AETIOLOGY OF HYPERTENSION

We are still uncertain of the way in which environment and heredity interact to produce increased arterial pressure in patients with essential hypertension. Few indisputable abnormalities can be demonstrated. Of these there is universal agreement that structural vessel hypertrophy is present and thi...

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Bibliographic Details
Published in:British journal of anaesthesia : BJA 1984-07, Vol.56 (7), p.677-688
Main Author: SWALES, J.D.
Format: Article
Language:English
Subjects:
Animals
Autonomic Nervous System - physiopathology
Biological Transport
Blood Pressure
Cell Membrane - physiology
Dogs
Humans
Hypertension - etiology
Hypertension - physiopathology
Muscle, Smooth, Vascular - physiopathology
Rats
Renin-Angiotensin System
Sodium - metabolism
Water-Electrolyte Balance
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Summary:We are still uncertain of the way in which environment and heredity interact to produce increased arterial pressure in patients with essential hypertension. Few indisputable abnormalities can be demonstrated. Of these there is universal agreement that structural vessel hypertrophy is present and this acts probably as a maintenance and perhaps amplifying system resulting from an initial increase in arterial pressure. It cannot of course explain an increase in arterial pressure ab initio. Most of the well defined systems of arterial pressure control do not show any marked abnormality, although there is some evidence for a modest degree of sympathetic nervous system overactivity. Although some of the changes in cation fluxes across erythrocyte and leucocyte membranes are still debatable, there is general agreement that cation handling by erythrocytes and leucocytes is abnormal in many patients with essential hypertension and that some of these abnormalities are shared by the normotensive relatives of hypertensive patients. The most promising approach is that there is an abnormality of the cell membrane vascular smooth muscle which is partly genetically determined and perhaps also involves the autonomic nervous system. This produces an increased pressor response to environmental stimuli which becomes perpetuated and perhaps amplified by structural hypertrophy of the resistance vessels.
ISSN:0007-0912
1471-6771
DOI:10.1093/bja/56.7.677