Peripheral vasculature in essential hypertension.
1. Haemodynamic evidence shows that in essential hypertension minimum vascular resistance and vascular pressor response are increased and that the vascular reserve is decreased. 2. The haemodynamic changes are most easily explained in terms of a generalized narrowing of the vasculature and an increase in the ratio between the thickness of the tunica media and the lumen diameter (media: lumen ratio), with no change in the functional properties of the smooth muscle itself. 3. Histological and in vitro studies of resistance vessels confirm these predictions. Moreover, the evidence indicates that these changes are associated mainly with remodelling (rearrangement of the same amount of material) of the vessels, rather than growth. 4. Although the alteration in small artery structure is usually appropriate to the actual blood pressure, the structure appears not only to be a secondary adaptation, but is also dependent on other factors, including neurohumoral factors. 5. The available evidence shows that normalization of the resistance vessel structure (by increasing lumen diameter and decreasing the media:lumen ratio) should be achieved not by inhibition of growth but by (reverse) remodelling. Recent evidence from clinical investigations shows that this can be achieved in essential hypertensive patients treated with the angiotensin-converting enzyme inhibitor perindopril. 6. The role of the resistance vasculature as a primary determinant of blood pressure remains unclear. It is suggested that the requirement for normalization of resistance vascular structure is due to a need to increase the vascular reserve.
Mulvany
M J
MJ
Department of Pharmacology, University of Aarhus, Denmark.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects*; D001808:Blood Vessels / Q000033:anatomy & histology / Q000473:pathology* / Q000503:physiopathology* / Q000648:ultrastructure; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D007211:Indoles / Q000627:therapeutic use; D020913:Perindopril; D014655:Vascular Resistance / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D007211:Indoles; D020913:Perindopril