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Impaired collateral artery development in spontaneously hypertensive rats
Jay L Tuttle1, Bridget M Sanders, Harold M Burkhart
1Department of Surgery, Indiana University Medical Center, Indianapolis, IN 46202-2879, USA.
Microcirculation (New York, N.Y. : 1994)
|October 11, 2002
Summary
Collateral artery development is impaired in spontaneously hypertensive rats compared to normotensive rats. This reduced expansion is linked to lower endothelial cell growth and no increase in eNOS expression.
Area of Science:
- Cardiovascular research
- Vascular biology
- Hypertension research
Background:
- Hypertension is a major risk factor for cardiovascular diseases.
- Impaired collateral circulation can exacerbate ischemic conditions.
- Understanding mechanisms of collateral development is crucial for therapeutic strategies.
Purpose of the Study:
- To investigate if collateral artery development is hindered in spontaneously hypertensive rats (SHR) compared to normotensive WKY rats.
- To elucidate the cellular and molecular mechanisms underlying potential differences in collateralization.
Main Methods:
- A surgical model of collateral artery induction was created by ligating sequential mesenteric arteries in SHR and WKY rats.
- Collateral artery diameter was measured in vivo before and after ligation.
- Histological, morphometric, and Western blot analyses were performed to assess endothelial cell proliferation and eNOS expression.
Main Results:
- Collateral artery expansion was significantly greater in WKY rats (38%) than in SHR (13%) one week post-ligation.
- Endothelial cell proliferation increased by 80% in WKY collaterals versus only 22% in SHR collaterals.
- eNOS expression increased by 128% in WKY collaterals but remained unchanged in SHR collaterals.
Conclusions:
- Collateral artery development, evidenced by luminal expansion, is suppressed in SHR compared to WKY rats.
- This impairment is associated with reduced endothelial cell proliferation and a lack of eNOS upregulation in SHR.
- These findings suggest that hypertension compromises the adaptive capacity of collateral circulation.