Abstract

Aging reduces skeletal muscle blood flow, but the mechanism remains unclear. The hypothesis was that aging results in less heat‐induced attenuation of vasoconstriction and this is attributable to decreased sensitivity of P2X receptors to heat. Femoral arteries from 28 young (2–3 months old) and 23 old (24 months old) rats were prepared for wire myography. Dose response curves for the P2X agonist, αβ‐methylene ATP (mATP: 10−7 to 10−3M), the α1‐agonist, phenylephrine (PE: 10−7 to 10−4M), the smooth muscle constrictor, potassium chloride (KCl: 20 to 80mM), and field stimulation (2–60Hz for 144 impulses) were performed at bath temperatures of 37°C and 41°C. The response to mATP was attenuated with heat in young (37°C: 0.95±0.14; 41°C: 1.48±0.12 g/log M mATP; p<0.05) and old (37°C: 1.05±0.16; 41°C: 1.67±0.20 g/log M mATP; p<0.05) femoral arteries. Phenylephrine dose response curves were not heat sensitive in young arteries, but were potentiated with 41°C in old arteries (p<0.05). KCl dose response curves were potentiated by 41°C in the young (37°C: 2.10±0.25; 41°C: 2.67±0.19g peak tension; p<0.05) and old arteries (37°C: 1.95±0.22; 41°C: 2.53±0.10g peak tension; p<0.05). The tension produced by field stimulation was attenuated by a greater amount in old (−78±10%) than in young (−43±12%). Heat‐induced attenuation of vasoconstriction via P2X receptors is preserved in old femoral arteries. Unexpectedly, old femoral arteries exhibit heat potentiation of α1‐receptor mediated vasoconstriction.

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