Function of myocardial α-adrenoceptors

Benfey, B. G.

doi:10.1016/0024-3205(82)90421-0

Cited by 75 publications

(14 citation statements)

References 74 publications

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“…1, 2, and 3). In a recent review, Benfey (1982) noted that in studies designed to assess myocardial alpha-adrenoceptor function, the alpha-adrenoceptor agonkt must be effective in relatively low concentrations and the study must be conducted in the presence of beta-adrenoceptor antagonism. In the presence of beta-adrenoceptor antagonism (timolol), there was a significant inhibition of the chronotropic response of right atria when stimulated by phenylephrine (75 and 5596, control and diabetic, respectively; Fig.…”

Section: Discussionmentioning

confidence: 98%

Alterations in alpha₁-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Jackson¹,

McGrath²,

McNeill³

1986

Can. J. Physiol. Pharmacol.

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This purpose of this investigation was to determine the influence of experimental diabetes (3 months) on the responsiveness of rat isolated atria to alpha 1-adrenoceptor stimulation by phenylephrine. Diabetes was chemically induced with streptozotocin (65 mg/kg i.v.) in 42- to 43-day-old, nonfasted male Sprague-Dawley derived rats. Chronotropic (right atria) and inotropic (left atria) indices were recorded in response to alpha 1-adrenoceptor stimulation by phenylephrine. These experiments were performed in the presence of beta-adrenoceptor antagonism (timolol). Isolated right atria from diabetic rats demonstrated a greater increase in heart rate in response to phenylephrine than did corresponding control atria. Left atria were supersensitive (decrease in EC50 values) and hyperresponsive to alpha 1-adrenoceptor stimulation by phenylephrine when compared with stimulation of control left atria. Diabetic left atria in response to phenylephrine were observed to exchange more radioactive calcium (45Ca2+) than control left atria, whereas both diabetic and control left atria exchanged the same amount of 45Ca2+ during basal contractile conditions. Phenylephrine had no effect on 45Ca2+ efflux from either diabetic or control atria. These results indicate that 3 months of uncontrolled experimental diabetes in the rat produces an enhancement of alpha 1-adrenoceptor activation of isolated atria, and that there is an alteration in Ca2+ mobilization which may contribute to the enhanced receptor activation.

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Section: Discussionmentioning

confidence: 98%

Alterations in alpha₁-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Jackson¹,

McGrath²,

McNeill³

1986

Can. J. Physiol. Pharmacol.

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“…The existence of a myocardial a-adrenergic receptor has been reported. 22 When stimulated, these receptors produce trophic changes. It is tempting to speculate that inhibition of the same receptors could lead to improvement in ventricular compliance and filling.…”

Section: Clinical Importancementioning

confidence: 99%

Left ventricular function in mild hypertension after adrenergic blockade.

et al. 1988

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We previously used the Doppler transmitral flow velocity ratio A/E (A = late ventricular filling peak velocity; E = early ventricular filling peak velocity) and the age-adjusted ratio A/E/Age to detect left ventricular filling abnormalities in untreated mild hypertension. This study is a double-blind assessment of the effect of combined a-and /3-blockade (labetalol) and ^-blockade alone (atenolol) on left ventricular filling in mild hypertension. Twenty-seven patients blindly randomized to labetalol (12 patients) and atenolol (15 patients) treatment completed the echocardiographic and Doppler studies. Clinical and echo-DoppIer data obtained at baseline and 6 weeks after initiation of therapy showed no difference between the two groups for age (49 ± 10 vs 46 ± 10 years), mean blood pressure (before therapy, 118 ± 9 vs 117 ± 8 mm Hg; after therapy, 108 ± 12 vs 108 ± 10 mm Hg), left ventricular dimensions, wall thickness, systolic function, and mean late filling velocity A. There was no significant change in left ventricular mass and mass index with labetalol (left ventricular mass, 211 ± 3 6 vs 216 ±38; mass index, 110 ±17 vs 112 ±16) or atenolol (245 ± 4 1 vs 271 ±65; 120 ± 18 vs 130 ± 35). The mean velocity E, A/E, and A/E/Age ratios significantly unproved with labetalol (p<0.05) but did not change significantly with atenolol. The improvement in A/E and PJEJkge ratios was primarily due to an increase in early filling velocity E. There was a significant correlation between improvement in velocity E and reduction in systolic blood pressure (r = 0.57, p< 0.05) and mean blood pressure with labetalol (r = 0.63, p < 0.05). In conclusion, short-term combined a-and /S-adrenergic blockade improves diastolic filling in mild hypertension. (Hypertension 11 [Suppl I]: I-98-I-102, 1988) KEYWORDS inhibition Doppler echocardiography • ventricular filling • a-and/3-adrenergic receptor

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“…It is generally accepted that stimulation of myocardial a,-adrenoceptors results in a positive inotropic effect in various mammalian species (for reviews, see Scholz, 1980;Schumann, 1980;Benfey, 1982). The question has remained unsettled as to whether myocardial a,-adrenoceptors have a functional or physiological role in the regulation of myocardial contractility.…”

Section: Introductionmentioning

confidence: 99%

Induction by endogenous noradrenaline of an α₁‐adrenoceptor‐mediated positive inotropic effect in rabbit papillary muscles

Hattori

Takeda

Nakaya

et al. 1993

British J Pharmacology

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-1 The possible involvement of xl-adrenoceptors in the inotropic and electrophysiological responses to endogenous noradrenaline released by tyramine was examined in rabbit papillary muscles. 2 A concentration-dependent positive inotropic effect was produced by tyramine. This effect of tyramine was not observed in muscles from rabbits pretreated with reserpine. 3 The positive inotropic effect of tyramine was greatly inhibited by propranolol, but not altered by prazosin. However, when P-adrenoceptors were blocked by pretreatment with propranolol, tyramine still produced a positive inotropic effect, an effect which was antagonized by prazosin. 4 Tyramine caused a decrease in action potential duration (APD) and an increase in action potential amplitude in a concentration-dependent manner. Isoprenaline also produced the same electrophysiological effects. These electrophysiological effects of both agents were inhibited by propranolol. 5 When ,B-adrenoceptors were blocked by propranolol, the observed prazosin-sensitive positive inotropic effect of tyramine was not accompanied by any change in APD. In contrast, APD was markedly prolonged by al-adrenoceptor stimulation with phenylephrine in the presence of propranolol, in association with the positive inotropic effect. 6 It is concluded that in rabbit papillary muscles, endogenous noradrenaline causes a positive inotropic effect predominantly mediated by P-adrenoceptors, but can still evoke a positive inotropic effect through ax-adrenoceptors when P-adrenoceptor stimulation is eliminated. This suggests that the a,-adrenoceptormediated positive intropic mechanism(s) may be masked by simultaneous activation of P-adrenoceptors. In addition, this study indicates that APD prolongation is not involved in the a,-adrenoceptor-mediated inotropic responses to endogenous noradrenaline.

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Function of myocardial α-adrenoceptors

Cited by 75 publications

References 74 publications

Alterations in alpha₁-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Alterations in alpha₁-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Left ventricular function in mild hypertension after adrenergic blockade.

Induction by endogenous noradrenaline of an α₁‐adrenoceptor‐mediated positive inotropic effect in rabbit papillary muscles

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Function of myocardial α-adrenoceptors

Cited by 75 publications

References 74 publications

Alterations in alpha1-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Alterations in alpha1-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Left ventricular function in mild hypertension after adrenergic blockade.

Induction by endogenous noradrenaline of an α1‐adrenoceptor‐mediated positive inotropic effect in rabbit papillary muscles

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Alterations in alpha₁-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Alterations in alpha₁-adrenoceptor stimulation of isolated atria from experimental diabetic rats

Induction by endogenous noradrenaline of an α₁‐adrenoceptor‐mediated positive inotropic effect in rabbit papillary muscles