Wild blueberry diets attenuate phenylephrine (Phe)‐induced vasoconstriction via NO‐sGC‐cGMP signaling, but not the COX pathway in spontaneously hypertensive rats (SHR)

The role of wild blueberries on the NO and COX pathways was examined in 20 week‐old SHRs after eight weeks of a control (C, n=10) or an 8% wild blueberry (WB, n=10) diet. Phenylephrine‐induced vasoconstriction was examined in aortic rings in the absence or presence of LNMMA (10 −5 M), ODQ (10 −5 M) and sildenafil (10 −5 M), inhibitors of NO synthase (NOS), soluble guanylyl cyclase (sGC) and phosphodiesterase‐5 (PDE 5 ) respectively; or MFA (10 −5 M), TCP (10 −5 M) and dazoxiben (10 −5 M), inhibitors of COX, prostaglandin I 2 (PGI 2 ) synthase and thromboxane A 2 (TXA 2 ) synthase, respectively. The maximum force of contraction (Fmax) was lower in the WB, 0.79±0.01g, than in the C rats, 0.96±0.01g, (p≤0.05). Application of LNMMA led to a higher but similar Fmax in both groups, whereas inhibition of sGC resulted in a higher F max in the WB, 1.61±0.01g vs 1.52±0.01g in the C group (p≤0.05). Sildenafil application decreased Fmax to a similar level in both groups. Additionally, concentration of aortic cGMP was higher in the WB‐fed SHRs, 5.49□0.20 vs 4.07□0.20 pg/ml/mg, (p≤0.05). A similar reduction of Fmax in both groups was elicited by MFA, TCP or dazoxiben, indicating that COX is not involved in the reduced Phe vasoconstriction in the SHRs fed a WB diet. Therefore, wild blueberries modulate NO‐sGC‐cGMP signaling, without a significant effect on the COX pathway in the SHR model.