%0 Journal Article
%1 Webe_2002_182
%A Weber, Christopher R
%A Piacentino, Valentino
%A Ginsburg, Kenneth S
%A Houser, Steven R
%A Bers, Donald M
%D 2002
%J Circ. Res.
%K 11834700 ATPase, Action Adenocarcinoma, Adult, Allosteric Animal, Animals, Blockers, Calcium, Cell Cells, Channel Channels, Congestive, Contraction, Diastole, Disease Electric Electrophysiology, Esophageal Exchanger, Failure, Fatal Fluid, Gov't, Guinea Heart Heart, Humans, In Intracellular Ion Kinetics, Male, Maxillary Membrane Membrane, Models, Muscle Myocardial Myocardium, Neoplasms, Nickel, Non-U.S. Outcome, P.H.S., Patch-Clamp Pigs, Potentia, Potentials, Rabbits, Re, Regulation, Research Reticulum, Sarcoplasmic Separation, So, Sodium Sodium, Sodium-Calcium Stimulation, Strophanthidin, Support, Techniques, Tetrodotoxin, Transport, U.S. Ventricles, Vitro, dium-Calcium ls, search {N}a$^{+}$-{K}$^{+}$-Exchanging
%N 2
%P 182--189
%T Na$^+$-Ca$^2+$ exchange current and submembrane Ca$^2+$
	during the cardiac action potential.
%U http://circres.ahajournals.org/cgi/content/full/90/2/182
%V 90
%X Na$^+$-Ca$^2+$ exchange (NCX) is crucial in the regulation
	of Ca$^2+$(i) and cardiac contractility, but key details of
	its dynamic function during the heartbeat are not known. In the present
	study, we assess how NCX current (I(NCX)) varies during a rabbit
	ventricular action potential (AP). First, we measured the steady-state
	voltage and Ca$^2+$(i) dependence of I(NCX) under conditions
	when Ca$^2+$(i) was heavily buffered. We then used this relationship
	to infer the submembrane Ca$^2+$(i) (Ca$^2+$(sm)) sensed
	by NCX during a normal AP and Ca$^2+$(i) transient (when the
	AP was interrupted to produce an I(NCX) tail current). The Ca$^2+$(i)
	dependence of I(NCX) at -90 mV allowed us to convert the peak inward
	I(NCX) tail currents to Ca$^2+$(sm). Peak Ca$^2+$(sm)
	measured via this technique was >3.2 micromol/L within < 32 ms of
	the AP upstroke (versus peak Ca$^2+$(i) of 1.1 micromol/L at
	81 ms measured with the global Ca$^2+$ indicator indo-1). The
	voltage and Ca$^2+$(sm) dependence of I(NCX) allowed us to
	infer I(NCX) during the normal AP and Ca$^2+$ transient. The
	early rise in Ca$^2+$(sm) causes I(NCX) to be inward for the
	majority of the AP. Thus, little Ca$^2+$ influx via NCX is expected
	under physiological conditions, but this can differ among species
	and in pathophysiological conditions.