Figure 4.
Interdependence of AT1R and ETA/BR in the response of renal interlobar arteries to activating autoantibodies. Small vessel myography of artery rings exposed to 1.0 mg/mL Control IgG or SRC IgG and natural ligands with and without pretreatment with receptor blockers as indicated. (A) Additional stimulation with 1000 nM AngII±ETA/BRB (bosentan). n =11–18. **P <0.01, ***P <0.001. (B) Additional stimulation with 100 nM ET-1±AT1RB (valsartan). n =6–12. ***P <0.001 for all comparisons. Contraction is expressed as % of the maximal contraction in response to 60 mM KCl of each individual vessel. Mean±SEM. Ang II: angiotensin II; AT1RB: Ang II type 1 receptor blocker; Control IgG: IgG isolated from healthy controls; ETA/BRB: dual ET-1 type A and type B receptor blocker; SRC IgG: IgG isolated from patients with scleroderma renal crisis

Interdependence of AT1R and ETA/BR in the response of renal interlobar arteries to activating autoantibodies. Small vessel myography of artery rings exposed to 1.0 mg/mL Control IgG or SRC IgG and natural ligands with and without pretreatment with receptor blockers as indicated. (A) Additional stimulation with 1000 nM AngII±ETA/BRB (bosentan). n =11–18. **P <0.01, ***P <0.001. (B) Additional stimulation with 100 nM ET-1±AT1RB (valsartan). n =6–12. ***P <0.001 for all comparisons. Contraction is expressed as % of the maximal contraction in response to 60 mM KCl of each individual vessel. Mean±SEM. Ang II: angiotensin II; AT1RB: Ang II type 1 receptor blocker; Control IgG: IgG isolated from healthy controls; ETA/BRB: dual ET-1 type A and type B receptor blocker; SRC IgG: IgG isolated from patients with scleroderma renal crisis

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