The systemic vascular resistance response: a cardiovascular response modulating blood viscosity with implications for primary hypertension and certain anemias

Abstract

Without an active regulatory feedback loop, increased blood viscosity could lead to a vicious cycle of ischemia, increased erythropoiesis, further increases of blood viscosity, decreased tissue perfusion with worsened ischemia, further increases in red cell mass, etc. We suggest that an increase in blood viscosity is detected by mechanoreceptors in the left ventricle which upregulate expression of cardiac natriuretic peptides and soluble erythropoietin receptor. This response normalizes systemic vascular resistance and blood viscosity at the cost of producing 'anemia of chronic disease or inflammation' or 'hemolytic anemia' both of which are better described as states of compensated hyperviscosity. Besides its role in disease, this response is also active in the physiologic adaptation to chronic exercise. Malfunction of this response may cause primary hypertension.

Prospective Safety Evaluation of a Cardiovascular Health Dietary Supplement in Adults with Prehypertension and Stage I Hypertension

“…29–32 Hematocrit in particular is the prevailing determinant of blood viscosity and as a result plays a role in long-term modulation of blood pressure. 29,33 It is plausible that the slight decreases in RBC count, hemoglobin, and hematocrit observed after 6 months are related to the decreases in systolic and diastolic blood pressure demonstrated in the first 3 months of the study.…”

Why Atherothrombosis is in Principle a Hematologic Disease: The Effect of Disorders and Drugs which Affect Thrombosis on the Development of Atherosclerotic Plaques

“…We hypothesize that the anemias of chronic disease and inflammation are compensatory mechanisms which normalize systemic vascular resistance. This response causes the anemias in congestive heart failure [83], monoclonal gammopathies and reactive hypergammaglobulinemias, hemolytic anemias, and others [113].…”

Apolipoprotein(a) is the Product of a Pseudogene: Implications for the Pathophysiology of Lipoprotein(a)

“…It also provides insight into the protection against atherothrombosis afforded by HDL, which decreases blood viscosity [ 36 ], the failure of cholesteryl ester transfer protein inhibitors [ 37 ] and the excess cardiovascular mortality caused by consumption of the Western diet and trans fats [ 38 ]. Our study of blood viscosity has also provided insight into the cause of several anemias, including those associated with heart failure [ 39 ], chronic disease and inflammation, and hemolytic anemias [ 40 ].…”