Mechanisms of the circadian regulation of β-adrenoceptor density and adenylyl cyclase activity in cardiac tissue from normotensive and spontaneously hypertensive rats

Witte, Klaus; Parsa-Parsi, Ramin W; Vobig, Michael A.; Lemmer, Björn

doi:10.1016/0022-2828(95)90055-1

Cited by 25 publications

(15 citation statements)

References 29 publications

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“…At the same time, the decreased number and function of β 1 AR, relatively increased the activity of β 2 AR in the heart [41] in the hypertensive individuals. This results were supported by Witte et al [42] who found that the total density of βAR in the membrane of cardiomyocytes declined significantly, due to the decline of the density of β 1 AR in spontaneous hypertension. Therefore, when met with stress, instantaneous emergence of a large number of catecholamines activate more β 2 AR in hypertensive patients.…”

Section: Scm Profile In Patients With Chronic Diseasessupporting

confidence: 80%

Stress Cardiomyopathy was Prone to Occur in Patients with Chronic Diseases: Maybe a Good Thing

Chong¹,

Hou²,

Zhang³

2016

Cardiovasc Pharm Open Access

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Background：Stress Cardiomyopathy (SCM) is an increasingly reported disease as a syndrome of acute, severe, but reversible, which is commonly triggered by an acute strong physical or emotional stress. But little is known whether chronic diseases may contribute to the occurrence of SCM.Method：The case reports about SCM from January 1998 to May 2014 were searched in the PubMed using the Medical Subject Headings: "tako-tsubo cardiomyopathy" or "stress cardiomyopathy" or ''ampulla syndrome'' or ''apical ballooning syndrome'' or ''broken heart syndrome''. The publications were excluded which didn't meet the inclusion criteria. SCM patients with and without chronic diseases were CD group and NCD group, respectively. The CD group was further classified into nine subgroups according to underlying chronic diseases. The circulatory diseases group which had the highest percentage in CD group was analyzed further.Results: 1331 literatures about SCM were collected, in which 1052 documents were eligible. In these documents, 1206 patients were reported, 795 had chronic diseases, 411 had no significant past medical history. The average age in NCD group was younger than that in CD group (57.3 ± 0.9 years versus 62.4 ± 0.6 years, P < 0.01). The number of SCM patients with Circulatory diseases was the most, then was Endocrine, Digestive, Respiratory, etc. The proportion of hypertension was 74.0% in circulatory diseases followed by dyslipidemia 29.3%, arrhythmia 10.1%, coronary artery disease 5.8%, etc.Conclusion：According to our results, the chronic diseases, especially hypertension, rose the rate of occurrence and delayed the onset age of SCM.

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Section: Scm Profile In Patients With Chronic Diseasessupporting

confidence: 80%

Stress Cardiomyopathy was Prone to Occur in Patients with Chronic Diseases: Maybe a Good Thing

Chong¹,

Hou²,

Zhang³

2016

Cardiovasc Pharm Open Access

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“…Surprisingly, we also found evidence for the existence of endogenous ≈12-h rhythm in cardiovascular biomarkers, specifically in platelet aggregability and in the reactivity to exercise of epinephrine and norepinephrine. Such 12-h patterns could be related to 12-h rhythms as have been demonstrated in animal studies, e.g., cardiac β-adrenergic receptor density and function (23), hormonal rhythms with a shaping role for the SCN (24), and gene transcription in various tissues, including liver, heart, kidney, and adrenals (25). Endogenous 12-h rhythms may have specific relevance to anticipating the daily transitions of dusk and dawn (25).…”

Section: Discussionmentioning

confidence: 73%

“…S2). There are daily rhythms in sensitivity to catecholamines in different organ systems including the heart, due in part to the down-regulation of adrenergic receptors after stimulation (23,(37)(38)(39). The circadian-mediated rapid rise in epinephrine that we observed at ≈8:00 AM may be particularly problematic in the setting of the concomitant circadian peak in cortisol because cortisol has permissive effects on adrenergic receptors (40).…”

Section: Discussionmentioning

confidence: 80%

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Scheer

Evoniuk

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

265

249

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The risk of adverse cardiovascular events peaks in the morning (≈9:00 AM) with a secondary peak in the evening (≈8:00 PM) and a trough at night. This pattern is generally believed to be caused by the day/night distribution of behavioral triggers, but it is unknown whether the endogenous circadian system contributes to these daily fluctuations. Thus, we tested the hypotheses that the circadian system modulates autonomic, hemodynamic, and hemostatic risk markers at rest, and that behavioral stressors have different effects when they occur at different internal circadian phases. Twelve healthy adults were each studied in a 240-h forced desynchrony protocol in dim light while standardized rest and exercise periods were uniformly distributed across the circadian cycle. At rest, there were large circadian variations in plasma cortisol (peak-to-trough ≈85% of mean, peaking at a circadian phase corresponding to ≈9:00 AM) and in circulating catecholamines (epinephrine, ≈70%; norepinephrine, ≈35%, peaking during the biological day). At ≈8:00 PM, there was a circadian peak in blood pressure and a trough in cardiac vagal modulation. Sympathetic variables were consistently lowest and vagal markers highest during the biological night. We detected no simple circadian effect on hemostasis, although platelet aggregability had two peaks: at ≈noon and ≈11:00 PM. There was circadian modulation of the cardiovascular reactivity to exercise, with greatest vagal withdrawal at ≈9:00 AM and peaks in catecholamine reactivity at ≈9:00 AM and ≈9:00 PM. Thus, the circadian system modulates numerous cardiovascular risk markers at rest as well as their reactivity to exercise, with resultant profiles that could potentially contribute to the day/night pattern of adverse cardiovascular events.

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“…A number of studies found that both AR-b 1 and AR-b 2 were downregulated in SHR. [28][29][30][31] Chruscinski et al 32,33 reported that AR-b 1 had a dominant role in mediating vasodilation in mice. Hirota et al 34 found AR-b 2 stimulation improved inotropic and lusitropic function in the failing heart and Communal et al 35 reported that AR-b 2 inhibited cardiocyte apoptosis through a Gi-coupled pathway in rats.…”

Section: Discussionmentioning

confidence: 99%

Is overall blockade superior to selective blockade of adrenergic receptor subtypes in suppressing left ventricular remodeling in spontaneously hypertensive rats?

et al. 2010

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To test the hypothesis that nonselective blockade of adrenergic receptor (AR) subtypes is superior to selective blockade of AR subtypes in suppressing left ventricular (LV) remodeling induced by hypertension. Sixty-four spontaneously hypertensive rats (SHR) were randomly divided into four groups: bisoprolol-treated, propranolol-treated, carvedilol-treated and no treatment groups (n¼16, each). Sixteen Wistar-Kyoto (WKY) rats served as a control group. Echocardiography and cardiac catheterization were carried out to record the mitral flow velocity ratio of E wave to A wave (E/A), LV mass index (LVMI), maximal rising (dp/dt max ) and falling (Àdp/dt max ) rate of the LV pressure and LV relaxation time constant (s). The mRNA and protein expression levels of AR, protein kinase(PK) and G-protein subtypes, intracellular free calcium (Ca 2+ ) concentration and cardiocyte apoptoisis rate were determined. Three drug-treated groups showed higher velocity ratio of E wave to A wave (E/A) and Àdp/dt max and lower systolic blood pressure (SBP), LVMI, s, apoptosis rate and intracellular free Ca 2+ concentration than the no treatment group. The mRNA expression levels of AR-a 1B in the carvedilol group were significantly lower than the other two drug-treated groups. The mRNA expression levels of AR-b 1 , AR-b 2 and Gsa were significantly higher in the three drug-treated groups than in the no treatment group, with the expression levels of AR-b 2 being the highest in the carvedilol-treated group. The protein expression levels of PKA and PKC subtype a and d were lower in the three drug-treated groups than in the no treatment group. Overall blockade of AR subtypes is not superior to selective blockade of AR subtypes in suppressing LV remodeling in SHR. Although carvedilol is the most effective in attenuating cardiocyte apoptosis, normalizing AR-a 1B and Gsa expression and increasing AR-b 2 expression.

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Mechanisms of the circadian regulation of β-adrenoceptor density and adenylyl cyclase activity in cardiac tissue from normotensive and spontaneously hypertensive rats

Cited by 25 publications

References 29 publications

Stress Cardiomyopathy was Prone to Occur in Patients with Chronic Diseases: Maybe a Good Thing

Stress Cardiomyopathy was Prone to Occur in Patients with Chronic Diseases: Maybe a Good Thing

Impact of the human circadian system, exercise, and their interaction on cardiovascular function

Is overall blockade superior to selective blockade of adrenergic receptor subtypes in suppressing left ventricular remodeling in spontaneously hypertensive rats?

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