Influence of the Renin-Angiotensin System Stimulation on Erythropoietin Production in Patients with Various Forms of Arterial Hypertension

Nowicki, Michał; Kokot, F; Wiȩcek, Andrzej

doi:10.1159/000187558

Cited by 12 publications

(10 citation statements)

References 18 publications

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“…This indirectly shows that there were no differences in the salt-sensitivity of patients between the studied groups, an finding important with respect to the study of Naomi et al (37) who found that sodium-sensitivity index may determine EPO response to changes in dietary sodium intake. It is noteworthy that we found a slight decline in EPO levels in response to sodium restriction in all groups, a finding which we reported not only in essential but also in some secondary forms of hypertension (27). These results are, however, difficult to explain because in agreement with the hypothesis of Kurtz and Eckardt (38) we should expect that the decrease in the fractional sodium excretion indicating increased tubular reabsorption of sodium, i. e., "metabolic strain" for proximal tubules, should result in the stimulation of EPO production.…”

Section: Discussionsupporting

confidence: 79%

“…Despite these findings little interest has been focused so far on the contribution of endogenous erythropoietin to the pathogenesis of essential hypertension (26,27). Taking the aforementioned findings into account, in the present study we tried to test the hypothesis that endogenous erythropoietin is involved in the pathogenesis of obesity-related hypertension.…”

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confidence: 96%

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Endogenouw Erythropoietin Levels in patients with Obesity-Related Hypertension.

Nowicki¹,

Kokot²,

Kokot³

et al. 1994

Hypertens Res

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The coincidence of increased red blood cell mass with obesity and hypertension has been confirmed in a number of studies. Since erythropoietin (EPO) induces hypertonic effect, we aimed to study the possible involvement of endogenous EPO in the pathogenesis of obesity-related hypertension (ORH). Seventy-two non-obese (body mass index-BMI < 25kg/m2) and 47 obese (BMI > 30 kg/m2) patients with essential hypertension, and 32 non-obese normotensive control subjects were studied on 120 mmol Na/24 h diets for 3 days and 30 mmol Na/24 h diets for the following 3 days. Serum EPO levels, plasma renin activity (PRA), aldosterone (PAC) and urinary sodium and potassium excretion were estimated under both conditions. Hematocrit, hemoglobin and serum iron, ferritin and TIBC were measured in basal conditions. Patients with ORH showed significantly higher hematocrit values, hemoglobin levels and erythrocyte counts (p < 0.05) than non-obese essential hypertensives and controls, although no differences in serum EPO levels (13.6 ± 1.1 and 12.8 ± 1.0 mU/ml, 15.3 ± 1.2 and 13.3 ± 1.1, 12.2 ± 2.0 and 10.95 ± 1.7, respectively) and log EPO X %Hct product were found between groups. In both hypertensive groups, BMI but not blood pressure positively correlated with hematocrit. A negative correlation between changes in EPO and PRA induced by sodium restriction was found in lean hypertensive subjects only (r = -0 .42, p < 0.01). This finding suggests that in contrast to non-obese patients with essential hypertension, in subjects with ORH activity of the renin-angiotensin-aldosterone system does not seem to be related to EPO secretion. Since in both lean and obese essential hypertensive subjects EPO and log EPO X %Hct product are within normal range, the contribution of endogenous EPO to the pathogenesis of hypertension in these patients is unlikely. (H ppertens Res 1994; 17: 43-48)

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 96%

Endogenouw Erythropoietin Levels in patients with Obesity-Related Hypertension.

Nowicki¹,

Kokot²,

Kokot³

et al. 1994

Hypertens Res

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“…In patients with hypertension and normal renal excretory function, a direct correlation between plasma renin activity and serum Epo was seen in patients with glomerulonephritis or pyelonephritis. 18 Previous work from this laboratory documents anaemia due to Epo deficiency in patients with Type 1 diabetes 10 with hyporeninaemic hypoaldosteronism. Plasma renin activity is significantly lower in haemodialysis patients requiring exogenous Epo to maintain a haematocrit of approximately 30%, compared with similar patients who do not require Epo.…”

Section: Discussionmentioning

confidence: 99%

Losartan may modulate erythropoietin production

Donnelly

Miller

2001

J Renin Angiotensin Aldosterone Syst

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Erythropoietin (Epo) is distinct amongst haematopoietic hormones, in that it is produced remote from the bone marrow. The tissue oxygen pressure required to trigger the Epo gene under physiological conditions is uniquely sited at a restricted area in the kidney termed the critmeter. Angiotensin II (Ang II) increases sodium reabsorption and hence oxygen consumption at any given blood flow rate; therefore, it may affect the balance of renal oxygen supply vs. demand and hence Epo production. The purpose of this study was to determine whether Epo production is modulated by the renin-angiotensin system (RAS). Twenty normal subjects on a controlled sodium and protein diet had glomerular filtration rate (GFR) and renal plasma flow (RPF) assessed by standard methods of inulin and para-aminohippurate clearance, respectively, at baseline, hourly after the administration of losartan (25 mg) and after each 30 minute period of the infusion of Ang II at doses of 0.5, 1.5 and 2.5 ng/kg/minute. The baseline GFR was 115±4.0 ml/minute/1.73 m 2 , RPF 650±29 ml/minute/1.73 m 2 and Epo 12.4±0.8 U/L. In spite of a marked increase in filtration fraction (FF) with Ang II, no changes in serum Epo levels were observed at two hours (11.7±1.3 U/L, p=n.s. compared with baseline). After the administration of losartan, there was a variable effect on FF, but a strong correlation of the change in serum Epo concentration and the change in FF (r=0.648, p=0.002), suggesting that the RAS may modulate Epo production.

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“…Insulin and plasma aldosterone were measured with radioimmunoassay as previously described [13]and all other parameters with standard laboratory methods.…”

Section: Methodsmentioning

confidence: 99%

Nonselective Beta-Adrenergic Blockade Augments Fasting Hyperkalemia in Hemodialysis Patients

Nowicki

Miszczak-Kuban²

2002

Nephron

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Background/Aim: Fasting hyperkalemia in patients with end-stage renal failure is a well-documented phenomenon. Both a decreased secretion of insulin and decreased β-adrenergic receptor sensitivity may take part in this effect. Methods: Twelve anuric, long-term (6.4 ± 2.7 years; mean ± SD) hemodialysis patients underwent three periods of 18-hour fasting (from 6 p.m. to 12 a.m.). At the beginning of each fasting period a single dose of the nonselective β-blocker, nadolol (80 mg), or the β₁-selective blocker, betaxolol (20 mg), or placebo were given in a random order and in blinded fashion. The wash-out period was 7 days. Results: The mean decrease in blood pressure was similar after nadolol and betaxolol (18 ± 10 vs. 19 ± 11 mm Hg) as was a decrease in heart rate (20 ± 3 and 19 ± 6, respectively). Serum potassium was not different before each of the fasting periods. The increase in serum potassium during fasting was highly significant in each case. The mean increase in serum potassium was 1.2 ± 0.4 mmol/l after nadolol, 0.9 ± 0.6 after betaxolol and 0.6 ± 0.6 after placebo. This effect was significantly larger after nadolol than after placebo (p = 0.01), but this relation was not significant with respect to betaxolol (p = 0.30). Serum insulin as well as glucose decreased significantly and to a similar extent during each fasting period. Plasma aldosterone was unchanged. Conclusion: Nonselective β-adrenergic blockade increases the hyperkalemic effect of fasting in hemodialysis patients.

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Influence of the Renin-Angiotensin System Stimulation on Erythropoietin Production in Patients with Various Forms of Arterial Hypertension

Cited by 12 publications

References 18 publications

Endogenouw Erythropoietin Levels in patients with Obesity-Related Hypertension.

Endogenouw Erythropoietin Levels in patients with Obesity-Related Hypertension.

Losartan may modulate erythropoietin production

Nonselective Beta-Adrenergic Blockade Augments Fasting Hyperkalemia in Hemodialysis Patients

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