Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lim, P.O.
Right arrow Articles by MacDonald, T.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lim, P.O.
Right arrow Articles by MacDonald, T.M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Q J Med 2000; 93: 703-705
© 2000 Association of Physicians


Editorial

Step test in hypertension

P.O. Lim and T.M. MacDonald

Department of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4KN

The physiological basis of essential hypertension is a continuing rise in the systemic vascular resistance (SVR) over time, a process which does not appear to be halted by drug treatment that normalizes diastolic blood pressure (BP).1 Since SVR is a major determinant of BP in the absence of left ventricular (LV) systolic dysfunction, BP rises in parallel with the SVR. This can easily be demonstrated with drugs such as phenylnephrine or cyclosporin that increase the SVR. It was previously thought that peripheral vasoconstriction was a ‘protective’ response to an early hyperkinetic circulation. However, this hypothesis has largely been discounted.2 Hypertension is thus the response to an increased SVR, the aetiology of which is still unclear. The increased pressure generated within the left ventricle to maintain a high level of systemic arterial BP has an inherent tendency to cause . . . [Full Text of this Article]

References


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
CJASNHome page
R. Agarwal and R. P. Light
Physical Activity and Hemodynamic Reactivity in Chronic Kidney Disease
Clin. J. Am. Soc. Nephrol., November 1, 2008; 3(6): 1660 - 1668.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
R. S. Vasan, J. C. Evans, M. G. Larson, P. W.F. Wilson, J. B. Meigs, N. Rifai, E. J. Benjamin, and D. Levy
Serum Aldosterone and the Incidence of Hypertension in Nonhypertensive Persons
N. Engl. J. Med., July 1, 2004; 351(1): 33 - 41.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
P. O. Lim and T. Rankinen
Role of Aldosterone in the Pathogenesis of Hypertension * Response
Hypertension, February 1, 2002; 39 (2): e14 - e14.
[Full Text] [PDF]