Key result
Increased blood flow caused lumen enlargement with reduced smooth muscle cell apoptosis in normotensive rats, but increased wall-to-lumen ratio with enhanced cell growth in hypertensive rats.
Increased blood flow induces maladaptive vascular remodeling in hypertensive rats, contrasting with adaptive lumen enlargement in normotensive rats, suggesting shear stress contributes to hypertensive vascular remodeling.
Caution warranted before clinical extrapolation from rat models; leaves open shear stress contribution to human hypertensive remodeling.
The effect of an increased blood flow on vascular remodeling was studied in the mesenteric arteries of 11-12-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY). Increased blood flow was induced by selective ligation of mesenteric arteries. Nearby arteries with normal blood flow were used as controls. 7-10 days after the ligation procedure, mesenteric arteries were fixed in situ at maximal relaxation by perfusion fixation. Morphometric measurement of vascular dimension was carried out with confocal microscopy. Apoptotic cells were detected by the TdT-mediated dUTP nick-end labelling method. Cell growth was quantified by using proliferating cell nuclear antigen (PCNA) in sections of paraffin-embedded vessels. In SHR, elevated blood flow increased the vessel wall dimension and the number of smooth muscle cell (SMC) layers and also increased the wall-to-lumen ratio and the number of PCNA-positive SMC, but did not change lumen size or number of apoptotic SMC. In WKY, on the other hand, increased blood flow resulted in an increase in lumen diameter, a reduction of apoptotic SMC, but no change in wall-to-lumen ratio, number of SMC layers, or number of PCNA-positive SMC. These results showed that mesenteric arteries from hypertensive and normotensive rats respond to an increase in blood flow differently: a lumen enlargement with reduced SMC apoptosis in WKY, but an increased wall-to-lumen ratio with enhanced SMC growth in SHR. Although it remains to be determined whether flow alteration is one of the initiating factors in the development of vascular remodeling in hypertension, we speculate that an increase in cardiac output, and therefore an increase in shear stress that occurs in young SHR, contributes to vascular remodelling in this model of hypertension.
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Gao et al. (2008) studied Hypertension. Increased blood flow via selective ligation of mesenteric arteries vs. Nearby arteries with normal blood flow was evaluated on Vascular dimension, apoptosis, and cell growth. Increased blood flow caused lumen enlargement with reduced smooth muscle cell apoptosis in normotensive rats, but increased wall-to-lumen ratio with enhanced cell growth in hypertensive rats.
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