Regulation of stretch-activated ANP secretion by chloride channels

Han, Jeong Hee; Bai, Guang Yi; Park, Jae‐Hyeong; Yuan, Kuichang; Park, Woo Hyun; Kim, Sung Zoo; Kim, Suhn Hee

doi:10.1016/j.peptides.2007.12.003

Cited by 21 publications

(7 citation statements)

References 27 publications

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“…Interestingly, S645648, a dimethyl‐pyrazolyl anthranilic acid derivative obtained from the Sigma rare compound collection, failed to block TRP channels and was not considered further. The fenamate niflumic acid, which has been intensively used as a pharmacological tool to interfere with cell volume regulation (Parkerson and Sontheimer, 2003; Moreland et al ., 2006; Han et al ., 2008), was less potent than flufenamic acid in blocking the four TRP channels in our study. Based on the fact that flufenamic acid has been used for the modulation of TRP channels it was surprising that the mono‐ and dichloro‐methyl‐phenyl anthranilic acid derivatives, meclofenamic acid and tolfenamic acid, as well as the mono‐chloro‐phenyl‐chloro anthranilic acid derivative DCDPC, outperformed flufenamic acid in blocking TRP channels, with TRPC6 as the only exception (Table 1A and B).…”

Section: Resultsmentioning

confidence: 99%

Fenamates as TRP channel blockers: mefenamic acid selectively blocks TRPM3

Klose

Straub

Riehle

et al. 2011

British J Pharmacology

102

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BACKGROUND AND PURPOSEFenamates are N-phenyl-substituted anthranilic acid derivatives clinically used as non-steroid anti-inflammatory drugs in pain treatment. Reports describing fenamates as tools to interfere with cellular volume regulation attracted our attention based on our interest in the role of the volume-modulated transient receptor potential (TRP) channels TRPM3 and TRPV4. EXPERIMENTAL APPROACHFirstly, we measured the blocking potencies and selectivities of fenamates on TRPM3 and TRPV4 as well as TRPC6 and TRPM2 by Ca 2+ imaging in the heterologous HEK293 cell system. Secondly, we further investigated the effects of mefenamic acid on cytosolic Ca 2+ and on the membrane voltage in single HEK293 cells that exogenously express TRPM3. Thirdly, in insulinsecreting INS-1E cells, which endogenously express TRPM3, we validated the effect of mefenamic acid on cytosolic Ca 2+ and insulin secretion. KEY RESULTSWe identified and characterized mefenamic acid as a selective and potent TRPM3 blocker, whereas other fenamate structures non-selectively blocked TRPM3, TRPV4, TRPC6 and TRPM2. CONCLUSIONS AND IMPLICATIONSThis study reveals that mefenamic acid selectively inhibits TRPM3-mediated calcium entry. This selectivity was further confirmed using insulin-secreting cells. KATP channel-dependent increases in cytosolic Ca 2+ and insulin secretion were not blocked by mefenamic acid, but the selective stimulation of TRPM3-dependent Ca 2+ entry and insulin secretion induced by pregnenolone sulphate were inhibited. However, the physiological regulator of TRPM3 in insulin-secreting cells remains to be elucidated, as well as the conditions under which the inhibition of TRPM3 can impair pancreatic b-cell function. Our results strongly suggest mefenamic acid is the most selective fenamate to interfere with TRPM3 function.

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Section: Resultsmentioning

confidence: 99%

Fenamates as TRP channel blockers: mefenamic acid selectively blocks TRPM3

Klose

Straub

Riehle

et al. 2011

British J Pharmacology

102

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“…The height, internal diameter, and slope of outflow catheter connected to atria were 5 cmH 2 O, 2.0 mm and 70°, respectively. To induce high atrial stretch, the height of outflow catheter was increased from 5 cmH 2 O to 7.5 cmH 2 O by connecting 2.5 cm length catheter after a 10 min control collection period and atrial perfusate was collected for 40 min [ 24 ]. The loaded volume to atria during diastole in low- and high-stretched conditions was 434 and 736 µl, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Group 1 and 2 were high-stretched atria perfused with either vehicle (n=15) or Ang-(4-8) (0.01 µM, n=10; 0.1 µM, n=10; 1 µM, n=10) [ 16 ]. After a 10 min control collection period, the height of outflow catheter was increased from 5 cmH 2 O to 7.5 cmH 2 O and Ang-(4-8) or vehicle was simultaneously perfused for 40 min [ 24 ]. Group 3, 4, and 5 were high-stretched atria perfused with Ang-(4-8) in the presence of AT 1 R, AT 2 R, or AT 4 R antagonist.…”

Section: Methodsmentioning

confidence: 99%

Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats

Phuong

Park

et al. 2017

Korean J Physiol Pharmacol

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Angiotensin II (Ang II) is metabolized from N-terminal by aminopeptidases and from C-terminal by Ang converting enzyme (ACE) to generate several truncated angiotensin peptides (Angs). The truncated Angs have different biological effects but it remains unknown whether Ang-(4-8) is an active peptide. The present study was to investigate the effects of Ang-(4-8) on hemodynamics and atrial natriuretic peptide (ANP) secretion using isolated beating rat atria. Atrial stretch caused increases in atrial contractility by 60% and in ANP secretion by 70%. Ang-(4-8) (0.01, 0.1, and 1 µM) suppressed high stretch-induced ANP secretion in a dose-dependent manner. Ang-(4-8) (0.1 µM)-induced suppression of ANP secretion was attenuated by the pretreatment with an antagonist of Ang type 1 receptor (AT1R) but not by an antagonist of AT2R or AT4R. Ang-(4-8)-induced suppression of ANP secretion was attenuated by the pretreatment with inhibitor of phospholipase (PLC), inositol triphosphate (IP3) receptor, or nonspecific protein kinase C (PKC). The potency of Ang-(4-8) to inhibit ANP secretion was similar to Ang II. However, Ang-(4-8) 10 µM caused an increased mean arterial pressure which was similar to that by 1 nM Ang II. Therefore, we suggest that Ang-(4-8) suppresses high stretch-induced ANP secretion through the AT1R and PLC/IP3/PKC pathway. Ang-(4-8) is a biologically active peptide which functions as an inhibition mechanism of ANP secretion and an increment of blood pressure.

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“…Atrial natriuretic peptide (ANP) is an important hormone that is involved in blood pressure regulation. ANP secretion is mediated by stretch-activated Cl channels [20]. K ATP channels are also suggested to regulate ANP secretion [21].…”

Section: Other Physiological Heart Functions Involved In Mechanosensimentioning

confidence: 99%

Mechanobiology in cardiac physiology and diseases

Takahashi

Kakimoto

Toda

et al. 2013

J Cellular Molecular Medi

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Mechanosensitivity is essential for heart function just as for all other cells and organs in the body, and it is involved in both normal physiology and diseases processes of the cardiovascular system. In this review, we have outlined the relationship between mechanosensitivity and heart physiology, including the Frank–Starling law of the heart and mechanoelectric feedback. We then focused on molecules involved in mechanotransduction, particularly mechanosensitive ion channels. We have also discussed the involvement of mechanosensitivity in heart diseases, such as arrhythmias, hypertrophy and ischaemic heart disease. Finally, mechanobiology in cardiogenesis is described with regard to regenerative medicine.

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Regulation of stretch-activated ANP secretion by chloride channels

Cited by 21 publications

References 27 publications

Fenamates as TRP channel blockers: mefenamic acid selectively blocks TRPM3

Fenamates as TRP channel blockers: mefenamic acid selectively blocks TRPM3

Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats

Mechanobiology in cardiac physiology and diseases

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