Aerobic Capacity Correlates with Urinary Thromboxane Concentration in Pre-Hypertensive African Americans
Sheara T. WilliamsonDeborah L. FeairhellerKeith M. DiazKathleen M. SturgeonMichael D. BrownSusan A. Jansen
0
Citation
0
Reference
20
Related Paper
Keywords:
Aerobic capacity
Cite
Captopril
Plasma renin activity
Renal circulation
Cite
Citations (61)
Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s). Urinary kallikrein excretion was compared in outpatients with essential hypertension, mineralocorticoid hypertension (primary aldosteronism and 17α-hydroxylase deficiency), and in normal subjects of the same race. No significant difference in urinary kallikrein excretion of patients with LREH vs. normal renin essential hypertension (NREH) was found for either black (4.1±0.4 vs. 4.8±0.5 esterase units (EU)/24 h, mean±SE, for 27 LREH and 38 NREH, respectively) or white patients (12.2±2.3 vs. 11.7±1.4 EU/24 h for 13 LREH and 25 NREH, respectively). Urinary kallikrein was decreased in black vs. white hypertensive patients and normal subjects. However, in patients with normal renal function (creatinine clearance ≥80 ml/min) urinary kallikrein was not significantly decreased in either black hypertensive vs. black normal subjects (4.3±0.3 vs. 5.4±0.6 EU/24 h) or in white hypertensive vs. white normal subjects (11.9±1.2 vs. 8.4±0.9 EU/24 h). In contrast, hypertensive patients with mild renal insufficiency (creatinine clearance of 41.8±78.5 ml/min) had reduced (P < 0.05) urinary kallikrein (3.3 EU/24 h with creatinine clearance of 63.6±2.0 for 24 black patients and 4.2±0.7 EU/24 h with creatinine clearance of 67.0±3.5 for 6 white patients). These results suggest that a reduction in urinary kallikrein excretion rate is an early accompaniment of hypertensive renal injury. Urinary kallikrein excretion in response to a 6-d 10-meq sodium diet and a 3-d Florinef (0.5 mg b.i.d.) administration was compared in hypertensive patients with normal renal function vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3±2.7 [n = 9], NREH = 11.7±1.8 [n = 10], LREH = 10.9±1.5 [n = 12]; white normals = 21.2±2.9 [n = 11], essential hypertension = 20.9±3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2±2.4 [n = 10], NREH = 10.1±2.7 [n = 10], LREH = 7.4±1.1 [n = 13]; white normals = 19.1±2.7 [n = 13], essential hypertension = 17.5±2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3±2.7 vs. 33.3±6.4 μg/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.
Primary Aldosteronism
Essential hypertension
Plasma renin activity
Mineralocorticoid
Cite
Citations (106)
Cite
Citations (0)
Cite
Citations (121)
Thromboxane B2
Essential hypertension
Cite
Citations (20)
Background:The relationship between urinary vasoactive factors and sodium excretion has not been adequately addressed in humans.
Vasoactive
Cite
Citations (28)
To compare renin-sodium profile and renal prostaglandins (PGs) of Black normotensive and hypertensive patients, with the same parameters of Caucasian normotensives and hypertensives, e.g. to reveal some of the ethnic differences in the pathogenesis of systemic (essential) hypertension.27 Black Zimbabwean normotensive and 27 hypertensive patients were matched by age, sex and number to Caucasian normotensives and hypertensives (systolic blood pressure > 160 mm Hg or diastolic blood pressure > 95 mm Hg, or both). All were examined during two protocols producing sodium depletion (less than 40 mmol sodium diet/day) for five days, followed by sodium loading (300 mmol sodium diet/day) for another five days. Changes in plasma renin activity (PRA), urinary aldosterone (Aldo), prostaglandin E2(PGE2) and prostaglandin F2 alpha (PGF2 alpha) excretions were simultaneously assessed by radioimmunoassay.Compared to caucasians the Blacks showed similar basal aldosterone and Na+ excretion but significant Na+ retention (30pc) during Na+ loading. Their basal PRA was lower (32pc) and poorly responding to sodium depletion/loading. They had suppressed PG synthesis, the PGE2/PGF2 ratio being significantly decreased 11pc. Renin profiles, obtained by plotting PRA against urinary Na+ excretion showed prevalence of low renin hypertension (62pc) in Black patients. All Caucasian patients had normal renin hypertension. At basal level the Black hypertensives had suppressed synthesis of vasodilator PGF2/PGF2 alpha ratio by 32pc. This finding was in accordance with their low renin hypertension. During sodium depletion the PGs excretion was increased in both hypertensive groups. The opposite effect was found during sodium loading.This study shows ethnic differences in renin-sodium profile and renal PG synthesis, during changes in dietary sodium. It addresses an old medical controversy about the usefulness of renin profiling in identifying hypertensive patients who are at increased risk for heart attack (Whites with normal/high renin hypertension) or increased risk of stroke (Blacks with low renin, sodium mediated hypertension).
Plasma renin activity
Basal (medicine)
Essential hypertension
Low sodium diet
Pathogenesis
Urine sodium
Cite
Citations (7)
Plasma renin activity
Cite
Citations (54)
Fourteen normotensive and 14 hypertensive black men with mild essential low-renin hypertension were examined during two protocols producing sodium depletion (less than 40 mmol sodium diet per day) for 5 days, followed by sodium loading (300 mmol sodium diet per day) for another 5 days. Changes in plasma renin activity, urinary aldosterone excretion, and excretion rates of stable breakdown products of thromboxane A2 (thromboxane B2) and prostacyclin (6-keto PGF1 alpha) were simultaneously assessed by radioimmunoassay. On the basis of low-renin status and paradoxically normal aldosterone excretion in both normotensives and hypertensives, thromboxane B2 excretion was increased by 14% (not significant); 6-keto PGF1 alpha was significantly decreased by 47% in the hypertensives compared to the normotensives. As a result, thromboxane B2/6-keto PGF1 alpha ratio was significantly increased from 1.29 +/- 0.10 in the normotensives to 2.78 +/- 0.12 in the hypertensive patients. The same ratio increased significantly after sodium loading in both groups, but more distinctly in the hypertensives (40%). Prostacyclin is a vasodilator, a natriuretic, and a potent inhibitor of platelet aggregation. Thromboxane A2 has opposite effects. The impaired prostacyclin biosynthesis we found in the hypertensive patients could account for the increased vascular resistance and some complications typical for hypertensive state.
Plasma renin activity
Thromboxane B2
Cite
Citations (3)
Renal sodium reabsorption
Plasma renin activity
Cite
Citations (30)