Systemic blood pressure is determined, in part, by arterial smooth muscle cells (myocytes). Several Transient Receptor Potential (TRP) channels are proposed to be expressed in arterial myocytes, but it is unclear if these proteins control physiological blood pressure and contribute to hypertension in vivo. We generated the first inducible, smooth muscle-specific knockout mice for a TRP channel, namely for PKD2 (TRPP1), to investigate arterial myocyte and blood pressure regulation by this protein. Using this model, we show that intravascular pressure and α1-adrenoceptors activate PKD2 channels in arterial myocytes of different systemic organs. PKD2 channel activation in arterial myocytes leads to an inward Na+ current, membrane depolarization and vasoconstriction. Inducible, smooth muscle cell-specific PKD2 knockout lowers both physiological blood pressure and hypertension and prevents pathological arterial remodeling during hypertension. Thus, arterial myocyte PKD2 controls systemic blood pressure and targeting this TRP channel reduces high blood pressure.
Pubmed ID: 30511640 RIS Download
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View all literature mentionsThis polyclonal secondary targets IgG (H+L)
View all literature mentionsThis polyclonal targets TRPM4 antibody
View all literature mentionsThis monoclonal targets actin
View all literature mentionsThis monoclonal targets Human TMEM16A
View all literature mentionsThis monoclonal targets PKD2 (431.2)
View all literature mentionsThis monoclonal targets Cav1.2 calcium channel
View all literature mentionsMus musculus with name B6.FVB-Tg(Myh11-icre/ERT2)1Soff/J from IMSR.
View all literature mentionsThis monoclonal targets Polycystin-1 (7E12)
View all literature mentionsThis polyclonal targets TRPC6 - Aminoterminal end
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