Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension (HTN) is a common complication of recombinant erythropoietin (EPO) therapy, but the mechanism of the EPO-associated HTN is uncertain. In the present study we examined the effects of EPO and the vehicle alone on rat caudal artery contractile response and basal and thrombin-stimulated platelet cytosolic Ca2+ concentration ([Ca2+]i) in vitro and on blood pressure (BP) and heart rate in vivo. At high concentrations (200 U/ml) EPO caused a small but consistent contraction in the caudal artery rings (P < 0.01) without affecting the response to either angiotensin II (ANG II) or the alpha 1-agonist methoxamine. Incubation with EPO significantly increased basal platelet [Ca2+]i (P < 0.01) and augmented the thrombin-induced rise of [Ca2+]i in Ca(2+)-free medium (P < 0.05). Long-term EPO administration led to a significant elevation of BP within 2 wk regardless of whether the hematocrit was allowed to rise or was kept constant by dietary iron deficiency. In contrast, single intravenous administration of high-dose EPO (400 and 5,000 U/kg), estimated to yield plasma concentrations comparable with those employed in vitro, failed to either alter BP or modify the BP response to ANG II during a 60-min observation period. This was associated with a significant rise in plasma guanosine 3',5'-cyclic monophosphate but no discernible change in plasma atrial natriuretic peptide, suggesting enhanced nitric oxide (NO) release. Thus, at high concentrations, EPO appears to possess a fast-acting pressor effect in vitro but not in vivo. The observed discrepancy may be due to enhanced NO release with EPO administration in vivo. However, HTN does occur with repeated EPO administration in a time-dependent and hematocrit-independent manner. This suggest that expression of the hypertensive effect of EPO in vivo involves a gradual conditioning process.
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PMID:In vivo and in vitro pressor effects of erythropoietin in rats. 859 78

Anemia is a common disease in elderly people. However, since hemoglobin concentration often decreases subclinically with aging because of nutritional impairment, its pathological significance is unclear. To investigate the pathological significance of low hemoglobin concentration, we studied the relation between hemoglobin levels and arrhythmia, as well as circulatory parameters. Arrhythmia was detected by Holter type ambulatory electrocardiography in 42 elderly people (aged 60 or over) living in a nursing home. Plasma concentrations of human atrial natriuretic peptide (hANP) after iron therapy were determined by immunoradiometric assay. Changes in circulatory parameters in elderly people with iron deficiency anemia were examined. Supraventricular and ventricular premature contractions significantly increased in elderly people with low hemoglobin concentrations or hematocrit. hANP increased significantly as the hemoglobin concentration decreased in 22 elderly people. Of these 22 subjects, 11 showed a low serum concentration of iron, and were administered ferrous salts. No side effects, such as nausea, occurred. After iron supplementation, the average hemoglobin level increased from 9.0 to 10.5 g/dl, and the average hANP level was reduced from 58.3+/-23.5 to 41.2+/-27.9 pg/ml, which was statistically significant by Wilcoxon's signed rank sum test. The increase in the hemoglobin level inversely correlated with the hANP level. Heart rate, blood pressure and body weight of subjects decreased significantly after iron supplementation therapy. Although hemoglobin levels were increased by iron supplementation therapy after a long period of anemia, the duration of the period with low hemoglobin levels showed no significant relation to initial hANP concentration. In conclusion, low hemoglobin levels induced secretion of hANP, and treatment of iron deficiency might exert favorable effects on the circulatory system.
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PMID:Atrial natriuretic peptide in aged patients with iron deficiency anemia. 1537 90