In canine skeletal muscle in vivo, ACE inhibition modulates noradrenaline overflow depending on alpha-adrenoceptor status, but circulating Ang II does not facilitate noradrenaline release.
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Animal data on ACE inhibition and noradrenaline overflow warrant no clinical translation yet; leaves open mechanisms of sympathetic regulation by the renin-angiotensin system.
Schwieler et al. (1992) studied this question.
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