Importance of receptor regulation in the pathophysiology and therapy of congestive heart failure
References (54)
- et al.
Tolerance to dobutamine after a 72-hour continuous infusion
Am J Med
(1980) - et al.
Chronic heart failure in the guinea pig increases cardiac alpha1- and beta-adrenoceptors
Eur J Pharmacol
(1980) A depressed response of left ventricular contractile force to isoproterenol and norepinephrine in dogs with congestive heart failure
Am Heart J
(1977)Myocardial beta-adrenergic receptor down regulation in heart failure
Int J Cardiol
(1984)- et al.
Catecholamine excretion and cardiac stores of norepinephrine in congestive heart failure
Am J Med
(1965) - et al.
Plasma norepinephrine in congestive heart failure
Am J Cardiol
(1978) Cardiovascular injury induced by sympathetic catecholamines
Prog Cardiovasc Dis
(1974)- et al.
Lack of correlation between the positive inotropic effect evoked by alpha-adrenoceptor stimulation and the levels of cyclic AMP and/or cyclic GMP in the isolated ventricular strip of the rabbit
J Mol Cell Cardiol
(1978) Prolongation of the myocardial functional refractory period by phenylephrine
Life Sci
(1967)- et al.
Platelet alpha2-adrenoceptors in chronic congestive heart failure
Am J Cardiol
(1983)
Intermittent continuous outpatient dobutamine infusion in the management of congestive heart failure
Am J Cardiol
Alpha-adrenoceptors in the ventricular myocardium: clonidine, naphazoline and methoxamine as partial alpha agonists exerting a competitive dualism in action to phenylephrine
Eur J Pharmacol
Systemic hemodynamic effects of dopamine, (±)-dobutamine and (+)- and (-)-enantiomers of dobutamine in anesthetized normotensive rats
Eur J Pharmacol
Possible value of H2-receptor agonists for treatment of catecholamine-insensitive congestive heart failure
Pharmac Ther
Decreased lymphocyte beta-adrenergic receptor density in patients with heart failure and tolerance to the beta-adrenergic agonist pirbuterol
N Engl J Med
Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts
N Engl J Med
Beta-adrenergic receptor measurements in normal and failing human right and left ventricle
Circulation
Selective down-regulation of beta1-adrenergic receptors in the failing human heart
Circulation
Beta-adrenergic receptor binding in human endomyocardial biopsy tissue
JACC
Effects of the H2-receptor agonist impromidine in human myocardium from patients with heart failure due to mitral and aortic valve disease
J Cardiovasc Pharmacol
Myocardial performance and extracellular ionized calcium in a severely failing human heart
Ann Intern Med
Impaired beta-adrenergic inotropic response in severe heart failure
Circulation
Regulation of beta1- and beta2-adrenergic receptors in human atria
Circulation
Beta2-receptors are coupled to muscle contraction in human ventricular myocardium
Circulation
The classification of beta-adrenoceptors
Trends Pharmacol Sci
Beta receptor desensitization in lympho-cytes from patients with congestive heart failure
Pharmacologist
Correlation between beta-adrenergic receptors in human lymphocytes and heart
Circulation
Cited by (32)
Heart failure and its treatment from the perspective of sympathetic nerve activity
2022, Journal of CardiologyCitation Excerpt :However, adrenaline did not increase plasma noradrenaline levels in the rabbits with heart failure induced by doxorubicin both in the anesthetized rabbits and the pithed rabbits with stimulated sympathetic outflow [24]. These findings suggest that presynaptic β-receptors may be down-regulated by the elevated plasma noradrenaline caused by heart failure, which is consistent with a study that reported that β-receptors were down regulated in heart failure [25]. Thus, involvement of presynaptic β-receptors in noradrenaline release may be different according to the severity of heart failure.
The historical evolution of knowledge of the involvement of neurohormonal systems in the pathophysiology and treatment of heart failure
2019, Revista Portuguesa de CardiologiaCardiac vagal control in a knock-in mouse model of dilated cardiomyopathy with a troponin mutation
2017, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Therefore, we cannot rule out the possibility that peripheral, as well as central impairment also might contribute to the reduction of cardiac vagal activity in more advanced stages of congestive heart failure in our DCM mouse model. Although others have frequently reported downregulation of adrenergic signaling and postsynaptic dysfunction in sympathetic regulation of the heart in heart failure (Ruffolo and Kopia, 1986; Vatner et al., 1999), our data suggested that vagal postsynaptic function was preserved in the DCM mouse. Electrical stimulation of cervical vagal nerve at both 5 and 10 Hz increased cardiac interval and myocardial interstitial ACh level in WT mice as well as in DCM mice, and there were no differences in these responses between WT and DCM mice (Figs. 1 and 3).
Neonatal Blood Pressure Support: The Use of Inotropes, Lusitropes, and Other Vasopressor Agents
2012, Clinics in PerinatologyCitation Excerpt :Therefore, in neonates with escalating dopamine infusion, the pattern of receptor stimulation is first dopaminergic, then α-adrenergic, and finally β-adrenergic (Fig. 3).3,4,28 Of note is that the hemodynamic effects and the clinical response to dopamine (and other vasopressors and inotropes) is altered by downregulation of adrenergic receptors caused by the critical illness–associated prolonged endogenous and the treatment-associated exogenous receptor stimulation.27 Furthermore, because cardiovascular adrenergic receptor expression is regulated by corticosteroids,26 the documented higher incidence of relative adrenal insufficiency29 also contributes to the observed attenuated hemodynamic response and the development of vasopressor-dependence in preterm and term neonates.
Reduction of vasopressor requirement by hydrocortisone administration in a patient with cerebral vasospasm
2001, British Journal of AnaesthesiaCitation Excerpt :In animal studies, adrenoceptor down-regulation and decreased responsiveness occur when catecholamines are given in large doses and/or for long periods.7–9 Similar findings occur in human subjects.10–12 In this report, phenylephrine was infused for three days before a progressive increase in dose requirement, to achieve the same target blood pressure, was observed (Fig.1).