Pathogenesis of Essential Hypertension

Ulrych, Milos
February 1979
Angiology;Feb1979, Vol. 30 Issue 2, p104
Academic Journal
There is no blood volume overload in essential hypertension. However there is evidence for capacitance bed constriction which, in spite of the lowered blood volume (and partly causing it), leads most likely to an increase in "circulatory filling." Blood volume may relate to circulatory filling inversely rather than directly, and thus its size is more likely misleading than helpful as an indicator of circulatory filling. Too much attention has been given to volume alone, without consideration of capacitance. An increased glomerular filtration fraction can be present either (1) as the same defect operating in the peripheral circulation, i.e., increased postcapillary constriction (intrinsic renal defect), or (2) as part of general circulatory adjustments to the shift to Starling's curve to the right (regulatory mechanisms cause the kidney to retain sodium), as in congestive heart failure. Future concepts will have to consider both intrinsic venous mechanisms and substances acting on the venous part of circulation (which can hardly be any of the currently commonly considered hormones) to explain the whole question of volume, circulatory filling, and volume retention in hypertension. Despite all of the attempts of all the other subspecialties, hypertension remains primarily a vascular disease. However, much remains to be elucidated before we understand the disease well enough to find the cure.


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