“…In addition, ACE inhibitors may impair erythropoiesis via either suppression of angiotensin-mediated Epo production or bone marrow response to Epo [53]. The relationship between the use of ACEI and ERI is still controversial, some investigations showed no relationship [54][55][56] while others [57,58] confirmed this study's finding and showed reduction in response to ESA.…”
Section: Individual Response Variations To Erythropoietin Stimulatingsupporting
“…In addition, ACE inhibitors may impair erythropoiesis via either suppression of angiotensin-mediated Epo production or bone marrow response to Epo [53]. The relationship between the use of ACEI and ERI is still controversial, some investigations showed no relationship [54][55][56] while others [57,58] confirmed this study's finding and showed reduction in response to ESA.…”
Section: Individual Response Variations To Erythropoietin Stimulatingsupporting
“…The underlying pathomechanism of this clinical observation is that ensuing renal hypoperfusion activates the reninangiotensin system (as described in detail above) and that angiotensin II stimulates erythropoiesis through stimulating Epo secretion and through its directs stimulating effect on erythropoiegenesis in the bone marrow (85). This mechanisms explains why effective blockage of the renin-angiotensin system through ACE inhibitors and/or angiotensin receptor blockers is often associated with a decrease in hematocrit (86,87) and that ACE inhibitors are effective in normalizing post-transplant erythrocytosis (88).…”
Section: Interplay Of Renin-angiotensin and Epo Systemsmentioning
Long overlooked as the virtual compartment and then strictly characterized through descriptive morphologic analysis, the renal interstitium has finally been associated with function. With identification of interstitial reninand erythropoietin-producing cells, the most prominent endocrine functions of the kidney have now been attributed to the renal interstitium. This article reviews the functional role of renal interstitium.
“…Recent research has provided some new insights into this aspect. Angiotensin II, a component of the regulatory pathway initiated by renin, acts directly as a growth factor through the AT1 receptor, stimulating proliferation of erythroid progenitors in bone marrow and, additionally, it enhances erythropoietin secretion (Vlahakos et al, 2010). This mechanism also explains anaemia that has been described as a side effect of drugs interfering with the renin-angiotensin system (Sica and Mannino, 2007).…”
Section: Blood Rheology and The Pathophysiology Of Hypertensionmentioning
Blood rheology is impaired in hypertensive patients. The alteration involves blood and plasma viscosity, and the erythrocyte behaviour is often abnormal. The hemorheological pattern appears to be related to some pathophysiological mechanisms of hypertension and to organ damage, in particular left ventricular hypertrophy and myocardial ischemia. Abnormalities have been observed in erythrocyte membrane fluidity, explored by fluorescence spectroscopy and electron spin resonance. This may be relevant for red cell flow in microvessels and oxygen delivery to tissues. Although blood viscosity is not a direct target of antihypertensive therapy, the rheological properties of blood play a role in the pathophysiology of arterial hypertension and its vascular complications.
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