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Objective: Extracellular vesicles are increasingly recognized to be central in intercellular communication, delivering messages through their content, including DNA, RNAs, proteins, and lipids, expelled particularly under cellular activation or stress. While microparticles are 100-1000 nm in size and bud of the cytoplasmic membrane, exosomes are distinct nano-sized particles (<100 nm) originating from intracellular multivesicular bodies via exocytosis. These structures are increasingly recognized to regulate biological processes including vascular repair and angiogenesis, and are seen as targets for therapeutic interventions, but their role in hypertension is little understood. We previously showed that hypertension is associated with loss of myofibrils and migration of smooth muscle cells (SMCs) towards and across the intima of the vascular wall. Cell-to-cell communication is thought to be essential in orchestrating these functional and structural adaptions to mechano or other stresses of the vessel wall. Therefore, we analyzed the differences in exosomes in the vessel wall of resistance-sized arteries from normotensive vs hypertensive patients. Design and method: We assessed with transmission electron microscopy the ultrastructure of resistance-sized arteries (200-400 μm), isolated from omental samples obtained during fibroid surgery from 17 women (8 hypertensive), mean age 42 y (SE 1). Results: Endothelial cells (ECs) and SMCs from normotensives showed few multivesicular bodies (MVBs; (mean 0.45 (0.6) per cell) containing on average 5.0 (0.7) exosomes/MVB. The number of MVBs and exosomes progressively increased with blood pressure increase, in both ECs and SMCs, to a mean of 5 MVBs (0.9)/cell) and 8.8 (1.1) exosomes/MVB in hypertensive patients (a 20-fold increase in exosomes/cell), displaying a prominent basal (abluminal) location in ECs of hypertensives (Figure). Conclusions: Our study demonstrates that blood pressure increase is associated with intensified intercellular communication in resistance arteries. The increases in MVBs and exosomes at the abluminal side of the endothelium suggest a possible autocrine and paracrine role in mediating EC-to-SMC communication during vascular remodeling. Exosomes released just beneath the endothelial layer can be internalized by SMCs, transferring bioactive materials that may affect SMC phenotype and function. Our study might inform further studies on intercellular communication in the vascular wall with increasing blood pressure.
Brewster et al. (Wed,) studied this question.