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Angiotensin II rapidly stimulates the short‐circuit current in opossum kidney cells expressing rat Na,K‐ATPase
Author(s) -
Yingst Douglas R.,
Hou Xia,
Li Quanwen,
Mattingly Raymond R.,
Sun Fei
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.912.23
Subject(s) - chemistry , angiotensin ii , medicine , endocrinology , sodium , renal sodium reabsorption , ouabain , reabsorption , transcellular , amiloride , apical membrane , stimulation , renin–angiotensin system , paracellular transport , receptor , biophysics , permeability (electromagnetism) , biology , membrane , biochemistry , blood pressure , organic chemistry
The binding of angiotensin II (Ang II) to the angiotensin receptor (AT 1 ) stimulates Na,K‐ATPase activity that drives sodium reabsorption in the proximal tubule, which reabsorbs 2/3 of the filtered sodium. To determine how quickly Ang II can stimulate Na,K‐ATPase in the proximal tubule, the α‐1 subunit of rat kidney Na,K‐ATPase and the AT 1a receptor were stably co‐expressed in opossum kidney cells. Cells were grown on permeable supports and mounted in an Ussing Chamber containing Ringer's solution. The addition of 10 μM Ang II to the basolateral side increased the short‐circuit current (Isc), which is proportional to net sodium transport, in ≤ ~10 sec. Isc peaked at ~20 sec and declined to a plateau above baseline for over 3 min. The subsequent addition of 200 μM nystatin to increase the sodium permeability of the apical membrane, and thereby the concentration of intracellular sodium, increased Isc to the level of the Ang II‐dependent peak. Subsequently adding 600 μM ouabain, which inhibits Na,K‐ATPase, reduced Isc to its original baseline value. Thus, Ang II significantly stimulated Na,K‐ATPase activity and transcellular sodium transport in 10 seconds or less. We hypothesize that such rapid Ang II‐dependent stimulation of sodium reabsorption in the proximal tubule is part of a mechanism to help the body to recover from a sudden drop in blood pressure. Supported in part by HL096800 to F.S.