Adrenergic–cholinergic interactions in left atria: Interaction of carbachol with alpha- and beta-adrenoceptor agonists

1986 ◽  
Vol 64 (5) ◽  
pp. 597-601 ◽  
Author(s):  
K. M. MacLeod
Keyword(s):  
Left Atrial ◽  
Muscarinic Agonist ◽  
Muscarinic Agonists ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Β Receptor ◽  
Inotropic Responses ◽  
Beta Adrenoceptor Agonists ◽  
Camp Levels ◽  
Dose Dependent

The purpose of the present investigation was to determine the nature of the functional interaction of muscarinic agonists with cAMP-generating and cAMP-independent agonists in left atria. Negative inotropic responses of rabbit isolated left atrial strips to the muscarinic agonist, carbachol were measured in the absence and presence of equi-active inotropic doses of the β-adrenoceptor stimulant isoproterenol (Iso), the mixed α- and β-adrenoceptor stimulant phenylephrine (PE) plus 1 μM timolol to block the β-receptor mediated component of its response, and elevated extracellular Ca2+. Carbachol produced dose-dependent negative inotropic responses in left atrial strips, which were much greater than control in the presence of either Iso, or PE plus timolol. However, carbachol responses were of a similar magnitude to the control in the presence of elevated extracellular Ca2+. In the presence of timolol, PE had no significant effect on cAMP levels in left atrial strips, and inotropic responses to carbachol alone and in combination with PE plus timolol were accompanied by significant increases in cGMP levels but no change in cAMP levels. Carbachol attenuated Iso-induced increases in cAMP levels, but decreases in left atrial tension were proportionally greater than the decreases in cAMP levels produced by carbachol in the presence of Iso. These results suggest that the antiadrenergic effects of muscarinic receptor stimulation may occur by a different mechanism in left atria than has been previously reported in ventricular muscle. While the nature of this mechanism is unknown, it may involve antagonism by muscarinic agents of both α-and β-adrenoceptor mediated increases in Ca2+ influx.

Adrenergic–cholinergic interactions in left atria. II. Comparison of the antagonism of inotropic responses to α- and β-adrenoceptor stimulation and BAY K 8644 by carbachol, D-600, and nifedipine

1987 ◽  
Vol 65 (10) ◽  
pp. 2059-2064 ◽  
Author(s):  
K. M. MacLeod
Keyword(s):  
Bay K 8644 ◽  
Muscarinic Agonist ◽  
Functional Interaction ◽  
Low Concentrations ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Β Blocker ◽  
Β Receptor ◽  
The Right ◽  
Inotropic Responses

The muscarinic agonist carbachol has previously been shown to reverse positive inotropic responses of rabbit left atrial strips to equiactive doses of the β-adrenoceptor agonist isoproterenol and to the α-adrenoceptor agonist phenylephrine. Responses to phenylephrine were measured in the presence of the β-blocker timolol. However, carbachol was not able to reverse the increase in tension produced by elevating the extracellular Ca2+ concentration. To gain more information about the nature of the functional interaction of carbachol with α- and β-receptor stimulants in left atria, the interaction of carbachol with these agonists, as well as with elevated Ca2+ and the Ca2+ activator compound BAY K 8644, was compared with that of the Ca2+ antagonists D-600 and nifedipine. The results demonstrate that the Ca2+ antagonists exhibit a selectivity similar to that of carbachol, in that responses to both isoproterenol and phenylephrine plus timolol were blocked by low concentrations of D-600 and nifedipine, which had no effect on positive inotropic responses to elevated Ca2+. Higher concentrations of these antagonists shifted the Ca2+ dose–response curve to the right. In addition, although phenylephrine and BAY K 8644 increased tension to a similar extent, responses to phenylephrine were more sensitive than responses to BAY K 8644 to inhibition by both carbachol and D-600. These similarities between the effects of low concentrations of D-600 and nifedipine and those of carbachol are consistent with the hypothesis that carbachol antagonizes responses to α- and β-receptor stimulation in left atria primarily by blocking increases in Ca2+ influx produced by these agonists. In addition, the observation that responses of left atria to α- and β-adrenoceptor agonists are blocked more readily than responses to elevated Ca2+ and those to BAY K 8644 by both carbachol and the Ca2+ antagonists may be indicative of differences in the way agonists on one hand, and elevated Ca2+ and BAY K 8644 on the other, increase Ca2+ influx into myocardial cells.

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.

scholarly journals The effect of beta-adrenoceptor agonists and antagonists on gastric emptying in man.

1980 ◽  
Vol 10 (6) ◽  
pp. 551-554 ◽  
Author(s):  
MR Rees ◽  
RA Clark ◽  
CD Holdsworth ◽  
DC Barber ◽  
PJ Howlett
Keyword(s):  
Gastric Emptying ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonists ◽  
Beta Adrenoceptor Agonists
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