Effect of arginine vasopressin and ANP on intracellular pH and cytosolic free [Ca2+] regulation in MDCK cells

Oliveira‐Souza, Maria; Mello-Aires, Margarida

doi:10.1046/j.1523-1755.2001.00993.x

Cited by 12 publications

(19 citation statements)

References 21 publications

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“…Vasopressin was shown to induce Ca 2ϩ influx across the apical membrane of renal collecting duct cells, and alterations in intracellular Ca 2ϩ levels are known to affect Na ϩ reabsorption in these tubules (34 -36). In addition, it has been suggested that the action of other hormones, including atrial natriuretic peptide (ANP), parathyroid hormone (PTH), bradykinin, and prostaglandins on transport processes involve Ca 2ϩ signaling (37)(38)(39). The tonicity of the pre-urine osmotically challenges tubular epithelial cells constantly, and the resulting cell volume regulation is facilitated by Ca 2ϩ signaling, which has been shown to encompass Ca 2ϩ release from intracellular stores followed by Ca 2ϩ influx from the extracellular compartment (40,41).…”

Section: Discussionmentioning

confidence: 99%

Localization and Regulation of the Epithelial Ca2+ Channel TRPV6 in the Kidney

Nijenhuis¹,

Hoenderop²,

Kemp³

et al. 2003

Journal of the American Society of Nephrology

188

142

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Abstract. The family of epithelial Ca 2ϩ channels consists of two highly homologues members, TRPV5 and TRPV6, which constitute the apical Ca 2ϩ entry mechanism in active Ca 2ϩ (re)absorption in kidney and small intestine. In kidney, TRPV5 expression has been extensively studied, whereas TRPV6 localization and regulation has been largely confined to the small intestine. The present study investigated the renal distribution of TRPV6 and regulation by 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ). In mouse kidney, TRPV6 was detected by immunohistochemistry at the apical domain of the distal convoluted tubules (DCT2), connecting tubules (CNT), and cortical and medullary collecting ducts (CD). Furthermore, several putative vitamin D-responsive elements were detected upstream of the mouse TRPV6 start codon, and 1,25(OH) 2 D 3 treatment significantly increased renal TRPV6 mRNA and protein expression. In DCT2 and CNT, TRPV6 co-localizes with the other known Ca 2ϩ transport proteins, including TRPV5 and calbindin-D 28K . Together, these data suggest a role for TRPV6 in 1,25(OH) 2 D 3 -stimulated Ca 2ϩ reabsorption in these segments. Interestingly, distribution of TRPV6 extended to the CD, where it localized to the apical domain of principal and intercalated cells, which are not generally implicated in active Ca 2ϩ reabsorption. In addition, TRPV6 mRNA levels were quantified in a large set of tissues, and in the order of decreasing expression level were detected: prostate Ͼ stomach, brain Ͼ lung Ͼ duodenum, kidney, bone, cecum, heart Ͼ colon Ͼ skeletal muscle Ͼ pancreas. Therefore, additional physiologic functions for TRPV6 are feasible. In conclusion, TRPV6 is expressed along the apical domain of DCT2, CNT, and CD, where TRPV6 expression is positively regulated by 1,25(OH) 2 D 3 .Active Ca 2ϩ absorption plays a key role in Ca 2ϩ homeostasis and takes place in Ca 2ϩ

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Section: Discussionmentioning

confidence: 99%

Localization and Regulation of the Epithelial Ca2+ Channel TRPV6 in the Kidney

Nijenhuis¹,

Hoenderop²,

Kemp³

et al. 2003

Journal of the American Society of Nephrology

188

142

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“…Natriuretic peptides attenuate elevations in cytosolic free Ca 2ϩ concentration ([Ca 2ϩ ] c ) in many cell types (37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50), including rat hepatocytes (51). Atrial natriuretic peptide (ANP) 3 is a circulating hormone released mainly by atrial myocytes (52) in response to stress conditions such as volume expansion or cardiac hypoxia.…”

Section: Elevations In Intracellular Camentioning

confidence: 99%

“…Similarly, calpain activation plays a key role in cellular injury in diverse pathologies, including oxidant-induced pancreatic acinar cell injury (27), myocardial ischemia-reperfusion injury (128), neurotoxicity (129), spinal cord injury (28), and endothelial dysfunction in type 2 diabetes (29). Because natriuretic peptides act on several organs (54) and attenuate elevations in [Ca 2ϩ ] c in many cell types (37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50), it is unlikely that their cytoprotective effects are restricted to liver. Indeed, natriuretic peptides may have an in vivo role as circulating inhibitors of pathophysiological elevations in [Ca 2ϩ ] c and calpain activity.…”

Section: Camentioning

confidence: 99%

Atrial Natriuretic Peptide Attenuates Elevations in Ca2+ and Protects Hepatocytes by Stimulating Net Plasma Membrane Ca2+ Efflux

Green

Stratton

Squires

et al. 2007

Journal of Biological Chemistry

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Elevations in intracellular Ca2؉ concentration and calpain activity are common early events in cellular injury, including that of hepatocytes. Atrial natriuretic peptide is a circulating hormone that has been shown to be hepatoprotective. The aim of this study was to examine the effects of atrial natriuretic peptide on potentially harmful elevations in cytosolic free Ca 2؉ (24) that plays a key role in initiation of cellular injury and subsequent necrosis or apoptosis (6,(25)(26)(27)(28)(29)(30). In hepatocytes, calpain promotes hepatocyte plasma membrane blebbing (31), induces the mitochondrial permeability transition in hepatocyte necrosis (32), and contributes to hepatocyte necrosis in anoxia (33). Calpain has been implicated in hepatotoxicity in ischemia-reperfusion injury (34, 35), hemorrhagic shock (36), and bile acid toxicity (20).In the search for cytoprotective agents and therapeutic interventions, those which suppress injurious [Ca 2ϩ ] i rises are considered highly promising (2-6, 30). Natriuretic peptides attenuate elevations in cytosolic free Ca 2ϩ concentration ([Ca 2ϩ ] c ) in many cell types (37-50), including rat hepatocytes (51). Atrial natriuretic peptide (ANP) 3 is a circulating hormone released mainly by atrial myocytes (52) in response to stress conditions such as volume expansion or cardiac hypoxia. In addition to its hypotensive, vasodilatory, and natriuretic effects in the cardiovascular and renal systems (53), increasing evidence supports a more widespread role for ANP in several other organs (54), including the liver. ANP elevates cGMP in rat hepatocytes (51,(55)(56) through the guanylyl cyclase A receptor (57), and is cytoprotective in both isolated hepatocytes (51,55,58) and perfused liver (57, 59 -62). An early preliminary study showed that ANP attenuated both oxidant-induced cell injury and the accompanying [Ca 2ϩ ] i rise (51), suggesting that the hepatoprotective effects of ANP may be mediated by mechanisms involved in Ca 2ϩ homeostasis (51, 55, 57). We have since examined the effects of ANP on physiological alterations in [Ca 2ϩ ] c ; we showed that ANP, through protein kinase G (PKG), attenuates [Ca 2ϩ ] c oscillations, dramatically increases the basal rate of plasma membrane Ca 2ϩ efflux and modestly inhibits basal Ca 2ϩ influx in rat hepatocytes (56).

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“…AVP dose-dependent biphasic effect on Na+/H+ exchanger: Figure 5 demonstrates the effect of AVP (10 -12 , 10 -9 or 10 -6 M) on (pHi)r and [Ca 2+ ]i in MDCK cells [335]. In control cells, the (pHi)r was 0.101 ± 0.005 pH units/min [79].…”

Section: Avp Receptors Involved In Distal Nephron Hco3-transportmentioning

confidence: 97%

“…However, it is known that PKC, when phosphorylated, may stimulate the Na + /H + exchanger [92]. In addition, in MDCK cells, the stimulatory effect of AVP on NHE1 is mediated by the activation of V1 receptors that are located on the basolateral cell membrane surface, while basolateral V2 receptors have a dose-dependent inhibitory effect [335].…”

Section: Avp Receptors Involved In Distal Nephron Hco3-transportmentioning

confidence: 99%

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

Mello-Aires¹,

Dellova²,

Castelo‐Branco³

et al. 2017

Nephrol Renal Dis

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This article reviews the main body of knowledge regarding NHE1 and NHE3 exchangers and their interaction with Angiotensin II, Angiotensin-(1-7), Aldosterone and Arginine Vasopressin, particularly their renal actions. This work addresses the biphasic effects of different hormonal doses on NHE1 or NHE3 in proximal tubule in Wistar, SHR (hypertensives) and their control WKY (normotensives) rats or MDCK cells (which share similarities with the collecting duct). The hormones were applied alone, with their inhibitors or plus agents that change the [Ca 2+ ]i. The data are compatible with hormonal stimulation of these exchangers by increases of [Ca 2+ ]i in lower range, and inhibition at high [Ca 2+ ]i. In MDCK cells and Wistar rats, low doses of ANG II, ALDO or AVP stimulated the exchangers, while high doses inhibited them. ANG-(1-7), in Wistar or WKY rats has inverse, dose-dependent effects. In SHR rats, the biphasic effects of ANG-(1-7) were similar to the effects of ANG II, ALDO or AVP in Wistar rats. The interactions between these effects may represent a mechanism that regulates extracellular volume. In hypertensives animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated hypertension. Figure 6 shows a schematic model to describe these biphasic hormonal effects.

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Effect of arginine vasopressin and ANP on intracellular pH and cytosolic free [Ca2+] regulation in MDCK cells

Cited by 12 publications

References 21 publications

Localization and Regulation of the Epithelial Ca2+ Channel TRPV6 in the Kidney

Localization and Regulation of the Epithelial Ca2+ Channel TRPV6 in the Kidney

Atrial Natriuretic Peptide Attenuates Elevations in Ca2+ and Protects Hepatocytes by Stimulating Net Plasma Membrane Ca2+ Efflux

ANG II, ANG-(1-7), ALDO and AVP biphasic effects on Na+/H+ transport: the role of cellular calcium

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