Elastase incubation abolished structural and mechanical differences between mesenteric resistance arteries from spontaneously hypertensive and normotensive rats.
Does elastin degradation reverse structural and mechanical alterations in mesenteric resistance arteries of spontaneously hypertensive rats?
Elastin restructuring within the internal elastic lamina plays a central role in small artery remodeling and increased stiffness in hypertension, which can be reversed by elastin degradation.
Chronic hypertension is associated with resistance artery remodelling and mechanical alterations. However, the contribution of elastin has not been thoroughly studied. Our objective was to evaluate the role of elastin in vascular remodelling of mesenteric resistance arteries (MRA) from spontaneously hypertensive rats (SHR). MRA segments from Wistar Kyoto rats (WKY) and SHR were pressurised under passive conditions at a range of physiological pressures with pressure myography. Confocal microscopy was used to determine differences in the quantity and organisation of elastin in intact pressure-fixed arteries. To assess the contribution of elastin to MRA structure and mechanics, myograph-mounted vessels were studied before and after elastase incubation. When compared with WKY, MRA from SHR showed: (1) a smaller lumen, (2) decreased distensibility at low pressures, (3) a leftward shift of the stress-strain relationship, (4) redistribution of elastin within the internal elastic lamina (IEL) leading to smaller fenestrae but no change in fenestrae number or elastin amount. Elastase incubation (1) fragmented the structure of IEL in a concentration-dependent fashion, (2) abolished all the structural and mechanical differences between strains, and (3) decreased distensibility at low pressures. The study shows the overriding role of elastin in determining vascular dimensions and mechanical properties in a resistance artery. In addition, it informs hypertensive remodelling. MRA remodelling and increased stiffness are accompanied by elastin restructuring within the IEL and elastin degradation reverses structural and mechanical alterations of SHR MRA. Differences in elastin organisation are, therefore, a central element in small artery remodelling in hypertension.
Briones et al. (Wed,) conducted a other in Hypertension. Elastase incubation vs. Before elastase incubation / WKY rats was evaluated on Vascular dimensions and mechanical properties (structure and mechanics of MRA). Elastase incubation abolished structural and mechanical differences between mesenteric resistance arteries from spontaneously hypertensive and normotensive rats.