Key result
Chronic NO restriction with L-NAME in hypertensive rats induced more pronounced intrinsic stiffening in the abdominal aorta than the thoracic aorta due to greater fibrosis.
Why the study?
The study aimed to compare thoracic and abdominal aortic stiffness in spontaneously hypertensive rats with reduced NO synthesis, untreated spontaneously hypertensive rats, and normotensive Wistar Kyoto rats.
Does chronic NO restriction via L-NAME increase thoracic and abdominal aortic stiffness in spontaneously hypertensive rats?
Does chronic NO restriction via L-NAME increase thoracic and abdominal aortic stiffness in spontaneously hypertensive rats?
Chronic NO restriction in hypertensive rats induces severe intrinsic stiffening in the abdominal aorta, but not the thoracic aorta, due to localized profibrotic material accumulation.
Hypothesis-generating for regional aortic fibrosis in hypertension; requires human validation before clinical relevance.
The spontaneously hypertensive rat model with reduced NO synthesis (SHRLN) shares features with aging and hypertension in humans, among other a severe aortic stiffening. The present in vivo study aimed to compare thoracic (TA) and abdominal (AA) aortic stiffness in the SHRLN (treated 5 weeks with L‐NAME), SHR, and normotensive Wistar Kyoto (WKY). Dynamic properties of TA and AA were measured in the same rats, using echotracking recording of aortic diameter coupled with blood pressure (BP). Measurements were performed first at operating BP and then after BP reduction in hypertensive rats, thus in isobaric conditions. Histological staining and immunohistochemistry were used for structural analysis at both sites. At operating pressure, BP and pulse pressure (PP) were higher in SHRLN compared with SHR. Stiffness index was also increased and distensibility decreased in both TA and AA in SHRLN. At WKY‐matched blood pressure, isobaric AA parameters remained specifically altered in SHRLN, whereas TA recovered to values identical to WKYs. Collagen, fibronectin, α 5‐selectin, and FAK were increased in SHRLN compared with SHR or WKY. Nevertheless, only the strong accumulations of fibronectin and collagen at the AA site in SHRLN were associated with intrinsic stiffening. In conclusion, we confirm that NO restriction associated with hypertension induces a severe pathological phenotype and shows that L‐NAME induced stiffening is more pronounced in AA than in TA as a result of greater fibrosis.
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Lindesay et al. (2019) studied Hypertension. L-NAME (NO restriction) vs. SHR and normotensive Wistar Kyoto (WKY) was evaluated on Thoracic (TA) and abdominal (AA) aortic stiffness and structural analysis. Chronic NO restriction with L-NAME in hypertensive rats induced more pronounced intrinsic stiffening in the abdominal aorta than the thoracic aorta due to greater fibrosis.
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