Table 1.

k_io Responsiveness to Metabolic Changes

kio increases with:	a	Increased NKA pump expression (5,9*)
	b	Increasing cytoplasmic ATP (9*)
	c	Increasing [Ko +] (at low [Ko +]), with an NKA Michaelis‐Menten signature (4,43)
	d	Hypoxia (10,44#)
	e	Cisplatin‐induced apoptosis (45)
	f	Xenograft tumor apoptotic regions (46#)
	g	Human brain metastasis radiosurgery (47#)
kio decreases with:	h	Ouabain NKA pump inhibition (2,5,9*,43)
	i	Increasing [Ko +] (at sufficient [Ko +] to cause membrane depolarization) (4)
	j	WZB117 glucose uptake inhibition (5)
	k	O2 → N2 switch (9*)
	l	Increasing mitochondrial reducing equivalents (6#)
	m	Intracellular lonidamine (48#) mitochondrial complex II inhibition (49)
	n	Extracellular tetrodotoxin voltage‐gated sodium channel inhibition (4)
	o	Extracellular AP5 plus DNQX† post‐excitatory neuronal activity inhibition (4)
	p	Glutamine deprivation (10)
	q	Hypertension in myocardium (28#)
	r	Chemotherapy of human breast tumors (50#)
	s	Phosphatase activation breast tumor therapy (51#)
kio correlates with:	t	Tumor metastatic potential (5,6#)
	u	Neuronal firing (4)
	v	Oxidative phosphorylation rate (52&)
	w	O2 consumption rate (4)
	x	Head and neck cancer mortality (53#)
	y	18Fluoro‐2‐deoxy‐D‐glucose breast tumor uptake (54#)

ATP, adenosine triphosphate; k_io, water efflux k (1/τ_i); NKA, Na⁺,K⁺‐ATPase (sodium pump).

^*For yeast, pump is PMA1, inhibitor is ebselen.

^#Employed shutter‐speed (к₁) dynamic‐contrast‐enhanced‐MRI.

^†(2R)‐Amino‐5‐phosphonovaleric acid plus 6,7‐dinitroquinoxaline‐2,3‐dione.

^&Indirect.