Effects of α‐adrenoceptor antagonists on clonidine‐induced inhibition of insulin secretion by isolated pancreatic islets

Langer, J; Panten, U.; Zielmann, S.

doi:10.1111/j.1476-5381.1983.tb11014.x

Cited by 44 publications

(15 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our present findings show that PE, an agonist with affinity for a2-adrenoceptors but with minimal central action, reproduced the inhibitory responses mediated by Clo (Figure 4). We propose therefore that the effects of Clo on blood glycerol and IRI levels are the result of a direct peripheral stimulation of inhibitory a2-adrenoceptors located on adipocytes and the pancreatic #-cell, confirming in this way previous in vitro data (Lafontan & Berlan, 1980;Nakaki et al, 1981;Langer et al, 1983;Hillaire-Buys et al, 1985).…”

Section: Discusionsupporting

confidence: 88%

“…direct radioligand binding and metabolic activity measurements (Garcia Sainz et al, 1980;Lafontan & Berlan, 1981;Carpene et al, 1983). Similarly the aadrenoceptor which mediates the insulin inhibitory response evoked by catecholamines appears to be of the a2-subtype (Nakaki et al 1981;Langer et al, 1983;Hillaire-Buys et al, 1985). However their effective role in vivo has not been fully studied.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Moratinos

Carpéné

Pablos

et al. 1988

British J Pharmacology

View full text Add to dashboard Cite

1 In conscious fasted rabbits an intravenous infusion of clonidine (2ygkg-min-1) induced hyperglycaemia. The increase in blood glucose was accompanied by an inhibition of insulin secretion and basal lipolysis. 2 Yohimbine infused at a rate of 20ogkg-min-' suppressed clonidine-induced hyperglycaemia and blocked the inhibitory effect on insulin secretion mediated by the a2-adrenoceptor agonist. 3 The intravenous infusion of amidephrine (10pgkg-'min-1) induced an increase in insulin secretion in the absence of patent hyperglycaemia. Prazosin, 0.3 mg kg1 s.c. selectively antagonized the effect of amidephrine on insulin secretion.4 Isoprenaline infusion (4.4 pgkg' min 1) evoked a significant increase in blood glycerol and immunoreactive insulin plasma levels. Both responses were clearly attenuated when a2-adrenoceptors were simultaneously stimulated by selective (clonidine) and less selective (phenylephrine, 20 yg kg-I min-') agonists. 5Amidephrine infusion did not induce appreciable changes in blood glycerol nor did it modify, isoprenaline-induced lipolytic response. 6 Simultaneous infusion of isoprenaline and amidephrine induced a remarkable increase in insulin secretion. 7 It is concluded that in normal fasted rabbits stimulation of oe2-adrenoceptors depresses basal and fl-adrenoceptor mediated lipolysis and insulin secretion. On the other hand, selective stimulation of a,-adrenoceptors does not affect lipolysis but induces insulin release. Simultaneous stimulation of a,-and fl-adrenoceptors potentiates the insulin secretory response.

show abstract

Section: Discusionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Moratinos

Carpéné

Pablos

et al. 1988

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…16,17 Likewise, the increase in blood glucose level after high-dose epinephrine administration is reported to be blunted by alpha 2-adrenoceptor antagonists. 18 In our study, we observed a fall in insulin levels after 5 h and a further decrease by high-dose epinephrine in control group due to fasting and epinephrine effect, respectively. These effects conform to normal physiology and are expected to happen in the control group.…”

Section: Discussionmentioning

confidence: 54%

Action of Cleistanthins A and B on Alpha Adrenoceptors in Rats

Lakshmanan¹,

Bobby²,

Raveendran³

2016

JYP

View full text Add to dashboard Cite

Objectives: Cleistanthins A and B (CAB), active phytochemicals present in Cleistanthus collinus, have been proven to have alpha 1-adrenoceptor blocking property. However action on alpha 2-adrenoceptor is not studied. We aimed to study the action of CAB on alpha 2-adrenoceptor by measuring platelet aggregation, insulin and blood glucose levels with yohimbine as a standard comparator control and alpha 1-adrenoceptor by measuring the blockade of relaxation induced by phenylephrine in the jejunum of Wistar albino rats. Materials and methods: Forty eight adult male Wistar rats were divided into eight drug groups of six each, namely control (CMC 0.5%), yohimbine 2 mg/kg, 10, 30 and 100 mg/kg doses of cleistanthin A and cleistanthin B. Blood samples were drawn at baseline, after 5 h and after high-epinephrine dose (5 mg/kg) from the retro-orbital sinus and used for estimation of platelet aggregation and plasma insulin levels. Blood glucose levels were estimated at six different time points. Degree of jejunal relaxation was studied by relaxing the acetylcholine pre-contracted jejunum with phenylephrine. Results: All groups, except control and cleistanthin A 10 mg/kg group, significantly inhibited the platelet aggregation when compared to the respective baseline values (p<0.05). No significant difference was observed between different drug groups in plasma insulin and blood glucose levels. With regard to phenylephrine induced jejunal relaxation, the median IC 50 for all three doses of cleistanthin A and cleistanthin B 100 mg/kg differ significantly from that of control (CMC 0.5%). Conclusion: CAB block both alpha 1 and 2-adrenoceptorand hence are non-selective alpha-adrenoceptor blockers.

show abstract

“…Adrenaline, at concentrations up to 100p1M, was without effect on ATP-sensitive K+ channels. Furthermore, clonidine acts on x2-adrenoceptors to inhibit insulin release at much lower concentrations (1-lOOnM) than those needed to affect the ATP-sensitive K + channels (Leclercq-Meyer et al, 1980;Nakaki et al, 1981;Langer et al, 1983;Bertrand & Henquin, 1990). A similar dissociation exists between the dose-dependency of the effects of phentolamine or yohimbine on c2-adrenoceptors and on ATP-sensitive K + channels (Plant & Henquin, 1990).…”

Section: Discussionmentioning

confidence: 98%

Clonidine inhibits ATP‐sensitive K⁺channels in mouse pancreatic β‐cells

Plant

Jonas²,

Henquin

1991

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of clonidine and adrenaline on adenosine 5'-triphosphate (ATP)-sensitive K + channels were studied in pancreatic #-cells from normal mice.2 When perifused with a medium containing 1 mm glucose, many of the ATP-sensitive K+ channels in the fl-cell membrane are open. Under these conditions, clonidine (5-100,uM) reversibly decreased 86Rb efflux from the islets, whereas adrenaline was ineffective at concentrations up to 100,UM.3 In 6 mm glucose, most of the ATP-sensitive K + channels in the fl-cell membrane are closed. Opening these channels by diazoxide (100pM) caused a marked acceleration of 86Rb efflux from the islets, which was attenuated by 100pM clonidine.4 ATP-sensitive K+ currents were measured in single fl-cells by the whole cell mode of the patch-clamp technique. At concentrations above 4pM, clonidine reversibly inhibited the ATP-sensitive K+ current in a dose-dependent manner.5 Voltage-sensitive K+ currents were unaffected by 20OpM but decreased slightly by 100pM clonidine.6 Calcium currents, measured by the whole cell or perforated patch technique, were unaffected by clonidine at concentrations up to 100pM. 7 It is concluded that high concentrations of the a2-adrenoceptor agonist clonidine, but not of adrenaline, can inhibit ATP-sensitive K+ channels in pancreatic fl-cells. Other ionic channels are only slightly affected or unaffected.

show abstract

Effects of α‐adrenoceptor antagonists on clonidine‐induced inhibition of insulin secretion by isolated pancreatic islets

Cited by 44 publications

References 32 publications

Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Action of Cleistanthins A and B on Alpha Adrenoceptors in Rats

Clonidine inhibits ATP‐sensitive K⁺channels in mouse pancreatic β‐cells

Contact Info

Product

Resources

About

Effects of α‐adrenoceptor antagonists on clonidine‐induced inhibition of insulin secretion by isolated pancreatic islets

Cited by 44 publications

References 32 publications

Role of α1‐ and α2‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Role of α1‐ and α2‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Action of Cleistanthins A and B on Alpha Adrenoceptors in Rats

Clonidine inhibits ATP‐sensitive K+channels in mouse pancreatic β‐cells

Contact Info

Product

Resources

About

Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Role of α₁‐ and α₂‐adrenoceptors in catecholamine‐induced hyperglycaemia, lipolysis and insulin secretion in conscious fasted rabbits

Clonidine inhibits ATP‐sensitive K⁺channels in mouse pancreatic β‐cells