The Schultz-Dale reaction of the guinea-pig ileum: Influence by beta-adrenoceptor agonists and theophylline

1979 ◽  
Vol 9 (4) ◽  
pp. 358-363 ◽  
Author(s):  
G. M. Laekeman ◽  
A. G. Herman
Keyword(s):  
Guinea Pig ◽  
Guinea Pig Ileum ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Beta Adrenoceptor Agonists

Inhibitory potency of isoprenaline on guinea-pig and gravid human myometrium following extraneuronal uptake blockade

1995 ◽  
Vol 7 (1) ◽  
pp. 59
Author(s):  
M Kousides ◽  
ME Story ◽  
JN Pennefather ◽  
SP Ziccone ◽  
AW Ross
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Human Myometrium ◽  
Inhibitory Effects ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Myometrial Contractility ◽  
Beta Adrenoceptor Agonists ◽  
Evoked Contractions

The hypothesis that inhibitory effects of isoprenaline on myometrial contractility may be constrained by activation of putative intracellular beta-adrenoceptors negatively-coupled to adenylate cyclase was examined. Field-stimulated preparations of guinea-pig and human myometrium were used to examine the influence of the catecholamine extraneuronal uptake2 inhibitors, corticosterone and beta-oestradiol, on the inhibitory effects of the beta-adrenoceptor agonist, isoprenaline, on uterine contraction. Longitudinal and circular myometrial layers were obtained from guinea-pigs in dioestrus, primed with oestrogen before progesterone, or pregnant (Days 62-65). In the guinea-pig myometrium, corticosterone (30 microM) did not affect responses to isoprenaline. beta-oestradiol (10 microM) induced a small potentiation of the effects of isoprenaline on longitudinal myometrium from dioestrus guinea-pigs. Myometrial preparations were obtained from pregnant women (36-40 weeks gestation) undergoing caesarean section. Isoprenaline inhibited stimulation-evoked contractions in 7 of 10 preparations of the inner myometrial layer and in 5 of 8 preparations of outer myometrial layer. Corticosterone (30 microM) reduced the effects of isoprenaline on the inner layer and did not affect the outer layer. These results do not support the existence of mechanism involving isoprenaline-sensitive intracellular receptors which constrain responses to beta-adrenoceptor agonists.

Interaction of iberiotoxin with beta-adrenoceptor agonists and sodium nitroprusside on guinea pig trachea

1993 ◽  
Vol 74 (4) ◽  
pp. 1879-1884 ◽  
Author(s):  
T. R. Jones ◽  
L. Charette ◽  
M. L. Garcia ◽  
G. J. Kaczorowski
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Sodium Nitroprusside ◽  
Airway Smooth Muscle ◽  
Plasma Membranes ◽  
K Channel ◽  
K Channels ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Beta Adrenoceptor Agonists

Airway smooth muscle plasma membranes contain a variety of functional K+ channels. In particular, there is a predominance of Ca(2+)-activated K+ channels (maxi-K). Inhibition of these K+ channels has been postulated to account for the ability of charybdotoxin (ChTX) to produce contraction of airway smooth muscle and to modify the relaxant effects of beta-adrenoceptor agonists and sodium nitroprusside (SNP). Iberiotoxin (IbTX) is more selective and more potent than ChTX at blocking maxi-K channels. In this study, pharmacological experiments were performed on guinea pig trachea to determine whether IbTX produced effects similar to ChTX. The concentration-response curves to salbutamol were markedly affected by IbTX, with a > 60-fold rightward shift being produced with 20 nM IbTX. The maximal relaxation to salbutamol was reduced to 49.3 +/- 0.9, 22.3 +/- 4.7, and 15.0 +/- 2.7% of control maximum in the presence of 20, 60, and 180 nM IbTX, respectively. Similar to salbutamol, the maximal relaxation to SNP was reduced to 80 +/- 1.6, 19 +/- 1.7, and 12 +/- 2.1% of control maximum in the presence of 20, 60, and 180 nM IbTX, respectively. IbTX (180 nM) failed to produce a significant alteration of relaxation to the ATP-dependent K+ channel agonist BRL-34915. Exposure of tissues to K(+)-rich medium (80 mM) inhibited responses to salbutamol > or = SNP > isoproterenol. These results confirm and extend our earlier observations that maxi-K channels may be involved in regulating tone and relaxation of carbachol-contracted guinea pig tracheal smooth muscle. This mechanism is of particular importance for beta 2-adrenoceptor- and SNP-induced relaxation.

scholarly journals Salbutamol-induced severe lactic acidosis in acute asthma

2020 ◽  
Vol 8 ◽  
pp. 2050313X2096902 ◽  
Author(s):  
Hamza Najout ◽  
Mohamed Moutawakil ◽  
Abdelghafour Elkoundi ◽  
Nawfal Doghmi ◽  
Hicham Bekkali
Keyword(s):  
Lactic Acidosis ◽  
Acute Asthma ◽  
Krebs Cycle ◽  
Bronchial Obstruction ◽  
Compensatory Mechanism ◽  
Severe Lactic Acidosis ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Lactate Formation ◽  
Beta Adrenoceptor Agonists

Selective beta-adrenoceptor agonists are worldwide prescribed to manage bronchial obstruction. However, they expose to a potential risk of hyperlactatemia and lactic acidosis even with normal doses. The mechanism still poorly understood and suggested that salbutamol diverts the metabolism of pyruvate acid from Krebs cycle toward lactate formation. We report the case of a 42-year-old patient, admitted to intensive care unit for acute severe asthma. He presented a transient lactic acidosis over the first 48 h, following an excessive use of salbutamol. The metabolic acidosis caused tachypnea, as a compensatory mechanism, leading to respiratory failure. The diagnosis of salbutamol-induced lactic acidosis must be made by elimination and only accepted after deleting the other causes. The main clinical character is the worsening of dyspnea despite regression of bronchospasm. It is transient and usually normalizes within 24–48 h after stopping or decreasing doses of salbutamol.

Cardiac function and responsiveness to beta-adrenoceptor agonists in rats with obstructive jaundice

1993 ◽  
Vol 265 (2) ◽  
pp. G314-G320 ◽  
Author(s):  
G. Jacob ◽  
N. Nassar ◽  
G. Hayam ◽  
S. Ben-Haim ◽  
Y. Edoute ◽  
...  
Keyword(s):  
Bile Duct ◽  
Obstructive Jaundice ◽  
Cardiac Function ◽  
Radioligand Binding ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Pithed Rats ◽  
Duct Ligation ◽  
Adrenoceptor Agonists ◽  
Beta Adrenoceptor Agonists

The function and role of the heart and the contribution of cardiac beta-adrenoceptors in the pathogenesis of circulatory failure in obstructive jaundice were studied in the 3-day bile duct-ligated (BDL) rat using three different techniques to measure cardiac function and beta-adrenoceptor activity, number, and affinity. The techniques were the pithed rat preparation, the isolated working heart preparation, and a competitive radioligand binding assay for beta-adrenoceptors. The results of these experiments were compared with those obtained in 3-day bile duct-manipulated (sham operated; SO) rats. Impaired indexes of basal cardiac contractility were observed in the BDL pithed rats and isolated working hearts. In these two preparations, responsiveness to norepinephrine and the beta-adrenoceptor agonists, isoproterenol and dobutamine, was unaffected by bile duct ligation. The affinity and number of cardiac beta-adrenoceptors in membranes from the hearts of SO and BDL rats were not significantly different from each other. These experiments have established for the first time that the 3-day BDL rat has a cardiac myopathy associated with intact responsiveness to beta-adrenoceptor agonists, a normal unchanged affinity and number of cardiac beta-adrenoceptors.

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