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Nephrol Dial Transplant (2000) 15: 1751-1754
© 2000 European Renal Association-European Dialysis and Transplant Association

Hypothesis

Is inactivity the origin of essential hypertension: should we all be runners?

Alexander L. Macnair

Cae'n y Bwlch Isaf, Talsarnau, Gwynedd, UK

Introduction

Irvine Page [1] thought that essential hypertension arose from ‘a constellation of facets, one or even none being more or less dominant’. On the other hand Guyton and his colleagues [2] posited a single pathogenetic mechanism. In their view, long-term arterial blood pressure control is a function of the fluid-balance system and depends upon the capacity of the kidney to excrete sodium and water. However, they clearly demonstrated that the relationship between blood pressure and fluid excretion is itself subject to feedback from a dozen or more variables which may modify the constituents, volume, pressure or rate of flow of blood, and glomerular filtrate within the vessels and tubules of the kidney. De Wardener [3] rejected Page's mosaic hypothesis in favour of a single triggering factor for essential hypertension, namely an abnormal kidney with diminished ability to excrete sodium. However, we are left with . . . [Full Text of this Article]

How is essential hypertensive initiated?

Blood flow in trained muscle

The relationship between obesity and essential hypertension

Autoregulation in untrained muscle

Effects of local activation of angiotensin II

Testing the hypothesis

Population-wide decline in activity

Notes

References


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