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1015 Impaired Angiogenesis in Malignant versus Non-malignant Experimental Hypertension

Objective: The pathogenesis of the vascular lesions of malignant hypertension is unclear. We hypothesized that an impaired angiogenic response characterizes the malignant course of experimental hypertension. Design and methods: Two-kidney, one-clip renovascular hypertension was induced in rats; controls (CON) were sham operated. To distinguish malignant hypertension (MH) from non-malignant hypertension (NMH), we performed split-half analyses for two factors: weight loss, and the number of typical vascular lesions (onion skin lesions and fibrinoid necroses) per kidney section of the nonclipped kidney. Animals in the upper half for both criteria were defined as MH. As a bioassay of the angiogenic response, polyvinyl discs were implanted subcutaneously, and the area of vascularization was measured as a fraction of the total area after sacrifice. Results: After 5 weeks, mean arterial blood pressure measured in conscious rats was elevated to the same degree in MH (207 ± 10 mmHg, N = 12) and NMH (201 ± 4 mmHg, N = 14, p = 0.4 versus MH) compared to CON (113 ± 3 mmHg, N = 25, P < 0.001 versus NMH and MH). Vascularization of discs was reduced in MH (0.65 ± 0.04, N = 9) compared to NMH (0.77 ± 0.02, N = 9, p = 0.028) and CON (0.76 ± 0.02, N = 12, p = 0.028). There was no difference between NMH and CON (p = 0.8). VEGF expression in the left ventricle tended to increase in NMH (1.29 fold, p = 0.1 versus CON) but decreased in MH (0.75 fold, p = 0.015 versus NMH). A similar pattern was observed for VEGF receptor 2. Conclusion: An impaired angiogenic response occurs in malignant renovascular hypertension but not in the non-malignant course of the disease despite comparable blood pressure levels.