ARTERIOLAR CONSTRICTION IN MILD-TO-MODERATE ESSENTIAL-HYPERTENSION - AN OLD CONCEPT REQUIRING RECONSIDERATION

Citation
Jhj. Muntinga et al., ARTERIOLAR CONSTRICTION IN MILD-TO-MODERATE ESSENTIAL-HYPERTENSION - AN OLD CONCEPT REQUIRING RECONSIDERATION, Journal of hypertension, 15(4), 1997, pp. 411-419
Citations number
39
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
02636352
Volume
15
Issue
4
Year of publication
1997
Pages
411 - 419
Database
ISI
SICI code
0263-6352(1997)15:4<411:ACIME->2.0.ZU;2-9
Abstract
Objective To investigate differences between in-vivo properties of a v ascular bed in hypertensive patients and normotensive controls, Design Despite the controversy about the origin of essential hypertension an d its accompanying vascular changes, it is generally assumed that the characteristic increase in peripheral resistance when hypertension pro gresses is caused by arteriolar constriction. Yet, there is little exp erimental evidence that this assumption generally holds in vivo. Metho ds A non-invasive technique was used for studying properties of the co mplete vascular bed of an upper arm segment under an occluding cuff in 23 previously untreated hypertensive patients and their matched normo tensive controls. The method used the segment's electrical impedance t o assess the volumes of extravascular fluid and of arterial and venous blood under varying arterial transmural pressures. Results Compared w ith that of matched normotensive controls, the compliance of the large arteries of the vascular bed was on average 50.9% lower (P < 0.001) i n the hypertensive patients, The compliance of the complete arterial b ed at the operating blood pressure level was also lower (40.0%, P < 0. 01), but appeared to be significantly higher (45.9%, P < 0.05) at the normotensive blood pressure level, On the venous side, the patients ha d a higher blood volume (60.0%, P < 0.01) and an increased myogenic re sponse (68.5%, P < 0.05). Conclusions The increase in vascular resista nce in the hypertensive patients is due primarily to changes in the la rge and small vessels of the arterial bed, We found no evidence for a generally increased arteriolar constriction.