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

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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 (10−5M), ODQ (10−5M) and sildenafil (10−5M), inhibitors of NO synthase (NOS), soluble guanylyl cyclase (sGC) and phosphodiesterase‐5 (PDE5) respectively; or MFA (10−5M), TCP (10−5M) and dazoxiben (10−5M), inhibitors of COX, prostaglandin I2 (PGI2) synthase and thromboxane A2 (TXA2) 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 Fmax 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.