Classification of the β-adrenoceptor subtype in the rat portal vein: effect of altered thyroid hormone levels

Chin, Jaye P. F.; Pennefather, Jocelyn N.

doi:10.1016/0014-2999(92)90330-7

Cited by 4 publications

(2 citation statements)

References 20 publications

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“…Atenolol (1 μ M) ( Chin and Pennefather, 1992 ; Arch and Kaumann, 1993 ; Suh et al ., 1999 ; Pourageaud et al ., 2005 ), 1 μ M SR59230A ( Nisoli et al ., 1996 ; Yurtcu et al ., 2006 ) and 300 n M CGP20712A would not be expected to block rodent β 2 ‐adrenoceptors. ICI118551 is, in contrast, a highly potent and selective β 2 ‐adrenoceptor antagonist with reported pA 2 values in rat tissues of greater than 9 ( Bilski et al ., 1983 ; Vidal‐Beretervide and Castaneda, 1988 ; Pourageaud 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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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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“…Together, these findings suggest that neural release of norepinephrine probably contributes to 8-OH-DPAT-induced venoconstriction and attenuation of metabolic acidosis to a greater extent than does increased circulating epinephrine. At the same time, sympathetic activation of epinephrine release could conceivably have contributed to stimulation of the high-density ␤-adrenergic receptor population found in the terminal splanchnic venous vasculature (e.g., the portal vein) and thereby reduced resistance to blood mobilization from splanchnic blood stores during norepinephrine release (5).…”

Section: Discussionmentioning

confidence: 99%

The spleen is required for 5-HT_1Areceptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat

Tiniakov¹,

Scrogin²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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The 5-HT(1A) receptor agonist, 8- OH-DPAT, increases whole body venous tone (mean circulatory filling pressure; MCFP), and attenuates metabolic acidosis in a rat model of unresuscitated hemorrhagic shock. To determine whether improved acid-base balance was associated with sympathetic activation and venous constriction, MCFP, sympathetic activity (SA), and blood gases were compared in hemorrhaged rats following administration of 5-HT(1A) receptor agonist 8-OH-DPAT, the arterial vasoconstrictor arginine vasopressin (AVP), or saline. To further determine whether protection of acid-base balance was dependent on splenic contraction and blood mobilization, central venous pressure (CVP), MCFP, and blood gases were determined during hemorrhage and subsequent 8-OH-DPAT-administration in rats subjected to real or sham splenectomy. Subjects were hemorrhaged to an arterial pressure of 50 mmHg for 25 min and subsequently were treated with 8-OH-DPAT (30 nmol/kg iv), AVP titrated to match the pressor effect of 8-OH-DPAT (approximately 2 ng/min iv), or infusion of normal saline. 8-OH-DPAT increased MAP, CVP, MCFP, and SA, and decreased lactate accumulation. AVP did not affect CVP or SA, but raised MCFP slightly to a level intermediate between 8-OH-DPAT- and saline-treated rats. Infusion of AVP also produced a modest protection against metabolic acidosis. Splenectomy prevented the rise in CVP, MCFP, and protection against metabolic acidosis produced by 8-OH-DPAT but had no effect on the immediate pressor response to the drug. Together, the data indicate that 8-OH-DPAT produces a pattern of cardiovascular responses consistent with a sympathetic-mediated venoconstriction that is, in part, responsible for the drug's beneficial effect on acid-base balance. Moreover, blood mobilization stimulated by the spleen is required for the beneficial effects of 8-OH-DPAT.

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BRL 37344 Inhibited Adrenergic Transmission In The Rat Portal Vein Via Atypicalβ -Adrenoceptors

Yousif

Oriowo

2002

Pharmacological Research

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Classification of the β-adrenoceptor subtype in the rat portal vein: effect of altered thyroid hormone levels

Cited by 4 publications

References 20 publications

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

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

The spleen is required for 5-HT_1Areceptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat

BRL 37344 Inhibited Adrenergic Transmission In The Rat Portal Vein Via Atypicalβ -Adrenoceptors

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Classification of the β-adrenoceptor subtype in the rat portal vein: effect of altered thyroid hormone levels

Cited by 4 publications

References 20 publications

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

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

The spleen is required for 5-HT1Areceptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat

BRL 37344 Inhibited Adrenergic Transmission In The Rat Portal Vein Via Atypicalβ -Adrenoceptors

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Resources

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

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

The spleen is required for 5-HT_1Areceptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat