In spontaneously hypertensive rats, VEGF expression and capillary density in the left ventricle are significantly increased, suggesting a compensatory angiogenic response to chronic hypertension.
Remains preclinical in hypertensive rats; leaves open whether VEGF-driven angiogenesis compensates for pressure overload in humans.
OBJECTIVE: The role of VEGF in vascular remodeling of target organs exposed to chronic hypertension is poorly understood. The authors compared capillary density (CD), capillary-to-fiber ratio (C/F), and VEGF mRNA expression in the hearts (left ventricle [LV]), and skeletal muscles (soleus and anterior tibialis [AT]) of 18-week-old male spontaneously hypertensive rats (SHR) and age-matched male Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats. METHODS: CD or C/F in LV, soleus, and AT of SHR, WKY, and SD rats was determined by analysis of randomly acquired digital images of cryosections stained with FITC-conjugated GS-I lectin. VEGF mRNA expressions in the tissues were determined by Northern blot. RESULTS: VEGF mRNA expressions in LV of SHR were 3.84- and 5.05-fold higher, compared to SD and WKY rats, respectively (n = 6; p < .01). There were no significant differences in VEGF mRNA expression in soleus or AT among SHR, WKY, and SD rats (p > .05). CD in LV of SHR (4975 +/- 167) was significantly higher than WKY or SD rats, 4151 +/- 169 and 3807 +/- 187 mm(-2), respectively (p < .05). In LV of SHR, C/F increased (35%) more significantly than CD (increased 20%), compared to WKY rats. CD, or C/F in soleus or AT of SHR was similar to that observed in WKY or 8D rats. CONCLUSIONS: VEGF expression, CD, and C/F in the heart (LV) of SHR are significantly increased, compared to WKY and SD rats. The data are consistent with the possibility that VEGF may contribute to capillary growth as a compensatory response to hypertension.
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Gu et al. (2004) studied this question.
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