Influence of β-adrenoceptor agonists on the pulmonary circulation. Effects of a β3-adrenoceptor antagonist, SR 59230A

Dumas, Monique; Dumas, Jean-Paul; Bardou, Marc; Rochette, Luc; Advenier, C.; Giudicelli, Jean‐François

doi:10.1016/s0014-2999(98)00146-0

Cited by 36 publications

(22 citation statements)

References 14 publications

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“…The participation of a third ␤-AR in vasorelaxation was suggested by in vitro and in vivo studies. Isoprenaline induced a vasodilation resistant to propranolol (a nonspecific ␤-AR antagonist) in rat carotid artery (7), aorta (8), pulmonary vessels (9), and in canine pulmonary artery (10). The use of preferential ␤ 3 -AR agonists confirmed these findings (7,8,11).…”

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confidence: 59%

Characterization of Beta3-Adrenoceptors in Human Internal Mammary Artery and Putative Involvement in Coronary Artery Bypass Management

Rozec

Serpillon

Toumaniantz

et al. 2005

Journal of the American College of Cardiology

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confidence: 59%

Characterization of Beta3-Adrenoceptors in Human Internal Mammary Artery and Putative Involvement in Coronary Artery Bypass Management

Rozec

Serpillon

Toumaniantz

et al. 2005

Journal of the American College of Cardiology

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“…As in rat soleus muscle ( Liu et al ., 1996b ), this effect of 10 p M BRL37344 was not blocked by the rodent β 3 ‐adrenoceptor antagonist SR59230A (1 μ M ), consistent with a report that very low concentrations of BRL37344 stimulated pyruvate and palmitate oxidation in soleus muscle of β 3 ‐adrenoceptor null mice ( Board et al ., 2000b ). SR59230A may not be a selective antagonist of human β 3 ‐adrenoceptors, in particular human cloned β 3 ‐adrenoceptors ( Arch, 2000 ), and it is a partial agonist of the human and mouse cloned β 3 ‐adrenoceptors ( Baker, 2005a ) and of the β 3 ‐adrenoceptor in some rodent tissues ( Dumas et al ., 1998 ; Horinouchi and Koike, 2001 ; Brahmadevara et al ., 2003 ). In 3T3‐F442A adipocytes, it was an antagonist of disodium ( R , R )‐5‐(2‐[{2‐(3‐chlorophenyl)‐2‐hydroxyethyl}‐amino]propyl)‐1,3‐benzodioxole‐2,2,dicarboxylate (CL316243)‐stimulated cAMP accumulation, but an agonist of the extracellular acidification rate ( Hutchinson et al ., 2005 ).…”

Section: Discussionmentioning

confidence: 99%

Metabolic responses to BRL37344 and clenbuterol in soleus muscle and C2C12 cells via different atypical pharmacologies and β₂‐adrenoceptor mechanisms

Ngala

O’Dowd

Wang

et al. 2008

British J Pharmacology

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Background and purpose: Picomolar concentrations of the b 3 -adrenoceptor agonist BRL37344 stimulate 2-deoxyglucose uptake in soleus muscle via undefined receptors. Higher concentrations alter uptake, apparently via b 2 -adrenoceptors. Effects of BRL37344 and b 2 -adrenoceptor agonists are compared. Key results: 10 pM BRL37344, 10 pM clenbuterol and 100 pM salbutamol stimulated 2-deoxyglucose uptake in soleus muscle by 33-54%. The effect of BRL37344 was prevented by 1 mM atenolol but not by 300 nM CGP20712A or ICI118551, or 1 mM SR59230A; that of clenbuterol was prevented by ICI118551 but not atenolol. 10 nM BRL37344 stimulated 2-deoxyglucose uptake, whereas 100 nM clenbuterol and salbutamol inhibited uptake. These effects were blocked by ICI118551. Similar results were obtained in C2C12 cells, in which only b 2 -adrenoceptor mRNA could be detected by RT-PCR. 10 nM BRL37344 and 10 pM clenbuterol stimulated muscle palmitate oxidation. In the presence of palmitate, BRL37344 no longer stimulated 2-deoxyglucose uptake and the effect of clenbuterol was not significant. Conclusions and implications: Stimulation of glucose uptake by 10 pM BRL37344 and clenbuterol involves different atypical pharmacologies. Nanomolar concentrations of BRL37344 and clenbuterol, probably acting via b 2 -adrenoceptors, have opposite effects on glucose uptake. The agonists preferentially stimulate fat rather than carbohydrate oxidation, but stimulation of endogenous fat oxidation cannot explain why 100 nM clenbuterol inhibited 2-deoxyglucose uptake.

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“…In guinea pig duodenum and gastric fundus endogenously expressing ␤ 3 -adrenoceptors, SR59230A is an agonist with a potency similar to isoprenaline (Horinouchi and Koike, 2001). At high concentrations, it causes relaxation of hypoxic pulmonary vasoconstriction in rats (Dumas et al, 1998) and rat aortic rings (Brahmadevara et al, 2003). We are further investigating the mechanism of SR59230A-mediated increases in ECAR.…”

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confidence: 99%

“…However, recent reports indicate that SR59230A also interacts with other ␤-adrenoceptors (Candelore et al, 1999;Brahmadevara et al, 2001;Hutchinson et al, 2001;Yamanishi et al, 2002), and agonist actions have been reported at the cloned human ␤ 3 -adrenoceptor (Strosberg and Pietri-Rouxel, 1997;Candelore et al, 1999) and ␤ 3 -adrenoceptor in some rodent tissues (Dumas et al, 1998;Brahmadevara et al, 2001;Horinouchi and Koike, 2001).…”

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confidence: 99%

Evidence for Pleiotropic Signaling at the Mouse β₃-Adrenoceptor Revealed by SR59230A [3-(2-Ethylphenoxy)-1-[(1,S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanol Oxalate]

Hutchinson

Sato²,

Evans³

et al. 2004

J Pharmacol Exp Ther

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This study examines the action of the ␤ 3 -adrenoceptor antagonist SR59230A [3-(2-ethylphenoxy)-1-[(1,S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanoloxalate] at cloned mouse ␤ 3 -adrenoceptors expressed in Chinese hamster ovary cells (CHO-K1-␤ 3 ) or endogenously expressed in 3T3-F442A adipocytes or ileum. SR59230A displayed partial agonist properties compared with thewith the intrinsic activity increasing with the level of receptor expression. Functional affinity values for SR59230A at each level of receptor expression were in agreement with pK I values determined by binding. In cytosensor microphysiometer studies, SR59230A was a full agonist for increases in extracellular acidification rates (ECARs) at all levels of receptor expression, and antagonist actions were measurable only in medium-or low-expressing cells. In 3T3-F442A adipocytes, SR59230A antagonized CL316243-mediated increases of cAMP and had no agonist actions. However, in the cytosensor microphysiometer, SR59230A (acting via ␤ 3 -adrenoceptors) was an agonist with an intrinsic activity greater than CL316243. In mouse ileum, SR59230A relaxed smooth muscle, although concentration-response curves were biphasic. Relaxant effects were produced by concentrations that did not affect cAMP levels. Differences in tissue responses to SR59230A were not caused by major differences in expression of G␣s. ECAR responses were not affected by pretreatment of cells with pertussis toxin, indicating that signaling did not involve Gi. Therefore, SR59230A displays agonist and antagonist actions at the mouse ␤ 3 -adrenoceptor. Because SR59230A only antagonized accumulation of cAMP in 3T3-F442A adipocytes yet in the same cells was an agonist for ECAR, cAMPindependent signaling pathways must mediate part of the agonist actions in the microphysiometer.␤ 3 -Adrenoceptors are pharmacologically characterized by a set of criteria (Arch and Kaumann, 1993;Emorine et al., 1994;Strosberg and Pietri-Rouxel, 1996) that include 1) low affinity and potency for conventional ␤-adrenoceptor antagonists and agonists, including radioligands; 2) low stereoselectivity of agonist and antagonist stereoisomers relative to those at typical ␤-adrenoceptors; 3) partial agonist activity of several ␤ 1 -/␤ 2 -adrenoceptor antagonists such as pindolol and CGP12177A; 4) high affinity and potency of selective agonists such as CL316243 and BRL37344; and 5) antagonism by the ␤ 3 -adrenoceptor antagonist SR59230A. ␤-Adrenoceptors exhibiting a pharmacologic profile consistent with that of the ␤ 3 -adrenoceptor have been cloned from various species, including mice, rats, and humans (Emorine et al., 1989;Granneman et al., 1991;Muzzin et al., 1991;Nahmias et al., 1991).

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Influence of β-adrenoceptor agonists on the pulmonary circulation. Effects of a β3-adrenoceptor antagonist, SR 59230A

Cited by 36 publications

References 14 publications

Characterization of Beta3-Adrenoceptors in Human Internal Mammary Artery and Putative Involvement in Coronary Artery Bypass Management

Characterization of Beta3-Adrenoceptors in Human Internal Mammary Artery and Putative Involvement in Coronary Artery Bypass Management

Metabolic responses to BRL37344 and clenbuterol in soleus muscle and C2C12 cells via different atypical pharmacologies and β₂‐adrenoceptor mechanisms

Evidence for Pleiotropic Signaling at the Mouse β₃-Adrenoceptor Revealed by SR59230A [3-(2-Ethylphenoxy)-1-[(1,S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanol Oxalate]

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Influence of β-adrenoceptor agonists on the pulmonary circulation. Effects of a β3-adrenoceptor antagonist, SR 59230A

Cited by 36 publications

References 14 publications

Characterization of Beta3-Adrenoceptors in Human Internal Mammary Artery and Putative Involvement in Coronary Artery Bypass Management

Characterization of Beta3-Adrenoceptors in Human Internal Mammary Artery and Putative Involvement in Coronary Artery Bypass Management

Metabolic responses to BRL37344 and clenbuterol in soleus muscle and C2C12 cells via different atypical pharmacologies and β2‐adrenoceptor mechanisms

Evidence for Pleiotropic Signaling at the Mouse β3-Adrenoceptor Revealed by SR59230A [3-(2-Ethylphenoxy)-1-[(1,S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanol Oxalate]

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Metabolic responses to BRL37344 and clenbuterol in soleus muscle and C2C12 cells via different atypical pharmacologies and β₂‐adrenoceptor mechanisms

Evidence for Pleiotropic Signaling at the Mouse β₃-Adrenoceptor Revealed by SR59230A [3-(2-Ethylphenoxy)-1-[(1,S)-1,2,3,4-tetrahydronapth-1-ylamino]-2S-2-propanol Oxalate]