A novel large vessel pressure myography technique demonstrated that isolated thoracic aortas from male mice were significantly larger than females (1358 vs 1287 µm) with similar vasomotor responses.
A novel large vessel pressure myography technique enables the ex vivo study of vasoreactivity and molecular mechanisms in intact murine thoracic aortas.
The vascular reactivity of the aorta influences hemodynamics which is crucial to delivering blood from the heart to the systemic circulation and attenuating the pulsatility of blood flow. Vasomotor responses (vasodilation and vasoconstriction) of the aorta rely on coordinated signals between the cell layers in the vessel wall, however, there are limited techniques to study these signals in large conduit blood vessels. Pressure myography, a technique where isolated vessels are cannulated and pressurized, is a widely used, physiologically relevant method to study cell signaling in intact vessels ex vivo, but technical limitations have restricted its use to small vessels. Our group has adapted this method to study vascular reactivity in large conduit vessels in murine models, specifically the thoracic aorta. In this study, thoracic aorta segments were exteriorized from 15-20-week-old C57BL/6J male and female mice and cannulated onto glass micropipettes inside a perfusion chamber. The temperature was maintained at 37°C, and the vessels were superfused with physiological salt solution (PSS). Intercostal arteries branching from the aorta were tied off with surgical suture to allow for pressurization without leaks. The intraluminal pressure of the aortas was set to 100mmHg using gravity-fed pressure lines. Pharmacological agents were delivered via the PSS superfusion solution. The vessel outer diameter was recorded using AmScope Imaging Software and analyzed post-hoc using VasoTracker software. Isolated, pressurized thoracic aortas from male mice were significantly larger in diameter than aortas from females outer diameter 1358µm ± 14 (males) vs. 1287µm ± 12 (females). Male and female mice had similar vasoconstrictor responses to the vascular smooth muscle cell (vSMC)-dependent alpha-1 adrenergic agonist phenylephrine logEC50(M)= -7.29 ± 0.09 (males) and -7.31 ± 0.05 (females). Between sexes, we found similar vasodilator responses to the endothelial cell-dependent muscarinic agonist acetylcholine logEC50(M)= -6.00 ± 0.43 (males) vs. -6.12 ± 0.15 (females) and the vSMC-dependent nitric oxide donor DEA-NONOate logEC50(M)= -6.35 ± 0.15 (males) vs. -6.70 ± 0.11 (females). Additionally, we observed flow-mediated vasodilation (FMD) in response to intraluminal flow, which was generated by raising the height of one gravity-fed pressure line by 10mmHg and lowering the other by 10mmHg. We found that FMD was consistent in male aortas, but female aortas demonstrated three distinct characteristic responses. Overall, we show here a new approach to studying the vasoreactivity of the ex vivo, pressurized thoracic aorta that maintains the intercellular connections and allows for probing of molecular mechanisms underlying vascular responses. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Kosmach et al. (Fri,) conducted a other in Vascular reactivity. Large vessel pressure myography vs. Male vs female mice was evaluated on Vessel outer diameter and vasomotor responses. A novel large vessel pressure myography technique demonstrated that isolated thoracic aortas from male mice were significantly larger than females (1358 vs 1287 µm) with similar vasomotor responses.
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