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Induction of angiogenesis in NO-deficient rat heart
L Okruhlicová1, N Tribulová, I Bernátová
1Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic. usrdokru@savba.sk
Insights
Long-term inhibition of nitric oxide (NO) production in rats induced hypertension, leading to cardiac capillary angiogenesis. This study reveals fibroblast activation and endothelial cell proliferation contributing to new blood vessel growth in the heart.
Area of Science:
- Cardiovascular Biology
- Pathophysiology
- Cellular Biology
Background:
- Hypertension is a known trigger for angiogenesis.
- Nitric oxide (NO)-deficient hypertension is associated with cardiac and coronary artery remodeling.
- Subcellular capillary alterations in hypertension require further investigation.
Purpose of the Study:
- To examine subcellular alterations of cardiac capillaries in rats with NO-deficient hypertension induced by L-NAME.
- To investigate the role of fibroblasts and endothelial cells in angiogenesis during NO-deficient hypertension.
Main Methods:
- Rats were treated with L-NAME (40 mg/kg/day) for 4 weeks to induce NO-deficient hypertension.
- Cardiac capillaries were analyzed for qualitative subcellular changes.
- Fibroblast and endothelial cell activity was assessed.
Main Results:
- Long-lasting NO inhibition activated fibroblast function, enhancing fibrotization and angiogenesis.
- Fibroblasts were observed near capillary pericytes, followed by detachment and migration.
- Capillaries showed proteosynthetic activity, capillary growth, and endothelial cell proliferation and migration.
Conclusions:
- L-NAME-induced NO-deficient hypertension triggers significant angiogenesis in cardiac capillaries.
- Fibroblast activation and endothelial cell proliferation are key mechanisms in this process.
- These findings highlight the role of NO deficiency in promoting cardiac vascular adaptation during hypertension.
Abstract:
Angiogenesis is known to be triggered by various stimuli including hypertension. It was previously found that NO-deficient hypertension is accompanied by structural remodeling of the cardiac muscle and large coronary arteries. This study was aimed to examine the qualitative subcellular alterations of capillaries in the heart of the rats treated with L-NAME (40 mg/kg/day for 4 weeks). The results showed that long-lasting inhibition of NO production induced an apparent activation of fibroblast function. This was associated with enhancement of fibrotization as well as with the induction of angiogenesis. Accordingly, fibroblasts were frequently located in the vicinity of capillary pericytes, which was followed by their detachment and migration. Moreover, besides inactive or even injured capillaries, the other ones exhibited extensive proteosynthetic activity linked to capillary growth, proliferation and migration of endothelial cells. The results strongly indicate enhanced triggering of the angiogenesis in L-NAME-induced NO-deficient hypertension.