Evidence for (+)-cicletanine sulfate as an active natriuretic metabolite of cicletanine in the rat

Garay, Ricardo P.; Rosati, Clelia; Fanous, Karine; Allard, Michel; Morin, Elisabeth; Lamiable, Denis; Vistelle, Richard

doi:10.1016/0014-2999(94)00731-l

Cited by 26 publications

(11 citation statements)

References 11 publications

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“…SULTs also play a role in the generation of bioactive compounds. Minoxidil, 18 triamterene, 19 cicletanine 20 and morphine, 21 in particular, are sulfated to more active compounds.…”

Section: Discussionmentioning

confidence: 99%

In-vitro sulfation of piceatannol by human liver cytosol and recombinant sulfotransferases

Miksits

Sulyok

Schuhmacher

et al. 2009

Journal of Pharmacy and Pharmacology

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“…SULTs also play a role in the generation of bioactive compounds. Minoxidil, 18 triamterene, 19 cicletanine 20 and morphine, 21 in particular, are sulfated to more active compounds.…”

Section: Discussionmentioning

confidence: 99%

In-vitro sulfation of piceatannol by human liver cytosol and recombinant sulfotransferases

Miksits

Sulyok

Schuhmacher

et al. 2009

Journal of Pharmacy and Pharmacology

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“…Drugs such as minoxidil [27,28], triamterene [30] and cicletanine [29,76] are bioactivated upon sulfonation, with the sulfate conjugate identified as the pharmacologically active agent. The 3-sulfate and, in particular, the 6-sulfate of morphine are potent analgesics if injected intraventricularly in mice [31].…”

Section: Bioactivation Of Xenobiotics and Endogenous Moleculesmentioning

confidence: 99%

Inhibition of Sulfotransferases by Xenobiotics

Wang

James²

2006

CDM

132

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The sulfotransferase (SULT) family comprises important phase II conjugation enzymes for the detoxification of xenobiotics and modulation of the activity of physiologically important endobiotics such as thyroid hormones, steroids, and neurotransmitters. SULT enzymes catalyze the transfer of a sulfuryl group, donated by 3'-phosphoadenosine-5'-phosphosulfate (PAPS), to an acceptor substrate that may be a hydroxy group or an amine group in a process originally called sulfation, but more correctly referred to as sulfonation or sulfurylation. SULT activity may be inhibited when humans are exposed to certain xenobiotics including drugs (mefenamic acid, salicylic acid, clomiphene, danazol etc.), dietary chemicals (catechins, food colorants, flavonoids and phytoestrogens etc.), and environmental chemicals (hydroxylated polychlorinated biphenyls, hydroxylated polyhalogenated aromatic hydrocarbons, pentachlorophenol, triclosan and bisphenol A, etc.). Inhibition of individual SULT isoforms may cause adverse effects on human health. For example, hydroxylated polychlorinated biphenyls have been shown to interfere with the transport of thyroid hormones, inhibit estradiol sulfonation, and inhibit thyroid hormone sulfonation, thereby potentially disrupting the thyroid hormone system. Formation of sulfate conjugates of toxic xenobiotics usually decreases their toxicity, so inhibition of this pathway may lead to prolonged exposure to the compounds. Conversely, some sulfate conjugates are chemically reactive, inhibition of their formation may protect from toxicity. This manuscript will review the literature concerning the inhibition of SULTs by xenobiotics including isoform-selective effects, inhibition kinetics and health effects resulting from the inhibition.

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“…Cicletanine is a furopyridine anti-hypertensive compound with direct vasorelaxant and natriuretic properties [1±3]. The mechanism of natriuretic effects of cicletanine is attributable to the inhibitory action of its sulphoconjugated ()-enantiomer on the apical Nadependent Cl/HCO 3 anion exchanger in the cortical diluting segment of the nephron [3]. The nature of the vasorelaxant activity of cicletanine is less well under-stood but is believed to be due to several mechanisms, including histamine antagonism [4], activation of prostacyclin production [5] and inhibition of low-K m cyclic GMP phosphodiesterase (cGMP-PDE) [6].…”

Section: Introductionmentioning

confidence: 99%

Cicletanine reverses vasoconstriction induced by the endogenous sodium pump ligand, marinobufagenin, via a protein kinase C dependent mechanism

Bagrov¹,

Dmitrieva²,

Дорофеева³

et al. 2000

Journal of Hypertension

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Cicletanine antagonizes vasoconstriction induced by Na/K-ATPase inhibition via a PKC-dependent mechanism that does not involve inhibition of cyclic GMP phosphodiesterase (cGMP-PDE). This mechanism of action may be relevant to the greater potency of cicletanine in salt-sensitive hypertension in which plasma levels of endogenous digitalis-like cardiotonic steroids are elevated. Our findings also suggest that PKC is an important factor for cardiotonic steroid-Na/K-ATPase interactions on the vascular tone, and is therefore a potential target for therapeutic intervention in hypertension.

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Evidence for (+)-cicletanine sulfate as an active natriuretic metabolite of cicletanine in the rat

Cited by 26 publications

References 11 publications

In-vitro sulfation of piceatannol by human liver cytosol and recombinant sulfotransferases

In-vitro sulfation of piceatannol by human liver cytosol and recombinant sulfotransferases

Inhibition of Sulfotransferases by Xenobiotics

Cicletanine reverses vasoconstriction induced by the endogenous sodium pump ligand, marinobufagenin, via a protein kinase C dependent mechanism

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