If I'm not mistaken adenosine is only released from cardiac tissue which leads to dilation of the coronary vessels. It should be the production of lactic acid from skeletal muscles which contributes to the decline in TPR.
Skeletal muscle is a very large organ (relatively speaking). Vasodilation of the blood vessels in the skeletal muscle >> vasoconstriction of splanchnic vessels. That's why, even though you see vasoconstriction in some beds, the overall effect is that the TPR decreases. Is that what you're asking?