Mechanical properties of mesenteric resistance arteries from Dahl salt-resistant and salt-sensitive rats: role of endothelin-1.
OBJECTIVE
Hypertension has been associated with altered structure and mechanics of resistance arteries. This study assessed whether the passive mechanics of mesenteric small arteries are altered in hypertensive Dahl salt-sensitive rats (Dahl-SS) vs normotensive Dahl salt-resistant rats (Dahl-SR). The role of endothelin-1 in determining small artery mechanics was also studied.


METHODS
Male Dahl-SR and Dahl-SS were treated with high sodium (4% NaCl) for 10 weeks. Subgroups of each strain were treated with the ETA-endothelin receptor antagonist, A-127722 (30 mg/kg/d), concomitantly. Third-order branches of mesenteric arteries were mounted in a pressure myograph and exposed to intraluminal pressures ranging up to 140 mmHg. Media thickness and lumen diameter were measured at each pressure, from which wall mechanics were calculated.


RESULTS
Tail-cuff systolic blood pressure was elevated with high sodium in Dahl-SS vs Dahl-SR. At the given dose, A-127722 decreased blood pressure in Dahl-SS slightly but significantly. Lumen diameter was lesser and media-lumen ratios were greater in vessels from Dahl-SS. Under isobaric conditions, vessels from Dahl-SS exhibited decreased wall stress and incremental elastic modulus. However, there were no changes in isobaric incremental distensibility or elastic modulus in relation to wall stress. A-127722 attenuated the changes in media:lumen ratio and isobaric stress observed in Dahl-SS.


CONCLUSIONS
Dahl salt-sensitive hypertension was associated with altered structure of mesenteric resistance arteries, which decreased wall stress. Endothelin-1 may be involved in these changes. These arteries exhibit decreased isobaric stiffness and no difference in geometry-independent stiffness, indicating that the decreased lumen diameter is a result of eutrophic remodeling.
Intengan
H D
HD
Clinical Research Institute of Montreal, Quebec, Canada.
Schiffrin
E L
EL
D000818:Animals; D000077868:Atrasentan; D001696:Biomechanical Phenomena; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D004548:Elasticity; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000502:physiology*; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D011759:Pyrrolidines / Q000494:pharmacology; D051381:Rats; D044022:Receptor, Endothelin A; D012965:Sodium Chloride; D014655:Vascular Resistance / Q000502:physiology
D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D011759:Pyrrolidines; D044022:Receptor, Endothelin A; D012965:Sodium Chloride; D000077868:Atrasentan