Biomechanics of resistance artery wall remodeling in angiotensin-II hypertension and subsequent recovery.
OBJECTIVE
To identify the relationship between systemic and local hemodynamics, as well as segmental biomechanical properties in a musculocutaneous resistance artery during angiotensin-II hypertension and its recovery.


METHODS
Rats were infused with angiotensin-II using implanted osmotic minipumps (ALZET 2ML4, 150 ng/kg/min) for 4 weeks. Measurements were made either immediately following infusion or after an additional 4-week recovery period. Parallel controls were created. Segmental geometry and blood flow were determined in vivo on microsurgically exposed segments of the saphenous arterial branch (350 mum). Pressure-radius plots of excised cylindrical segments were recorded by pressure arteriography.


RESULTS
Eutrophic hypertensive wall remodeling developed, with reduced passive radius, increased wall thickness, elevated low-stress elastic modulus, reduced norepinephrine contraction, and reduced endothelium-mediated dilation. Relaxed wall geometry fully healed in 4 weeks of recovery, but an increased contractility and a reduced in vivo lumen persisted. Regional hemodynamic resistance correlated positively with systemic arterial pressure and wall thickness in vivo, and negatively with in vivo lumen size throughout these studies.


CONCLUSIONS
A partial recovery of the biomechanical parameters was found. Healing of eutrophic hypertensive remodeling of the resistance artery wall is a complex biomechanical process, not a simple reversal of the original pathological sequel.
Nádasy
György L
GL
Department of Clinical Research and Human Physiology, Semmelweis University, Budapest, Hungary. nadasy@elet2.sote.hu
Várbíró
Szabolcs
S
Szekeres
Mária
M
Kocsis
Adrienn
A
Székács
Béla
B
Monos
Emil
E
Kollai
Márk
M
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004548:Elasticity; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D006977:Hypertension, Renal / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D009638:Norepinephrine