Interaction between the microcirculatory network and the systemic arterial pressure

• Main Authors: Jose Vilar, Antony W. Kedra, Jean-Jacques Mourad, Jean-Sébastien Silvestre, Bernard I. Lévy
• Format: Article
• Language: English
• Published: Atlantis Press 2010-12-01
• Series: Artery Research
• Online Access: https://www.atlantis-press.com/article/125929317/view

The large arterial system and the microcirculatory network are generally studied as separated entities. We aimed to establish a link between the remodelling of microcirculatory and arterial blood pressure. Experimental: Pre-hypertensive spontaneously hypertensive rats SHRs were maintained under hypoxic (12% O2) conditions for 8 weeks. The systolic blood pressure was lower by 26% in hypoxic vs. normoxic SHRs. Total peripheral vascular resistance was 30% lower in hypoxic than in normoxic SHRs. At the end of the hypoxic period, capillary density in skeletal muscle was 1.2-fold higher in hypoxic than in normoxic SHRs. Myocardial capillary density and VEGF-A protein contents were also 1.2- and 2.1-fold higher in hypoxic compared to normoxic SHRs. Thus, chronic normobaric hypoxia (1) activates VEGF-A-induced angiogenesis and thereafter (2) prevents or normalizes hypertension in the SHR. Clinical: Increase in blood pressure (BP) is a hallmark of anti-angiogenic treatments. We used video microscopy to measure dermal capillary densities in the dorsum of the fingers. Measurements were carried out in 18 patients before and after 6-month treatment with bevacizumab. BP was increased compared with baseline from 129 ± 13/75 ± 7 mmHg to 145 ± 17/82 ± 7 mmHg. Compared with the baseline, mean dermal capillary density was significantly lower (75 ± 12 versus 83 ± 13/mm2). Thus, bevacizumab treatment resulted in capillary rarefaction, possibly participating to the rise in BP observed in most patients. Thus, from experimental and clinical data, we might suggest that activation or blockade of angiogenesis may affect vascular resistance and, subsequently, blood pressure levels.