Angiotensin II-stimulated Ca2+ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na+/Ca2+ exchange

Fellner, Susan K.; Arendshorst, William J.

doi:10.1152/ajprenal.00244.2007

Cited by 55 publications

(37 citation statements)

References 63 publications

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“…These results are consistent with the observation that KB-R7943, a NCX inhibitor, decreased the peak [Ca 2ϩ ] i response to ANG II by 48%; the Ca 2ϩ entrymode NCX may therefore be an important Ca 2ϩ entry pathway that mediates ANG II vasoconstriction of afferent arteriole smooth muscle cells (8). Upregulation of this mechanism may help to explain the augmented myogenic responses and enhanced phenylephrine-induced vasoconstriction in ouabainhypertensive rat arteries as well as the increased BP (23).…”

Section: F577 and Ncx1supporting

confidence: 89%

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Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na⁺/Ca²⁺exchanger knockout mice

Zhao

Zhang

Blaustein

et al. 2011

American Journal of Physiology-Renal Physiology

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ϩ/Ϫ (109 Ϯ 2 to 134 Ϯ 3 mmHg, P Ͻ 0.001, n ϭ 8) and NCX1 smϪ/Ϫ (101 Ϯ 8 to 129 Ϯ 8 mmHg, P Ͻ 0.01, n ϭ 6) mice to a similar extent (⌬25 Ϯ 1 vs. ⌬28 Ϯ 4 mmHg, P Ͼ 0.05). In response to ANG II infusions, PAH clearance (CPAH) decreased from 1.39 Ϯ 0.27 to 0.98 Ϯ 0.22 ml·min Ϫ1 ·g Ϫ1 (P Ͻ 0.05) and glomerular filtration rate (GFR) was reduced from 0.50 Ϯ 0.09 to 0.32 Ϯ 0.06 ml·min Ϫ1 ·g Ϫ1 (P Ͻ 0.05) in NCX1 ϩ/Ϫ mice. In contrast, the NCX1 smϪ/Ϫ did not exhibit significant reductions in either CPAH (1.16 Ϯ 0.30 to 1.22 Ϯ 0.34 ml·min Ϫ1 ·g Ϫ1 , P Ͼ 0.05) or GFR (0.48 Ϯ 0.08 to 0.41 Ϯ 0.05 ml·min Ϫ1 ·g Ϫ1 , P Ͼ 0.05) during acute ANG II infusions. Using flometry to measure renal blood flow continuously, NCX1 smϪ/Ϫ mice had significantly attenuated responses to ANG II infusions (Ϫ34.2 Ϯ 3.9%, P Ͻ 0.05) compared with those in NCX1 ϩ/Ϫ mice (Ϫ48 Ϯ 2%) or in wild-type mice (Ϫ69 Ϯ 7%). These data indicate that renal vascular responses to ANG II are attenuated in NCX1 smϪ/Ϫ mice compared with NCX1 ϩ/Ϫ mice and that NCX1 contributes to the renal vasoconstriction response to acute ANG II infusions. sodium/calcium exchanger; renal vascular tone regulation; arterial pressure THE Na ϩ

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Section: F577 and Ncx1supporting

confidence: 89%

“…smϪ/Ϫ mice in response to ANG II as occurs under conditions where the NCX is pharmacologically blocked (8).…”

Section: Gfr and Rbf Responses To High-dose Ang II Are Attenuated In mentioning

confidence: 99%

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na⁺/Ca²⁺exchanger knockout mice

Zhao

Zhang

Blaustein

et al. 2011

American Journal of Physiology-Renal Physiology

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“…Likewise, calcium entry in afferent arteriolar smooth muscle also involved activation of TRPC channels (24). Because of the coupling of TRPC-mediated calcium entry in related contractile tissues, we proposed that adenosine activation of A 1 R in JG cells could also be mediated by TRPC channels.…”

Section: Discussionmentioning

confidence: 95%

Adenosine inhibits renin release from juxtaglomerular cells via an A₁ receptor-TRPC-mediated pathway

Ortiz-Capisano

Atchison

Harding

et al. 2013

American Journal of Physiology-Renal Physiology

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Ortiz-Capisano MC, Atchison DK, Harding P, Lasley RD, Beierwaltes WH. Adenosine inhibits renin release from juxtaglomerular cells via an A 1 receptor-TRPC-mediated pathway. Am J Physiol Renal Physiol 305: F1209 -F1219, 2013. First published July 24, 2013 doi:10.1152/ajprenal.00710.2012.-Renin is synthesized and released from juxtaglomerular (JG) cells. Adenosine inhibits renin release via an adenosine A 1 receptor (A1R) calcium-mediated pathway. How this occurs is unknown. In cardiomyocytes, adenosine increases intracellular calcium via transient receptor potential canonical (TRPC) channels. We hypothesized that adenosine inhibits renin release via A 1R activation, opening TRPC channels. However, higher concentrations of adenosine may stimulate renin release through A 2R activation. Using primary cultures of isolated mouse JG cells, immunolabeling demonstrated renin and A 1R in JG cells, but not A2R subtypes, although RT-PCR indicated the presence of mRNA of both A 2AR and A2BR. Incubating JG cells with increasing concentrations of adenosine decreased renin release. Different concentrations of the adenosine receptor agonist N-ethylcarboxamide adenosine (NECA) did not change renin. Activating A 1R with 0.5 M N6-cyclohexyladenosine (CHA) decreased basal renin release from 0.22 Ϯ 0.05 to 0.14 Ϯ 0.03 g of angiotensin I generated per milliliter of sample per hour of incubation (AngI/ml/mg prot) (P Ͻ 0.03), and higher concentrations also inhibited renin. Reducing extracellular calcium with EGTA increased renin release (0.35 Ϯ 0.08 g AngI/ml/mg prot; P Ͻ 0.01), and blocked renin inhibition by CHA (0.28 Ϯ 0.06 g AngI/ml/mg prot; P Ͻ 0. 005 vs. CHA alone). The intracellular calcium chelator BAPTA-AM increased renin release by 55%, and blocked the inhibitory effect of CHA. Repeating these experiments in JG cells from A 1R knockout mice using CHA or NECA demonstrated no effect on renin release. However, RT-PCR showed mRNA from TRPC isoforms 3 and 6 in isolated JG cells. Adding the TRPC blocker SKF-96365 reversed CHA-mediated inhibition of renin release. Thus A 1R activation results in a calcium-dependent inhibition of renin release via TRPC-mediated calcium entry, but A 2 receptors do not regulate renin release. renin; adenosine; calcium; A 1R; CHA; adenosine receptors; transient receptor potential canonical RENIN IS PRODUCED BY, STORED in, and released from juxtaglomerular (JG) cells located in the lamina media of the afferent arteriole at the entrance to the glomerulus (7, 31). Two main intracellular second-messenger systems are known to regulate renin secretion: stimulation of renin release by the cyclic nucleotide cAMP; and inhibition or renin secretion by increased intracellular calcium (1-3, 16, 25, 30).Adenosine is a purine nucleoside catabolite of ATP. Adenosine's effects are mediated by the activation of four G protein-coupled receptor (GPCR) subtypes: A 1 , A 2A , A 2B , and A 3 (13, 44). Adenosine inhibits renin secretion in vivo and in vitro (9, 37). It is considered that adenosine from the macula densa inhib...

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“…Several reports indicate that Ca 2ϩ homeostasis in arterial smooth muscle cells (ASMCs) is influenced not only by direct Ca 2ϩ entry through TRPC channels but also by Na ϩ entry through these nonselective cation channels. The entering Na ϩ apparently then also promotes Ca 2ϩ entry through Na ϩ /Ca 2ϩ exchanger type 1 (NCX1) (4,23,58,82).…”

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confidence: 99%

Upregulation of Na⁺/Ca²⁺exchanger and TRPC6 contributes to abnormal Ca²⁺homeostasis in arterial smooth muscle cells from Milan hypertensive rats

Zulian

Baryshnikov

Linde

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Zulian A, Baryshnikov SG, Linde CI, Hamlyn JM, Ferrari P, Golovina VA. Upregulation of Na ϩ /Ca 2ϩ exchanger and TRPC6 contributes to abnormal Ca 2ϩ homeostasis in arterial smooth muscle cells from Milan hypertensive rats. Am J Physiol Heart Circ Physiol 299: H624 -H633, 2010. First published July 9, 2010; doi:10.1152/ajpheart.00356.2010.-The Milan hypertensive strain (MHS) of rats is a model for hypertension in humans. Inherited defects in renal function have been well studied in MHS rats, but the mechanisms that underlie the elevated vascular resistance are unclear. Altered Ca 2ϩ signaling plays a key role in the vascular dysfunction associated with arterial hypertension. Here we compared Ca 2ϩ signaling in mesenteric artery smooth muscle cells from MHS rats and its normotensive counterpart (MNS). Systolic blood pressure was higher in MHS than in MNS rats (144 Ϯ 2 vs. 113 Ϯ 1 mmHg, P Ͻ 0.05). Resting cytosolic free Ca 2ϩ concentration (measured with fura-2) and ATP-induced Ca 2ϩ transients were augmented in freshly dissociated arterial myocytes from MHS rats. Ba 2ϩ entry activated by the diacylglycerol analog 1-oleoyl-2-acetyl-sn-glycerol (a measure of receptor-operated channel activity) was much greater in MHS than MNS arterial myocytes. This correlated with a threefold upregulation of transient receptor potential canonical 6 (TRPC6) protein. TRPC3, the other component of receptor-operated channels, was marginally, but not significantly, upregulated. The expression of TRPC1/5, components of store-operated channels, was not altered in MHS mesenteric artery smooth muscle. Immunoblots also revealed that the Na ϩ /Ca 2ϩ exchanger-1 (NCX1) was greatly upregulated in MHS mesenteric artery (by ϳ13-fold), whereas the expression of plasma membrane Ca 2ϩ -ATPase was not altered. Ca 2ϩ entry via the reverse mode of NCX1 evoked by the removal of extracellular Na ϩ induced a rapid increase in cytosolic free Ca 2ϩ concentration that was significantly larger in MHS arterial myocytes. The expression of ␣ 1/␣2 Na ϩ pumps in MHS mesenteric arteries was not changed. Immunocytochemical observations showed that NCX1 and TRPC6 are clustered in plasma membrane microdomains adjacent to the underlying sarcoplasmic reticulum. In summary, MHS arteries exhibit upregulated TRPC6 and NCX1 and augmented Ca 2ϩ signaling. We suggest that the increased Ca 2ϩ signaling contributes to the enhanced vasoconstriction and elevated blood pressure in MHS rats.adducin; hypertension; Milan normotensive rats; C-type transient receptor potential channels; receptor-operated calcium entry PRIMARY OR ESSENTIAL HYPERTENSION is a multifactorial disorder resulting from the complex interplay between genetic predisposition (genetic heritability, ϳ30%) and multiple environmental factors (1,44,71,74). The major difficulty in identifying genes contributing to hypertension is the etiological heterogeneity of hypertension (1). Genetic, physiological, and biochemical studies reveal that an alteration in the genes encoding adducin, a ubiquitously expressed membrane-ske...

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Angiotensin II-stimulated Ca²⁺ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na⁺/Ca²⁺ exchange

Cited by 55 publications

References 63 publications

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na⁺/Ca²⁺exchanger knockout mice

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na⁺/Ca²⁺exchanger knockout mice

Adenosine inhibits renin release from juxtaglomerular cells via an A₁ receptor-TRPC-mediated pathway

Upregulation of Na⁺/Ca²⁺exchanger and TRPC6 contributes to abnormal Ca²⁺homeostasis in arterial smooth muscle cells from Milan hypertensive rats

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Angiotensin II-stimulated Ca2+ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na+/Ca2+ exchange

Cited by 55 publications

References 63 publications

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na+/Ca2+exchanger knockout mice

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na+/Ca2+exchanger knockout mice

Adenosine inhibits renin release from juxtaglomerular cells via an A1 receptor-TRPC-mediated pathway

Upregulation of Na+/Ca2+exchanger and TRPC6 contributes to abnormal Ca2+homeostasis in arterial smooth muscle cells from Milan hypertensive rats

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Angiotensin II-stimulated Ca²⁺ entry mechanisms in afferent arterioles: role of transient receptor potential canonical channels and reverse Na⁺/Ca²⁺ exchange

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na⁺/Ca²⁺exchanger knockout mice

Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na⁺/Ca²⁺exchanger knockout mice

Adenosine inhibits renin release from juxtaglomerular cells via an A₁ receptor-TRPC-mediated pathway

Upregulation of Na⁺/Ca²⁺exchanger and TRPC6 contributes to abnormal Ca²⁺homeostasis in arterial smooth muscle cells from Milan hypertensive rats