͻ 0.001). Racial differences in urinary K excretion seem to reflect more than intake differences; further studies are needed to understand their potential impact on clinical outcomes.

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“…43 Examination of urine and fecal potassium in 10 black and 11 white South Africans revealed a urinary potassium excretion of 38.2 and 78.3 mmol for whites and blacks, respectively. 44 The 24-hour fecal excretion of the ion was 15.0 and 20.8 mmol for blacks and whites, respectively. The total 24-hour excretion of potassium via the urine and feces was indeed lower in blacks (53.2 mmol) than in whites (99.1 mmol), indicting a lower intake of potassium in South African blacks.…”

Section: Urinary Potassium Excretion In Blacksmentioning

confidence: 95%

Urinary Potassium Excretion and Sodium Sensitivity in Blacks

2004

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Abstract-Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle's loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure. Key Words: blacks Ⅲ hypertension, essential Ⅲ kidney Ⅲ potassium Ⅲ sodium B lood pressure of a subset of the human population rises as a result of an increase in the intake of salt (sodium chloride). 1 Individuals who manifest this trait are salt sensitive. As sodium (and chloride) balance must be preserved to sustain life, salt-sensitive and salt-resistant subjects maintain sodium balance. What distinguishes salt-sensitive from saltresistant subjects is that in the face of a high-salt intake, salt-sensitive subjects raise their blood pressure, ultimately maintaining sodium balance by resorting to pressure natriuresis. 2 However, a habitually high salt consumption in susceptible individuals may exert biological effects other than salt-evoked blood pressure elevation, including left ventricular hypertrophy, stiffness of conduit arteries, and stroke. [3][4][5] The kidneys are the main player in salt sensitivity, but mechanisms causing this trait are a matter of conjecture. Lessons from rare, monogenic forms of hypertension and hypotension arising from abnormalities in renal sodium handling 6 -8 suggest that salt sensitivity need not be a single entity; rather, it is probably a clinical manifestation of a number of renal disorders that result in altered electrolyte homeostasis and thus blood pressure elevation.Salt sensitivity in blacks has begged for a physiological explanation ever since the predilection of this group to essential hypertension and progressive renal damage has come to light. In a previous communication, we offered a paradigm that explains salt sensitivity in blacks. 9 This article further expands the model by proposing that the differences in renal potassium handling between blacks and whites reflect ethnic variation in the fractional reabsorption of sodium in specific renal tubular segments. Moreover, we propose that mechanisms in the renal regulation of sodium may explain the predisposition of blacks to sodium-induced elevation of blood pressure and also to sodium-induced glomerular damage. Here, we refer to salt sensitivity as "sodium sensitivity," albeit some research has suggested that not only sodium but also chloride, potassium, and perhaps other nutrients may contribute to the salt-sensitivity trait. 10 -13 Although irrefutable evidenc...

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A Study of 48-Hour Faecal and Urinary Electrolyte Excretion in Normotensive Black and White South African Males

Cited by 27 publications

References 0 publications

Relationship Between Urinary Salt Excretion and Pulse Pressure and Central Aortic Hemodynamics Independent of Steady State Pressure in the General Population

Relationship Between Urinary Salt Excretion and Pulse Pressure and Central Aortic Hemodynamics Independent of Steady State Pressure in the General Population

Racial Differences in Urinary Potassium Excretion

Urinary Potassium Excretion and Sodium Sensitivity in Blacks

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