Erythrocytosis: a key to understanding the hemodynamic changes in hypertension.
Theories that would propose to explain the increased vascular resistance that accompanies hypertension include the presence circulating vasoconstrictor substances (angiotensin II, vasopressin, epinephrine, etc.), a centrally mediated generalized increase in sympathetic tone, increased vascular smooth muscle tone due to increased calcium ion permeability, and perhaps others. While each of these may be valid in some circumstances there exists yet another mechanism, indirect and potent, that could account for much of the change in peripheral vascular resistance that accompanies hypertension. This is the erythrocytosis mechanism that is mainly controlled by the kidneys. This treatise concerns the manner in which the kidneys supposedly react to disturbances in oxygen transport coincident with the development of hypertension and the effect that this might have in modifying peripheral resistance to blood flow.
Gaar
K A
KA
L.S.U. Medical Center, Shreveport 71130.
D001810:Blood Volume; D002302:Cardiac Output; D006439:Hemodynamics; D006801:Humans; D006978:Hypertension, Renovascular / Q000378:metabolism / Q000503:physiopathology*; D008955:Models, Cardiovascular; D010100:Oxygen / Q000378:metabolism; D011086:Polycythemia / Q000378:metabolism / Q000503:physiopathology*; D012079:Renal Circulation; D014655:Vascular Resistance
D010100:Oxygen