Modulation of adrenergic receptors during regression of cardiac hypertrophy

Matsui, Hiroki; Makino, Naoki; Yano, Ken’ichi; Nakanishi, H; Hata, Tomoko; Yanaga, Takashi

doi:10.1097/00004872-199412000-00006

Cited by 9 publications

(4 citation statements)

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“…In contrast to ␤-adrenergic and muscarinic receptors, relatively little is known concerning the effect of hypoxia and of acclimatization to hypoxia on myocardial ␣-adrenergic receptor function. ␣-Adrenergic receptors have been implicated in the development of left ventricular hypertrophy secondary to aortic coarctation (14,23). Chronic hypoxia is an interesting model because it results in right ventricular hypertrophy (19) with little or no change in left ventricle mass.…”

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confidence: 99%

Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O₂ transport in exercise

Favret

Richalet

Henderson

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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The time course of changes in rat myocardial alpha(1)- and beta-adrenoceptors and of muscarinic cholinergic (M-Ach) receptor characteristics was studied parallel with the changes in exercise systemic O(2) transport during a 21-day period of hypoxia (barometric pressure 380 Torr) to assess the effects of receptor modification during acclimatization on maximal exercise capacity. Hypoxia resulted in polycythemia, pulmonary hypertension, right ventricular hypertrophy, and transient left ventricular weight loss. Maximal O(2) consumption at 30 min of hypoxia was reduced to 60% of the normoxic value and remained unchanged. This was partly due to a gradual decrease in maximal cardiac output and heart rate (HR(max)), which offset the increase in blood O(2) content. HR(max) correlated positively (r = 0.994) with beta-adrenoceptor density and negatively (r = -0.964) with M-Ach-receptor density, suggesting that HR(max) reduction results from intrinsic changes in myocardial receptor characteristics leading to reduced responses to adrenergic stimulation and elevated responses to cholinergic stimulation. alpha-Adrenoceptor density in both ventricles increased initially to eventually fall below normoxic values. The dissociation between the different patterns of right and left ventricular weight and the similar pattern of alpha-adrenoceptor change in both ventricles do not support a role for these receptors on right ventricular myocardial hypertrophy.

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confidence: 99%

Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O₂ transport in exercise

Favret

Richalet

Henderson

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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“…22 Furthermore, the heterogeneous efficacy in the regression of LVH induced by different antihypertensive drugs in hypertensive patients, despite similar blood pressure decreases, may only be explained by the non-haemodynamic mechanisms involved in the pathogenesis of this complication. 23 In this sense, LVH can only be prevented if blood pressure reduction is not associated with reflex cardiac sympathetic activation. 24 From another aspect, the myocardium in experimental animal models of hypertension is known to exhibit reduced cardiac inotropic and chronotropic responses to adrenergic stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…5 In fact, the sympathetic outflow to the heart, kidneys and skeletal muscle vasculature is commonly increased in younger patients with essential hypertension. 6 Cardiac inotropic and chronotropic responses to adrenergic stimuli have been reported to be reduced Correspondence: Dr Jordi Calls, Nephrology Unit, Fundació n Hospital de Manacor, Carretera de Manacor a Alcú dia s/n, 07500 Manacor, Mallorca, Islas Baleares, Spain Received 22 January 1999; revised 2 July 1999; accepted 23 July 1999 body mass index (P Ͻ 0.01), plasma noradrenaline levels (P Ͻ 0.05) and ␤ 2 -adrenoceptor density (P Ͻ 0.05) were higher in hypertensives than in controls. Left ventricular mass index correlated with body mass index both in normotensives and hypertensives, as well as with plasma noradrenaline levels only in normotensives.…”

Section: Introductionmentioning

confidence: 99%

β-adrenergic receptor density and function in left ventricular hypertrophy in young essential hypertensives

et al. 2000

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A sympathetic overactivity has been reported in the early stages of essential hypertension and has been involved in the pathogenesis of left ventricular hypertrophy (LVH) in essential hypertension. The state of ␤ 2 -adrenergic receptors as related to the presence of this complication was investigated in a group of 15 essential hypertensive patients and compared to 10 normotensive control subjects. Left ventricular mass index was determined by bidimensional echocardiography. Plasma catecholamine levels were measured by a radioenzymatic assay. ␤ 2 -adrenoceptor density was measured in intact lymphocytes by radioligand binding assay, using the hydrophilic ligand CGP 12177. ␤ 2 -adrenoceptor function was assessed by measuring intracellular cAMP levels in isoproterenol-stimulated lymphocytes. Left ventricular mass index (P Ͻ 0.05),

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“…There is increasing evidence that ACE inhibition attenuates sympathetic responses through an as yet undefined mechanism 11 . Possible mechanisms include the reduction in tissue AII concentrations with a consequential reduction in the facilitatory action of AII on adrenergic neurotransmission, 6 enhanced bradykinin and prostaglandin accumulation 12 or a reduction in α 1 adrenergic receptor number 13 …”

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confidence: 99%

Selective AT1 Receptor Antagonism Enhances Sympathetically Mediated Vasoconstriction in Man

Lyons

Jackson

Swift

2007

Clin Pharmacol Ther

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The vasoconstrictive action of angiotensin II (AII) is partly, sympathetically mediated and angiotensin-converting enzyme (ACE) inhibitors appear to exert a sympatholytic effect. We examine the effect of an orally administered, selective AT(1) receptor antagonist (losartan 50 mg) on sympathetically mediated vasoconstriction in healthy volunteers in an observer blind crossover study. Seven healthy, normotensive volunteers (21-32 years), were studied on two occasions at the end of each 6-week treatment period (losartan or placebo). Forearm blood flow (FABF) (ml/dl forearm/min) was measured by venous occlusion plethysmography during the application of lower body negative pressure (LBNP) (-20 cm H(2)O) and at the end of each incremental infusion of norepinephrine (60, 120, and 240 pmol/min). Comparison of blood flow changes was by repeated measures analysis of variance; P<0.05 was taken as statistically significant. Losartan did not alter blood pressure compared to placebo. It did significantly enhance LBNP-induced vasoconstriction in both the left arm compared to placebo (-36.6+/-3.4 vs -23.5+/-3.3%; P=0.017) and the right arm compared to placebo (-39.5+/-3.8 vs -21.0+/-3.6%; P=0.005). The FABF response to all doses of infused norepinephrine (60, 120, and 240 pmol/min) was also enhanced by losartan compared to placebo (-35.0+/-2.7 vs -18.2+/-6.0%; -43.6+/-4.3 vs -28.6+/-5.8%, and -53.9+/-3.2 vs -42.5+/-6.8%; P=0.057, respectively. Losartan enhances locally mediated sympathetic vasoconstriction in the forearm circulation of man, probably through its effect on circulating AII concentrations and we postulate that the adrenergic sympathetic constrictor action of AII is not mediated by the AT(1) receptor or is surmountable at this receptor.

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Modulation of adrenergic receptors during regression of cardiac hypertrophy

Cited by 9 publications

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Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O₂ transport in exercise

Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O₂ transport in exercise

β-adrenergic receptor density and function in left ventricular hypertrophy in young essential hypertensives

Selective AT1 Receptor Antagonism Enhances Sympathetically Mediated Vasoconstriction in Man

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Modulation of adrenergic receptors during regression of cardiac hypertrophy

Cited by 9 publications

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Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O2 transport in exercise

Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O2 transport in exercise

β-adrenergic receptor density and function in left ventricular hypertrophy in young essential hypertensives

Selective AT1 Receptor Antagonism Enhances Sympathetically Mediated Vasoconstriction in Man

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Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O₂ transport in exercise

Myocardial adrenergic and cholinergic receptor function in hypoxia: correlation with O₂ transport in exercise