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. Author manuscript; available in PMC: 2024 Oct 1.
Published in final edited form as: Hypertension. 2023 Aug 18;80(10):2072–2087. doi: 10.1161/HYPERTENSIONAHA.123.21392

Figure 3. Cellular senescence impairs endothelial function with aging by reducing nitric oxide (NO) bioavailability not by influencing vascular smooth muscle sensitivity to NO, and senolytic treatment increases vascular endothelial function in advanced age by increasing NO bioavailability, not by altering vascular smooth muscle sensitivity to NO.

Figure 3.

In young (6-8 months) and old (27-29 months) male and female (sexes combined) p16-3MR mice treated with vehicle (Veh; sterile saline) or ganciclovir (GCV, in sterile saline) at a dose of 25 mg/kg/day for five consecutive days via intraperitoneal injection: (A) Carotid artery endothelium-dependent dilation (EDD) to increasing doses of acetylcholine (ACh). (C) NO-mediated EDD calculated as peak EDD alone (−) peak EDD in the presence of L-NAME. (E) Carotid artery endothelium-independent dilation to increasing doses of the NO donor sodium nitroprusside (SNP). In old male C57BL/6N mice treated with vehicle (10% ethanol; 30% PEG400; 60% Phosal 50PG) or ABT-263 (in the vehicle) at a dose of 50 mg/kg/day via oral gavage following a one week on – two weeks off – one week on dosing regimen: (B) Carotid artery EDD to increasing doses of ACh. (D) NO-mediated EDD. (F) Carotid artery endothelium-independent dilation (EID) to increasing doses of SNP. All data are mean ± SEM. N = 15-20/group, p16-3MR study EDD, NO-mediated EDD, and EID. N = 10-14/group, ABT-263 study EDD, NO-mediated EDD, and EID. * P < 0.05, effect of aging within group; ‡ P < 0.05, effect of treatment within age group.