Guanosine 3' ,5'-Cyclic Monophosphate Assay at 10−15-Mole Level

Cailla, H.; Vannier, Christian; Delaage, M

doi:10.1016/s0378-5173(83)90100-x

Cited by 194 publications

(34 citation statements)

References 14 publications

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“…Pellet and supernatant were frozen and maintained at Ϫ20°C until assayed. The cGMP content was determined in thawed supernatant using a radioimmunoassay described previously (Cailla et al, 1976), modified by separation of free cGMP with activated charcoal (Koch and Lutz-Bucher, 1991). DNA was determined in the pellet according to Setaro and Morley (1976), and the cGMP content of the rings was expressed as fmol ⅐ g Ϫ1 DNA.…”

Section: Contraction-relaxation Experiments In Rat Aortic Ringsmentioning

confidence: 99%

Involvement of NO in the Endothelium-Independent Relaxing Effects of Nω-Hydroxy-l-arginine and Other Compounds Bearing a C=NOH Function in the Rat Aorta

Vetrovsky

Boucher²,

Schott³

et al. 2002

The Journal of Pharmacology and Experimental Therapeutics

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The mechanisms of vasorelaxation elicited by N -hydroxy-Larginine (L-NOHA) and other compounds bearing a CϭNOH function and the structural determinants governing this effect were investigated in rat aorta. L-NOHA, formamidoxime, five aromatic monosubstituted amidoximes, and one aromatic monosubstituted ketoxime elicited relaxation in endothelium-denuded rings. N-Hydroxyguanidine and substituted N-hydroxyguanidines were markedly less active. Relaxations induced by L-NOHA and by the most active studied compound, 4-chlorobenzamidoxime (ClBZA), were unmodified by the presence of endothelium. In endothelium-denuded rings, they were blunted by the NO scavenger 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (300 M) and by the inhibitor of guanylylcyclase activation 1H[1,2,4,]oxadiazolo[4,3-a]quinoxalin-1-one (1 M). In addition, L-NOHA-and ClBZA both caused cGMP accumulation. L-Arginine, but not D-arginine (1 mM), antagonized the effect of L-NOHA but not ClBZA. Both L-NOHA-and ClBZA-induced relaxations were inhibited by the NAD(P)H-dependent enzymes inhibitor diphenyliodonium (30 M) and the NAD(P)H-dependent reductases inhibitor 7-ethoxyresorufin (10 M), but they were unmodified by the cytochrome P450 (P450) inhibitor proadifen (10 M) and by the NO synthase inhibitor N -nitro-L-arginine methyl ester (L-NAME, 300 M). These results show that L-NOHA and other compounds with a CϭNOH function can cause endothelium-independent relaxation in the rat aorta. They suggest that activation of guanylyl cyclase and NO formation is implicated in relaxation and that a 7-ethoxyresorufin-sensitive NAD(P)H-dependent pathway is involved. On one hand, L-NOHA and amidoximes may be useful tools for characterizing this pathway in blood vessels and, on the other, may offer a novel approach for treating vascular diseases with impaired endothelial NO activity.

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Section: Contraction-relaxation Experiments In Rat Aortic Ringsmentioning

confidence: 99%

Involvement of NO in the Endothelium-Independent Relaxing Effects of Nω-Hydroxy-l-arginine and Other Compounds Bearing a C=NOH Function in the Rat Aorta

Vetrovsky

Boucher²,

Schott³

et al. 2002

The Journal of Pharmacology and Experimental Therapeutics

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“…The reaction was terminated by transferring the vessels into an ice-cold HCl solution (0.1 N). Following homogenization of the tissues, the cyclic GMP content was determined by radioimmunoassay (Cailla et al, 1976).…”

Section: Determination Of Tissue Cyclic Gmp Contentmentioning

confidence: 99%

Alteration by lipopolysaccharide of the relationship between intracellular calcium levels and contraction in rat mesenteric artery

Martínez

Müller

Stoclet

et al. 1996

British J Pharmacology

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1 The aim of this work was to investigate the effect of lipopolysaccharide (LPS) treatment on the relationship between the cytosolic Ca2+ ion concentration ([Ca2]i) and contraction in rat resistance arteries, and the involvement of the L-arginine-nitric oxide (NO)-guanosine 3'-5' cyclic monophosphate (cyclic GMP) pathway in these effects. 2 [Ca2+]i and tension were simultaneously recorded in small mesenteric arteries removed from rats 4 h after intraperitoneal injection of E. coUi LPS (30 mg kg-') or solvent. Cyclic GMP was assayed in vessels submitted to identical treatments.3 Basal [Ca21], was higher in vessels from LPS-treated rats compared to controls. LPS did not modify the concentration-contraction curve of noradrenaline. However, the increase in basal [Ca2+], produced by LPS resulted in a shift of the noradrenaline [Ca2+]i-contraction curve to higher [Ca2+], concentrations.4 L-Arginine (300 gM) relaxed noradrenaline (10 gM) pre-contracted arteries from LPS-treated but not from control rats. This effect of L-arginine was reversed by two inhibitors of NO synthase: Nw-nitro-Larginine-methyl-ester (L-NAME, 1 mM) and S-methyl-isothiourea (SMT, 0.1 mM). Both the relaxing effect of L-arginine and its reversal by L-NAME or SMT occurred without any change in [Ca21],.5 LPS treatment did not modify the cyclic GMP content of the small mesenteric arteries. In arteries removed from LPS-treated rats but not from controls, addition of L-arginine (300 gM) was associated with a significant increase in cyclic GMP content, an effect which was prevented by both L-NAME (1 mM) and SMT (0.1 mM). 6 L-NAME (1 mM) produced a greater reduction in cyclic GMP content than SMT (0.1 mM) in control vessels exposed to L-arginine (300 giM). Under the same conditions, SMT produced a larger decrease in cyclic GMP level than L-NAME in arteries taken from LPS-treated rats, consistent with selective inhibition by SMT of the inducible NO-synthase after LPS. 7 These results show that LPS produced two effects in small mesenteric arteries: (i) alterations in Ca21 handling and a decreased sensitivity of myofflaments to Ca2 , (ii) induction of NO-synthase activity resulting in exogenous L-arginine-dependent production of NO and cyclic GMP accumulation. Both effects are likely to be involved in the hyporeactivity induced by LPS in resistance arteries. Keywords: Calcium; endotoxin shock; resistance arteries Introduction Lipopolysaccharide (LPS)-administration decreases vascular resistance, produces vascular hyporeactivity to different vasoconstrictors and promotes the overproduction of nitric oxide (NO) through activation of the inducible isoform of NO synthase (iNOS) (see Stoclet et al., 1993). The effect of LPS on vascular reactivity and the involvement of NO in this effect have been well documented in large conductance arteries such as the aorta (Julou-Schaeffer et al., 1990). However, the sensitivity to noradrenaline was only slightly decreased in the femoral artery (Schneider et al., 1994) and was not significantly impaired in small mesenteric ...

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“…Tissues were thawed in 400 Al of perchloric acid (1 N), then homogenized with a Potter glass/glass homogenizer followed by sonication (UltrasonsAnnemasse, type 75TS) for 15 s. The homogenate was centrifuged at 10,000 g for 5 min and the cyclic nucleotide content (cyclic AMP (adenosine cyclic 3',5'-monophosphate), cyclic GMP) of the supernatant assayed by a radioimmunological method (Cailla et al, 1973;1976). The DNA content of each tissue segment was assayed by a fluorometric method as adapted by Schoeffter & Stoclet (1982).…”

Section: Determination Of Cyclic Nucleotide Levelsmentioning

confidence: 99%

Endothelial mediated inhibition of contraction and increase in cyclic GMP levels evoked by the α‐adrenoceptor agonist B‐HT 920 in rat isolated aorta

Miller

Mony

Schini

et al. 1984

British J Pharmacology

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1In the presence of endothelium maximal contractions of rat aorta preparations evoked by B-HT 920 were about 10% of those evoked in the absence of endothelium.2 6-Allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-(4,5-d)azepin dihydrochloride (B-HT 920, 0.1 jLM to 0.1 mM) induced concentration-dependent contractions of rat aorta in the absence of endothelium. Maximal contractions were comparable in magnitude to those induced by noradrenaline.3 In the presence of endothelium but not in its absence B-HT 920 (0.1 mM) stimulated an increase in tissue cyclic GMP levels of about 2 fold. Levels of cyclic AMP were unaffected. Removal of endothelium reduced basal tissue levels of cyclic GMP.4 The guanylate cyclase inhibitor methylene blue (0.5 pM) potentiated B-HT 920-induced contractions in the presence of endothelium and inhibited increases in cyclic GMP. 5 In the presence of endothelium 5,8,11,14-eicosatetraynoic acid (ETYA; 0.1 mM), an inhibitor of both lipoxygenase and cyclo-oxygenase systems, inhibited the B-HT 920-induced increase in cyclic GMP but did not potentiate B-HT 920-induced contractions. ETYA also antagonized B-HT 920-induced contractions in the absence of endothelium. 6 It is concluded that endothelium continuously releases a product or products which influence the smooth muscle. Inhibition of B-HT920-induced contractions in the presence of endothelium is associated with increased tissue levels of cyclic GMP.

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Guanosine 3' ,5'-Cyclic Monophosphate Assay at 10−15-Mole Level

Cited by 194 publications

References 14 publications

Involvement of NO in the Endothelium-Independent Relaxing Effects of Nω-Hydroxy-l-arginine and Other Compounds Bearing a C=NOH Function in the Rat Aorta

Involvement of NO in the Endothelium-Independent Relaxing Effects of Nω-Hydroxy-l-arginine and Other Compounds Bearing a C=NOH Function in the Rat Aorta

Alteration by lipopolysaccharide of the relationship between intracellular calcium levels and contraction in rat mesenteric artery

Endothelial mediated inhibition of contraction and increase in cyclic GMP levels evoked by the α‐adrenoceptor agonist B‐HT 920 in rat isolated aorta

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