Effects of Erythropoietin Administration on Blood Pressure and Urinary Albumin Excretion in Rats

Abstract

The effects of recombinant human erythropoietin (rHuEPO) administration on blood pressure and urinary albumin excretion were studied in normotensive Wistar-Kyoto rats (WKY), in spontaneously hypertensive rats (SHR), and in SHR rats treated with an angiotensin converting enzyme inhibitor (SHR-ACEi). Rats were housed in metabolic cages and treated with rHuEPO (150 U/kg body weight [bw] three times a week) for 6 weeks. Control animals received the vehicle only (0.25 mL of physiological saline). An angiotensin converting enzyme inhibitor was administered in the drinking water for 6 weeks (spirapril 5 mg/kg bw). Systolic blood pressure (SBP), and 24 h urinary albumin excretion (UAE) were measured once a week. No significant differences in SBP were observed between rHuEPO and vehicle-treated normotensive animals at the end of the treatment (171.9 +/- 4.9 v 172.1 +/- 5.6 mm Hg, respectively). After 6 weeks, SBP was significantly higher in SHR and SHR-ACEi groups treated with rHuEPO than in control groups (239.8 +/- 7.3 and 243.0 +/- 7.3 mm Hg v 218.1 +/- 6.0 and 187.9 +/- 4.6 mm Hg, respectively); UAE was significantly higher in groups treated with rHuEPO than in control groups (WKY: 265.9 +/- 19.5 v 127.0 +/- 12.3 microg/100 g bw, SHR: 1668.4 +/- 564.6 v 234.8 +/- 22.9 microg/100 g bw, and SHR-ACEi: 1522.7 +/- 448.3 v 143.0 +/- 18.9 microg/100 g bw, respectively). We concluded that erythropoietin treatment causes an increase in arterial pressure in SHR only, and an increase in UAE in both normotensive and hypertensive rats. The albuminuric effect was not entirely dependent on increased blood pressure. The treatment with an angiotensin converting enzyme inhibitor did not modify either the proteinuric or the pressor effects.

The Role of Serum Erythropoietin (EPO) and Vascular Endothelial Growth Factor (VEGF) in Pulse Wave Velocity (PWV) Among Hypertensive Patients: A Cross-Sectional Study

“…It has been observed that treating chronic kidney disease (CKD) patients with EPO may lead to severe arterial HTN. This could be attributed to EPO-induced increased blood viscosity and decreased hypoxic vasodilatation [ 18 ]. Furthermore, it has also been noted that EPO increases calcium ion influx via opening L-type calcium channels in vascular smooth muscle cells and causes vasoconstriction [ 19 ].…”

Cerebral Blood Volume and Vasodilation are Independently Diminished by Aging and Hypertension: A Near Infrared Spectroscopy Study

“…Cerebral blood volume was then calculated [21,22] as CBV (ml/100g) = [HbT]brain*MWHb*10 −4 / dt*[HbT]plasma*CLVHR, where [HbT]brain (mol/L) is the total hemoglobin concentration in brain tissue, MWHb = 64.5 kiloDalton molecular weight of hemoglobin, dt = 1.05 g/ml is the cerebral tissue density, [HbT]plasma (g/dl) is the hemoglobin concentration obtained from plasma and CLVHR = 0.69 is the cerebral to large vessel hematocrit ratio [23,24] (Further studies will be needed in order to understand the effect of age and hypertension on the cerebral-to-large vessel hematocrit ratio in order to improve the precision of CBV calculation). In the young animals, blood hemoglobin concentration was assumed to be 16 g/dL [22,[25][26][27].…”