Vasoconstriction caused by the ATP synthase subunit-coupling factor 6: a new function for a historical enzyme.

Enhancement of arterial vasoconstriction and depression of endothelial cell– dependent relaxation have been reported by many investigators as characteristics of vascular dysfunction in hypertension.1 These dysfunctions support the increase in total peripheral resistance observed in experimental and human forms of hypertension. Because arterial smooth-muscle cell hyperreactivity and reduced vasoactive function of the endothelial cell are observed in response to multiple stimuli (eg, serotonin, norepinephrine, KCl in smooth muscle; acetylcholine, bradykinin, A23187 in endothelial cell) and are thus not necessarily agonist-specific, researchers have investigated the idea that more general mechanisms of signal transduction are altered and support global changes in vascular function. These include alterations in composition and function of elements as diverse as potassium channels, calcium channels, sodium-potassium ATPase, G-proteins, membrane lipid composition, etc. In this issue of Hypertension, the study by Osanai et al2 reveals a new function for a protein subunit of an enzyme that is ubiquitously expressed in all tissues, the ATP synthase.