У нас вы можете посмотреть бесплатно EPicks: Stiffer large arteries and cerebral and skeletal muscle feed artery responses или скачать в максимальном доступном качестве, видео которое было загружено на ютуб. Для загрузки выберите вариант из формы ниже:
Если кнопки скачивания не
загрузились
НАЖМИТЕ ЗДЕСЬ или обновите страницу
Если возникают проблемы со скачиванием видео, пожалуйста напишите в поддержку по адресу внизу
страницы.
Спасибо за использование сервиса ClipSaver.ru
In this EPicks video, Ashley Walker (Department of Human Physiology at University of Oregon, USA) talks about her latest paper investigating whether stiffer large arteries affect cerebral and skeletal muscle feed artery responses to vasoconstrictors. Read more in Experimental Physiology: Cerebral and skeletal muscle feed artery vasoconstrictor responses in a mouse model with greater large elastic artery stiffness Ashley E. Walker, Elise K. Kronquist, Kerrick T. Chinen, Kelly D. Reihl, Dean Y. Li, Lisa A. Lesniewski & Anthony J. Donato. 104(3), pp. 434-442 https://physoc.onlinelibrary.wiley.co... Transcript: Hi, my name is Ashley Walker. I am an Assistant Professor in the Department of Human Physiology at University of Oregon. One of the hallmark feature of advancing age is an increase in stiffness of the large elastic arteries. Recent studies in humans have found correlations between large artery stiffness and cerebrovascular dysfunction, cognitive impairment, and an increased risk for Alzheimer’s disease. However, the mechanisms underlying this link between large artery stiffness and poor outcomes in the brain are unclear. In these studies we examined the effect of large artery stiffness on the cerebral artery response to vasoconstrictors. To examine the causative nature of this relation, we used a transgenic mouse model of large artery stiffness, the elastin heterozygote mouse. To perform these studies, we used isolated and pressurized middle cerebral arteries. We found that the vasoconstriction response to angiotensin II was greater in cerebral arteries from elastin heterozygote mice compared with wildtype mice. By using losartan, we demonstrated that this greater vasoconstriction was mediated by the angiotensin II type 1 receptor. To summarize, in these studies we found that in a mouse model of greater large artery stiffness there was a greater vasoconstrictor response to angiotensin II in the cerebral arteries. We also examined the dose responses to potassium chloride, norepinephrine, and endothelin-1 and found no differences between cerebral arteries from elastin heterozygote and wildtype mice. In parallel with these experiments in cerebral arteries, we also examined the response to the vasoconstrictors in gastrocnemius feed arteries. In this case, we found no difference between groups of elastin genotype on any vasoconstrictor response. These findings align with a previous study by our group that demonstrated that the elastin heterozygote mouse has impaired endothelial function in cerebral arteries, but not skeletal muscle feed arteries. These findings also align with the human literature, where it is found that the cerebral vasculature is one of the most susceptible circulations to the effects of large artery stiffness. Overall, these results indicate that increased responsiveness to angiotensin II may be one mechanisms linking age-related increases in large artery stiffness to cerebrovascular impairments.