Related Experiment Video
Updated: Jul 10, 2026

Cardiac Pressure-Volume Loop Analysis Using Conductance Catheters in Mice
Published on: September 17, 2015
Correction of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin
E L Schiffrin1, J B Park, H D Intengan
1Medical Research Council Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada. schiffe@ircm.qc.ca
Losartan, an angiotensin type 1 receptor antagonist, improved vascular structure and endothelial function in hypertension patients. Beta-blocker atenolol did not show these vascular benefits.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hypertension Research
Background:
- Vascular alterations are linked to hypertension complications.
- Angiotensin II may play a key role in these vascular abnormalities.
Purpose of the Study:
- To test if losartan corrects resistance artery abnormalities in hypertensive patients.
- To compare losartan's effects with atenolol on vascular structure and function.
Main Methods:
- 19 untreated essential hypertension patients received losartan or atenolol for 1 year.
- Resistance arteries were analyzed using a pressurized myograph.
- Vascular structure and endothelial function were assessed.
Main Results:
- Both drugs equally reduced blood pressure.
- Losartan significantly reduced media width to lumen diameter ratio.
- Losartan normalized endothelium-dependent relaxation, while atenolol did not.
Conclusions:
- Losartan corrected structural and endothelial dysfunction in resistance arteries.
- Atenolol did not improve these vascular parameters.
- AT(1) receptor antagonism offers vascular benefits beyond blood pressure reduction.
Related Concept Videos
Hypertension and Regulation of Blood Pressure
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Antihypertensive Drugs: Angiotensin II Receptor Blockers
Antihypertensive Drugs: Direct Renin Inhibitors
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Hypertension II: Pathophysiology

