On the mechanism of positive inotropic effects of alpha-adrenoceptor agonists

1989 ◽  
Vol 84 (1) ◽  
pp. 23-33 ◽  
Author(s):  
W. Schmitz ◽  
C. Kohl ◽  
J. Neumann ◽  
H. Scholz ◽  
J. Scholz
Keyword(s):  
Inotropic Effects ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Positive Inotropic Effects ◽  
Adrenoceptor Agonists

Interaction of Halogenated Anesthetics with α- and β-Adrenoceptor Stimulations in Diabetic Rat Myocardium

2004 ◽  
Vol 101 (5) ◽  
pp. 1145-1152 ◽  
Author(s):  
Julien Amour ◽  
Jean-Stéphane David ◽  
Benoît Vivien ◽  
Pierre Coriat ◽  
Bruno Riou
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Positive Inotropic Effect ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Inotropic Effect ◽  
Diabetic Rat ◽  
Inotropic Effects ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Positive Inotropic Effects

Background Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations. Although diabetes mellitus induces significant myocardial abnormalities, the interaction of halogenated anesthetics and adrenoceptor stimulation in diabetic myocardium remains unknown. Methods Left ventricular papillary muscles were provided from healthy and streptozotocin-induced diabetic rats. Effects of 1 minimum alveolar concentration halothane, isoflurane, and sevoflurane on the inotropic and lusitropic responses of alpha (phenylephrine)- and beta (isoproterenol)-adrenoceptor stimulations were studied at 29 degrees C with 12 pulses/min. Data shown are mean percentage of baseline active force +/- SD. Results Phenylephrine induced comparable positive inotropic effects in healthy and diabetic rats (143 +/- 8 vs. 136 +/- 18%; not significant), but the potentiation by halogenated anesthetics was abolished in the diabetic rats (121 +/- 20, 130 +/- 20, and 123 +/- 20% for halothane, isoflurane, and sevoflurane, respectively; not significant). In diabetic rats, the positive inotropic effect of isoproterenol was markedly diminished (109 +/- 9 vs. 190 +/- 18%; P < 0.05), but its potentiation was preserved with isoflurane (148 +/- 21%; P < 0.05) and sevoflurane (161 +/- 40%; P < 0.05) but not with halothane (126 +/- 16%; not significant). Halothane induced a deleterious effect on the sarcoplasmic reticulum, as shown by its impairment in the lusitropic effect of isoproterenol, compared with isoflurane and sevoflurane. Conclusion Potentiation of the positive inotropic effect of alpha-adrenoceptor stimulation by halogenated anesthetics is abolished in diabetic rats. In contrast, potentiation of beta-adrenoceptor stimulation is preserved with isoflurane and sevoflurane but not with halothane, probably because of its deleterious effects on sarcoplasmic reticulum.

Quantitative relationships between .alpha.-adrenergic activity and binding affinity of .alpha.-adrenoceptor agonists and antagonists

1984 ◽  
Vol 27 (4) ◽  
pp. 495-503 ◽  
Author(s):  
Pieter B. M. W. M. Timmermans ◽  
Adriaan De Jonge ◽  
Martin J. M. C. Thoolen ◽  
Bob Wilffert ◽  
Harry Batink ◽  
...  
Keyword(s):  
Binding Affinity ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenergic Activity ◽  
Adrenoceptor Agonists

Evidence for existence of postjunctional alpha 1- and alpha 2-adrenoceptors in cat pulmonary vascular bed

1985 ◽  
Vol 249 (4) ◽  
pp. H891-H898
Author(s):  
A. L. Hyman ◽  
P. J. Kadowitz
Keyword(s):  
Adrenergic Nerve ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Vascular Bed ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenoceptor Blocker ◽  
Adrenoceptor Agonists ◽  
Uk 14,304 ◽  
6 Hydroxydopamine ◽  
Pulmonary Vascular Bed

The subtypes of postjunctional alpha-adrenoceptors in the feline pulmonary vascular bed were studied using selective alpha-adrenoceptor agonists and antagonists. Under conditions of controlled pulmonary blood flow and constant left atrial pressure, intralobar injections of the alpha 1-adrenoceptor agonists, phenylephrine and methoxamine, and the alpha 2-adrenoceptor agonists, UK 14,304 and BHT 933, increased lobar arterial pressure in a dose-related manner. Prazosin, an alpha 1-adrenoceptor antagonist, reduced responses to phenylephrine and methoxamine to a greater extent than responses to UK 14,304 and BHT 933. Yohimbine, an alpha 2-adrenoceptor blocker, decreased responses to UK 14,304 and BHT 933 without altering responses to phenylephrine or methoxamine. The same pattern of blockade was observed in animals pretreated with 6-hydroxydopamine, an agent that destroys the integrity of adrenergic nerve terminals. However, in propranolol-treated animals, prazosin antagonized responses to phenylephrine and methoxamine without altering responses to UK 14,304 or BHT 933, and the selectivity of the blocking effects of yohimbine were preserved. Responses to intralobar injections of norepinephrine were markedly decreased by prazosin, whereas yohimbine had only a small effect. These data suggest the presence of both postjunctional alpha 1- and alpha 2-adrenoceptors mediating vasoconstriction in the pulmonary vascular bed. These results also indicate that the vasoconstrictor responses to injected norepinephrine in the cat pulmonary vascular bed are due mainly to activation of alpha 1-adrenoceptors.

scholarly journals Mediation of contraction in rat cauda epididymidis by alpha-adrenoceptors

Reproduction ◽  
2002 ◽  
pp. 887-892 ◽  
Author(s):  
G Chaturapanich ◽  
S Maythaarttaphong ◽  
V Verawatnapakul ◽  
C Pholpramool
Keyword(s):  
Pressure Transducer ◽  
Systemic Effects ◽  
Alpha Adrenoceptors ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Alpha Adrenoceptor Agonists ◽  
Adrenoceptor Agonists ◽  
Cauda Epididymidis ◽  
Spontaneous Contractions

Subtypes of alpha-adrenoceptors responsible for contractions of the rat cauda epididymidis were studied in vivo by micropuncture using a servo-nulling pressure transducer system. Administration of both non-selective and selective alpha-adrenoceptor agonists in doses of 1-40 microg noradrenaline kg(-1) body weight (BW), 1-100 microg clonidine kg(-1) BW, or 100-800 mg methoxamine kg(-1) BW enhanced contractions of the proximal cauda epididymidis in a dose-response manner. The potency of the agonists were noradrenaline > or = clonidine>methoxamine. Pre-treatments with selective alpha(1)-adrenoceptor antagonist (prazosin) and alpha(2)-adrenoceptor antagonist (yohimbine) at the doses of 400 and 800 microg kg(-1) BW, respectively, had very little effect on spontaneous contractions, but effectively blocked the responses to the maximal doses of methoxamine and clonidine. The responses could not be explained by the systemic effects of agonists and antagonists. The results suggest that contraction of the proximal cauda epididymidis of rats is mediated by both alpha(1)- and alpha(2)-adrenoceptors. The latter appears to be more abundant.

Coronary vasoconstriction mediated by alpha 1- and alpha 2-adrenoceptors in conscious dogs

1987 ◽  
Vol 253 (2) ◽  
pp. H388-H393 ◽  
Author(s):  
O. L. Woodman ◽  
S. F. Vatner
Keyword(s):  
Conscious Dogs ◽  
Similar Degree ◽  
Coronary Resistance ◽  
Coronary Vasoconstriction ◽  
Beta Adrenoceptor ◽  
Alpha Adrenoceptor ◽  
Alpha Adrenoceptor Agonists ◽  
Vasoconstrictor Response ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Coronary vasoconstriction was examined in response to the selective stimulation of alpha 1- and alpha 2-adrenoceptors in chronically instrumented conscious dogs. Norepinephrine (NE, 0.05 and 0.1 micrograms X kg-1 X min-1), a mixed alpha 1- to alpha 2-adrenoceptor agonist, phenylephrine (PE, 0.5 and 1.0 micrograms X kg-1 X min-1), a preferential alpha 1-adrenoceptor agonist, and B-HT 920 (1.0 micrograms X kg-1 X min-1), a preferential alpha 2-adrenoceptor agonist, were infused intravenously after ganglionic (hexamethonium, 30 mg/kg iv), beta-adrenoceptor (propranolol, 1.0 mg/kg iv), and muscarinic receptor (atropine methylbromide, 0.1 mg/kg iv) antagonism. Equipressor doses of the alpha-adrenoceptor agonists caused similar increases in calculated late diastolic coronary resistance (NE, 0.57 +/- 0.10 mmHg X ml-1 X min; PE, 0.61 +/- 0.13 mmHg X ml-1 X min; B-HT 920, 0.64 +/- 0.09 mmHg X ml-1 X min). Mechanically increasing aortic root pressure to levels similar to those observed in response to alpha-adrenoceptor stimulation did not increase coronary resistance. Preferential antagonism of alpha 1-adrenoceptors with prazosin (1 mg/kg iv) abolished the vasoconstrictor response to PE but had a lesser effect on the response to B-HT 920. Antagonism of alpha 2-adrenoceptors with rauwolscine (alpha-yohimbine, 0.1 mg/kg iv) abolished the vasoconstrictor response to B-HT 920 but had a lesser effect on the response to PE. The response to NE was reduced to a similar degree by either alpha 1- or alpha 2-adrenoceptor antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)

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