Mas Receptor Activation Contributes to the Improvement of Nitric Oxide Bioavailability and Vascular Remodeling During Chronic AT1R (Angiotensin Type-1 Receptor) Blockade in Experimental Hypertension.
TGR(mREN2)27 rats develop non-alcoholic fatty liver disease-associated portal hypertension responsive to modulations of Janus-kinase 2 and Mas receptor.
AngII/AT1R and Ang-(1-7)/Mas1 receptor signaling converge on anessential common pathway of importance for both angiogenesis and vasodilation in the renin-angiotensin system involving ERK1/2 and p38MAPK signaling.
Mas receptor antagonist abolished relaxation while bradykinin receptor antagonist only slightly reduced it suggesting that bradykinin-induced vasorelaxation is regulated also by other mechanisms than the classical BR1/BR2 pathway.
valsartan attenuates neointimal hyperplasiain balloon-injured rat aortic arteries through activation of the ACE2-angiotensin-(1-7)-Mas axis as well as inhibition of the ACE-angiotensin II-AT1 and p-ERK pathways.
It seems that co-blockade of all AT1R AT2R and MasR may alter Renal blood flow/kidney weight in male more than in female rats. These findings support a crosstalk between MasR and Ang II receptors in renal circulation.
results demonstrated that renovascular hypertension increased Mas receptors expression and nitric oxide production in the rats carotid which consequently increased Ang-(1-7)-vasorelaxant response.
Actually the peptides Ang-(1-7) have been involved in modulating pain sensitivity. This modulation appear be dependent of its interaction with Mas receptor
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