Signaling path of the action of AVP on distal K+ secretion

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Date of download: 6/25/2016 From: Nephrogenic Diabetes Insipidus Ann Intern Med. 2006;144(3): doi: / Water.
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Presentation transcript:

Signaling path of the action of AVP on distal K+ secretion José B.O. Amorim, Raif Musa-Aziz, Margarida Mello-Aires, Gerhard Malnic  Kidney International  Volume 66, Issue 2, Pages 696-704 (August 2004) DOI: 10.1111/j.1523-1755.2004.00800.x Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 1 Experimental setup: stationary microperfusion of cortical distal tubule. Double-barreled micropipette is inserted into late proximal tubule. Abbreviations are: C, colored castor oil; P, control perfusion solution; S, single micropipette for experimental solution. Double-barreled microelectrode in late distal tubule (initial collecting duct). Abbreviations are: IE, ion exchange resin; Ref, reference electrode. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 2 Potassium secretory flux (JK) during luminal perfusion with 10−5 mol/L 8-bromo-cyclic adenosine monophosphate (cAMP) (A) and with 10−8 mol/L phorbol 12-myristate 13-acetate (PMA) (B). 8-bromo-cAMP reduces JK, while PMA, known to stimulate protein kinase C (PKC), increases JK significantly. *P < 0.05; **P < 0.01. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 3 JK during luminal perfusion with 10−11 mol/L arginine vasopressin (AVP), alone or with 10−4 mol/L H89, (A) or with 10−5 mol/L staurosporin (B). Note that H89, a blocker of protein kinase A (PKA), does not affect JK, while staurosporin, a blocker of protein kinase C (PKC), causes a significant reduction of JK. #P < 0.01. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 4 JK during luminal perfusion with 10−11 mol/l arginine vasopressin (AVP) alone or plus 10−11 mol/L BAPTA-am. BAPTA, a calcium chelator, reduces JK, indicating that the effect of AVP depends on cell Ca2+.#P < 0.001. BAPTA, bis aminophenoxy ethane-tetraacetic acid. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 5 JK during luminal perfusion with 10−11 mol/L arginine vasopressin (AVP) alone and plus 5 mmol/L tetraethylammonium chloride (TEA), a blocker of Ca2+-dependent K+ channels (maxi-potassium).*P < 0.05. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 6 JK during luminal perfusion with 10−11 mol/L arginine vasopressin (AVP) alone or plus 10−7 mol/L iberiotoxin (IBX), a scorpion venom-derived toxin, highly specific inhibitor of maxi-potassium channels (A). (B) luminal perfusion with AV1, blocker of V1 receptors for AVP, alone or with iberiotoxin. *P < 0.05; **P < 0.01. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions

Figure 7 Schematic drawing of cell signaling mechanisms of luminal (V1 receptors) and basolateral (V2 receptors) action of arginine vasopressin (AVP). The role of V1 receptors and their signaling are derived from the present studies. The role of V2 receptors in ROMK channel stimulation is based on the studies of Cassola, Giebisch, and Wang6. Kidney International 2004 66, 696-704DOI: (10.1111/j.1523-1755.2004.00800.x) Copyright © 2004 International Society of Nephrology Terms and Conditions