PubMed · 10892097
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P Keto, A Haapanen, T Kallio. 1997. [Visualizing the arteries].. https://pubmed.ncbi.nlm.nih.gov/10892097/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
Consider renovascular hypertension (HT) when: Newly diagnosed hypertension presents with features that are atypical of essential hypertension; Resistant hypertension is associated with risk factors for atheroma; or Angiotensin-converting enzyme (ACE) inhibitor or angiotensin-II-receptor antagonist therapy is associated with increasing plasma creatinine levels. Atheromatous renovascular HT can often be managed medically, which includes intensive correction of cardiovascular risk factors. ACE inhibitors are probably second-line antihypertensives for patients with unilateral renal artery stenosis and two kidneys. First-line antihypertensives are diuretics, beta-blockers and calcium-channel blockers. Bilateral renal artery stenosis, or a unilateral stenosis in a patient with only one kidney, is an absolute contraindication to ACE inhibition.
We have previously shown that deficiency in the anti-inflammatory cytokine interleukin-10 (IL-10) is responsible for enhanced angiogenesis after hindlimb ischemia. This study examined the putative involvement of matrix metalloproteinase (MMP) activation in this process. Ischemia was produced by artery femoral occlusion in both C57BL6 IL-10(+/+) and IL-10(-/-) mice. Angiographic vessel density and laser Doppler perfusion data at day 28 showed significant improvement in ischemic/nonischemic leg ratio by, respectively, 1.8-fold and 1.4-fold in IL-10(-/-) mice compared with IL-10(+/+) mice. This was associated with an increase in vascular endothelial growth factor (VEGF) protein content in the ischemic hindlimb. Three days after ischemia, gelatin zymography showed a significant increase in both pro- and active forms of MMP-2 and MMP-9 in ischemic hindlimbs of IL-10(-/-) mice compared with IL-10(+/+) mice (P<0.01). This increase in MMP activity in IL-10(-/-) mice was completely inhibited by treatment with BB-94 (5 mg/kg IP), a specific MMP inhibitor. Furthermore, increases in both vessel density and blood perfusion indexes at day 28 in IL-10(-/-) mice were abolished after treatment with BB-94 (0.78+/-0.06 versus 1.17+/-0.09 and 0.62+/-0.02 versus 0.88+/-0.04, for vessel density and blood perfusion ratio, respectively, in IL-10(-/-) mice treated with BB-94 versus untreated IL-10(-/-) mice, P<0.05). In contrast, BB-94 treatment did not affect the rise in VEGF protein content. These findings in IL-10(-/-) mice underscore the critical role of MMP activation, in a context of increased VEGF expression, in promoting ischemia-induced angiogenesis.