Cardiovascular effects of ventrolateral periaqueductal gray (vlPAG) AT۱ receptors in normotensive and hemorrhagic rats
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 29، شماره: 2
سال انتشار: 1405
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 75
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شناسه ملی سند علمی:
JR_IJBMS-29-2_014
تاریخ نمایه سازی: 7 بهمن 1404
چکیده مقاله:
Objective(s): The ventrolateral periaqueductal gray (vlPAG) regulates cardiovascular function. Given the presence of Angiotensin II (AngII) and its AT۱ receptors (AT۱R) in the vlPAG, this study investigated their central and peripheral roles in cardiovascular control during normotensive and hemorrhage (Hem) conditions.Materials and Methods: Saline, three doses of AngII (۰.۱, ۰.۲, and ۰.۳ nmol) were microinjected into the vlPAG. The AT۱R blocker Losartan (Losa) was microinjected alone and before AngII in normotensive and Hem conditions. The peripheral mechanisms of AngII were examined by intravenous injection of hexamethonium (Hexa, a ganglion blocker) and atropine (Atro, a muscarinic receptor blocker), alone and before AngII (۰.۳ nmol), in both normotensive and Hem conditions. Time course and maximal changes (Δ) of mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) were recorded by the PowerLab apparatus and analyzed. Results: Higher doses of AngII significantly increased HR, SBP, and MAP (P<۰.۰۵-P<۰.۰۰۱) than saline. Losa attenuated these effects. Hexa significantly attenuated the pressor effect of AngII (P<۰.۰۰۱), while Atro increased HR (P<۰.۰۰۱). Hem decreased SBP/MAP and increased HR (P<۰.۰۱); these responses were augmented by AngII, and Losa blocked this AngII effect. Hexa reduced the cardiovascular improvement induced by AngII during Hem, and Atro enhanced the AngII-induced tachycardia.Conclusion: AngII in the vlPAG stimulates cardiovascular activity via AT۱R in both normotensive and Hem conditions. Furthermore, these peripheral effects of AngII are primarily mediated through sympathetic nervous system activation.
کلیدواژه ها:
نویسندگان
Esmaeil Hamounpeyma
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Reza Mohebbati
Department of Physiology, Faculty of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran
Mohammad Naser Shafei
Applied Biomedical Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran
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