Vasa recta pericytes express a strong inward rectifier K<sup>+</sup> conductance

Cao, Chunhua; Goo, Jae Hwan; Lee-Kwon, Whaseon; Pallone, Thomas L.

doi:10.1152/ajpregu.00877.2005

Cited by 35 publications

(40 citation statements)

References 43 publications

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“…1,5,6 Our finding that Kir is expressed in afferent and efferent arterioles is consistent with the suggestion that this channel is preferentially expressed in resistance vessels. The finding that the postglomerular efferent arterioles express Kir also agrees with a recent report by Cao et al 16 that Kir currents are observed in the contractile pericytes of the postglomerular descending vasa recta. In contrast, Prior et al 15 demonstrated a lack of Kir in the renal arcuate artery, a conduit vessel.…”

Section: Discussionsupporting

confidence: 92%

“…This study, in concert with the observations of Prior et al 15 and Cao et al, 16 suggest a similar distribution within the renal vascular bed.…”

Section: Discussionsupporting

confidence: 90%

“…Our laboratory found indirect evidence that Kir plays a prominent role in the afferent arteriole, 14 whereas Prior et al 15 found no evidence that Kir influences tone or membrane potential in the upstream arcuate artery, a conduit vessel that does not contribute to renal vascular resistance. Recently, Cao et al 16 demonstrated that the pericytes of the postglomerular descending vasa recta express a Kir current and exhibit K ϩ -induced hyperpolarization. The expression of Kir and its role in the efferent arteriole are unknown.…”

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confidence: 99%

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Inward Rectifier K+ Currents and Kir2.1 Expression in Renal Afferent and Efferent Arterioles

Chilton¹,

Loutzenhiser²,

Salinas³

et al. 2008

Journal of the American Society of Nephrology

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The afferent and efferent arterioles regulate the inflow and outflow resistance of the glomerulus, acting in concert to control the glomerular capillary pressure and glomerular filtration rate. The myocytes of these two vessels are remarkably different, especially regarding electromechanical coupling. This study investigated the expression and function of inward rectifier K ϩ channels in these two vessels using perfused hydronephrotic rat kidneys and arterioles and myocytes isolated from normal rat kidneys. In afferent arterioles pre-constricted with angiotensin II, elevating [K ϩ ] 0 from 5 to 15 mmol/L induced hyperpolarization (Ϫ27 Ϯ 2 to Ϫ41 Ϯ 3 mV) and vasodilation (6.6 Ϯ 0.9 to 13.1 Ϯ 0.6 m). This manipulation also attenuated angiotensin II-induced Ca 2ϩ signaling, an effect blocked by 100 mol/L Ba 2ϩ . By contrast, elevating [K ϩ ] 0 did not alter angiotensin II-induced Ca 2ϩ signaling or vasoconstriction in efferent arterioles, even though a significant hyperpolarization was observed (from Ϫ30 Ϯ 1 to Ϫ37 Ϯ 3 mV, P ϭ 0.003). Both vessels expressed mRNA for Kir2.1 and exhibited anti-Kir2.1 antibody labeling. Patch-clamp measurements revealed prominent inwardly rectifying and Ba 2ϩ -sensitive currents in afferent and efferent arteriolar myocytes. Our findings indicate that both arterioles express an inward rectifier K ϩ current, but that modulation of this current alters responsiveness of only the afferent arteriole. The expression of Kir in the efferent arteriole, a resistance vessel whose tone is not affected by membrane potential, is intriguing and may suggest a novel function of this channel in the renal microcirculation.

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Section: Discussionsupporting

confidence: 92%

“…This study, in concert with the observations of Prior et al 15 and Cao et al, 16 suggest a similar distribution within the renal vascular bed.…”

Section: Discussionsupporting

confidence: 90%

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confidence: 99%

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Inward Rectifier K+ Currents and Kir2.1 Expression in Renal Afferent and Efferent Arterioles

Chilton¹,

Loutzenhiser²,

Salinas³

et al. 2008

Journal of the American Society of Nephrology

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“…Where possible, inputs for the model were taken from recent studies of descending vasa recta pericytes (7,8,28) and cerebrovascular arteries (40). When parameters were not available for VSMC, they were extrapolated from data for cardiac cells (24,33).…”

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confidence: 99%

Ouabain modulation of cellular calcium stores and signaling

Edwards¹,

Pallone²

2007

American Journal of Physiology-Renal Physiology

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Ouabain-like factors modulate intracellular Ca2+ concentrations and Ca2+ stores. Recently, a role for Na+-K+-ATPase Na+ transport inhibition as a pivotal event in ouabain signaling was questioned (Kaunitz JD. Am J Physiol Renal Physiol 290: F995-F996, 2006). In the present study, we used a mathematical model of Ca2+ trafficking in cytoplasm and subplasmalemmal microdomains to simulate the pathways through which ouabain can affect Ca2+ signaling: inhibition of active transport by Na+-K+-ATPase alpha1- and alpha2-isoforms, activation of inositol trisphosphate (IP3) production, and increased IP3 receptor (IP3R) conductance. A fundamental prediction is that Na+-K+-ATPase inhibition favors sarcoplasmic reticulum Ca2+ store loading, whereas Src-mediated increases in IP3 production and IP3R sensitization favor store depletion. The model predicts that alpha2-isoform inhibition generates a peak-and-plateau pattern of cytosolic Ca2+ concentration ([Ca2+](cyt)) elevation, whereas alpha1-isoform inhibition yields a monophasic rise. The effects of ouabain-mediated increases in IP3 production or IP3R conductance on [Ca2+](cyt) depend on their relative distributions between cellular microdomains and the bulk cytoplasm. Simulations suggest that the intracellular localization of IP3 production is a pivotal determinant of the changes in compartmental Ca2+ concentrations that can be induced by ouabain. As a consequence of sequestration of the ouabain-sensitive alpha2-isoform into microdomains, inhibition of the alpha2-isoform in rodents is not predicted to significantly affect cytosolic Na+ concentration. Model simulations support the hypothesis that ouabain can enhance agonist-evoked [Ca2+](cyt) transients when its predominant effect is to inhibit alpha2-isoform Na+ transport and, thereby, increase Ca2+ loading into sarcoplasmic reticulum stores.

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“…DVR are composed of smooth muscle-like pericytes and an endothelial monolayer. Study of channel architecture in these vessels (3, 4, 17, 20, 21, 25, 29 -31) has verified the presence of voltage-gated cation channels and led to recent identification of a strong, inwardly rectifying K ϩ conductance in the pericytes (3). To date, there has been no identification of K IR in the endothelium of DVR or any other renal microvessel.…”

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confidence: 99%

Descending vasa recta endothelia express inward rectifier potassium channels

Cao

Lee-Kwon²,

Payne³

et al. 2007

American Journal of Physiology-Renal Physiology

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Descending vasa recta (DVR) are capillary-sized microvessels that supply blood flow to the renal medulla. They are composed of contractile pericytes and endothelial cells. In this study, we used the whole cell patch-clamp method to determine whether inward rectifier potassium channels (K(IR)) exist in the endothelia, affect membrane potential, and modulate intracellular Ca(2+) concentration ([Ca(2+)](cyt)). The endothelium was accessed for electrophysiology by removing abluminal pericytes from collagenase-digested vessels. K(IR) currents were recorded using symmetrical 140 mM K(+) solutions that served to maximize currents and eliminate cell-to-cell coupling by closing gap junctions. Large, inwardly rectifying currents were observed at membrane potentials below the equilibrium potential for K(+). Ba(2+) potently inhibited those currents in a voltage-dependent manner, with affinity k = 0.18, 0.33, 0.60, and 1.20 microM at -160, -120, -80, and -40 mV, respectively. Cs(+) also blocked those currents with k = 20, 48, 253, and 1,856 microM at -160, -120, -80, and -40 mV, respectively. In the presence of 1 mM ouabain, increasing extracellular K(+) concentration from 5 to 10 mM hyperpolarized endothelial membrane potential by 15 mV and raised endothelial [Ca(2+)](cyt). Both the K(+)-induced membrane hyperpolarization and the [Ca(2+)](cyt) elevation were reversed by Ba(2+). Immunochemical staining verified that both pericytes and endothelial cells of DVR express K(IR)2.1, K(IR)2.2, and K(IR)2.3 subunits. We conclude that strong, inwardly rectifying K(IR)2.x isoforms are expressed in DVR and mediate K(+)-induced hyperpolarization of the endothelium.

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Vasa recta pericytes express a strong inward rectifier K⁺ conductance

Cited by 35 publications

References 43 publications

Inward Rectifier K+ Currents and Kir2.1 Expression in Renal Afferent and Efferent Arterioles

Inward Rectifier K+ Currents and Kir2.1 Expression in Renal Afferent and Efferent Arterioles

Ouabain modulation of cellular calcium stores and signaling

Descending vasa recta endothelia express inward rectifier potassium channels

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Vasa recta pericytes express a strong inward rectifier K+ conductance

Cited by 35 publications

References 43 publications

Inward Rectifier K+ Currents and Kir2.1 Expression in Renal Afferent and Efferent Arterioles

Inward Rectifier K+ Currents and Kir2.1 Expression in Renal Afferent and Efferent Arterioles

Ouabain modulation of cellular calcium stores and signaling

Descending vasa recta endothelia express inward rectifier potassium channels

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Vasa recta pericytes express a strong inward rectifier K⁺ conductance