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Angiotensin II augments renal vascular smooth muscle soluble GC expression via an AT 1 receptor–forkhead box subclass O transcription factor signalling axis
Author(s) -
Galley Joseph C.,
Hahn Scott A.,
Miller Megan P.,
Durgin Brittany G.,
Jackson Edwin K.,
Stocker Sean D.,
Straub Adam C.
Publication year - 2022
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.15522
Subject(s) - medicine , endocrinology , angiotensin ii , angiotensin ii receptor type 1 , kidney , vascular smooth muscle , renovascular hypertension , receptor , vasodilation , renin–angiotensin system , receptor expression , biology , blood pressure , smooth muscle
Reduced renal blood flow triggers activation of the renin-angiotensin-aldosterone system (RAAS) leading to renovascular hypertension. Renal vascular smooth muscle expression of the NO receptor, soluble GC (sGC), modulates the vasodilator response needed to control renal vascular tone and blood flow. Here, we tested if angiotensin II (Ang II) affects sGC expression via an AT 1 receptor-forkhead box subclass O (FoxO) transcription factor dependent mechanism.