Coffee Blunts Mental Stress–Induced Blood Pressure Increase in Habitual but Not in Nonhabitual Coffee Drinkers

Sudano, Isabella; Spieker, Lukas E.; Binggeli, Christian; Ruschitzka, Frank; Lüscher, Thomas F.; Noll, Georg; Corti, Roberto

doi:10.1161/01.hyp.0000177448.56745.c7

Cited by 51 publications

(32 citation statements)

References 23 publications

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“…A test that relies on sympathetic mediation for NO release is the cold pressor test: A subject submerges her hand for 2 min in ice water. In healthy subjects, α 2-adrenoceptor-dependent vasodilatation as seen, e.g., in quantitative coronary angiography will prevail over α 1-adrenoceptor-mediated constriction (vice versa in dysfunctional endothelium) [32,33].…”

Section: How Can We Measure Endothelial Function?mentioning

confidence: 99%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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The endothelium has increasingly been recognized as a smart barrier and a key regulator of blood flow in microand macrovascular beds. Endothelial dysfunction marks a stage of atherosclerosis and is an important prognostic marker for cardiovascular disease. Yet, some people who tend to be slim and physically active and with rather low blood pressure show a propensity to respond to certain stimuli such as emotional stress with endothelial-mediated vascular dysregulation (Flammer syndrome). This leads to characteristic vascular symptoms such as cold hands but also a risk for vascularmediated diseases such as normal-tension glaucoma. It is the aim of this review to delineate the differences between Flammer syndrome and its Bcounterpart^endothelial dysfunction in the context of cardiovascular diseases.

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Section: How Can We Measure Endothelial Function?mentioning

confidence: 99%

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

et al. 2017

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“…Under resting conditions, caffeine causes an increase in blood pressure in caffeine-withdrawn subjects (50), whereas habitual coffee drinkers exhibited less or no effect of caffeine on blood pressure (51). Furthermore, caffeine-naive individuals may rapidly develop tolerance to its pressor effects over 2-3 d. However, other studies found that some people do not develop tolerance to the blood pressure-elevating effects of caffeine (52) and supplementation with caffeine alone has also been reported to evoke similar changes in blood pressure in habitual and nonhabitual caffeine users (53). Post hoc analyses conducted with the use of data from our studies (17,18) also found no differences between habitual and nonhabitual caffeine users in the effect of the ED in increasing blood pressure after 24 h of caffeine avoidance.…”

Section: Impact Of Caffeinementioning

confidence: 99%

Energy Drinks and Their Impact on the Cardiovascular System: Potential Mechanisms

Grasser

Miles-Chan

Charrière

et al. 2016

Advances in Nutrition

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Globally, the popularity of energy drinks is steadily increasing. Scientific interest in their effects on cardiovascular and cerebrovascular systems in humans is also expanding and with it comes a growing number of case reports of adverse events associated with energy drinks. The vast majority of studies carried out in the general population report effects on blood pressure and heart rate. However, inconsistencies in the current literature render it difficult to draw firm conclusions with regard to the effects of energy drinks on cardiovascular and cerebrovascular variables. These inconsistencies are due, in part, to differences in methodologies, volume of drink ingested, and duration of postconsumption measurements, as well as subject variables during the test. Recent well-controlled, randomized crossover studies that used continuous beat-to-beat measurements provide evidence that cardiovascular responses to the ingestion of energy drinks are best explained by the actions of caffeine and sugar, with little influence from other ingredients. However, a role for other active constituents, such as taurine and glucuronolactone, cannot be ruled out. This article reviews the potentially adverse hemodynamic effects of energy drinks, particularly on blood pressure and heart rate, and discusses the mechanisms by which their active ingredients may interact to adversely affect the cardiovascular system. Research areas and gaps in the literature are discussed with particular reference to the use of energy drinks among high-risk individuals. Adv Nutr 2016;7:950-60.

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“…The signal was integrated with a 0.1-second time constant, amplified with a gain of 50 000 to 80 000, band-pass filtered (700 to 2000 Hz), and acquired with a sampling rate of 1000 Hz through a digital acquisition system (ACQ-16, Gould Electronics). MSNA was identified according to the following criteria outlined in previous studies 3,16,17 : (1) electric stimulation through the electrode in the peroneal nerve elicited involuntary leg contractions but no paresthesia; (2) tapping or stretching the innervated muscle region elicited afferent mechanoreceptor discharges, whereas stroking the skin did not; and (3) spontaneous pulse-synchronous bursts, which increase in frequency during voluntary apnea but not after a loud noise, were displayed by the neurogram. The recording was considered acceptable if the signal:noise ratio exceeded the value of 3.…”

Section: Measurementsmentioning

confidence: 99%

Interactions Between Sympathetic Nervous System and Endogenous Endothelin in Patients With Essential Hypertension

et al. 2011

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Abstract-Experimental evidence indicates that endothelin 1 stimulates the sympathetic nervous system by activation of the subtype A receptor. The aim of the present study was to assess whether this mechanism is active in humans and to investigate its potential role in the pathogenesis of essential hypertension. In 15 hypertensive patients and 12 normotensive subjects, blood pressure, heart rate, and muscle sympathetic nerve activity were evaluated during intravenous 20-minute infusion of BQ123 (0.1 mg/kg per hour), an endothelin A receptor antagonist, and sodium nitroprusside (SNP; 0.4 g/kg per minute). In hypertensive patients, blood pressure was reduced similarly by BQ123 and SNP. In contrast, the increase in muscle sympathetic nerve activity induced by BQ123 (from 52.0Ϯ4.9 to 56.8Ϯ5.5 bursts per 100 heartbeats; PϽ0.05 versus baseline) was significantly lower (PϽ0.05) than that induced by SNP (from 50.6Ϯ4.9 to 61.1Ϯ5.1 bursts per 100 heartbeats; PϽ0.05 versus baseline). In normotensive subjects, SNP reduced blood pressure and increased muscle sympathetic activity, whereas BQ123 was ineffective. Thus, in a subgroup (nϭ9) of normotensive subjects, we administered BQ123 at a higher dose ( Key Words: hypertension Ⅲ sympathetic nervous system Ⅲ endothelin Ⅲ microneurography Ⅲ BQ123 E ssential hypertension is characterized by increased sympathetic nervous system (SNS) activity, as clearly demonstrated by sensitive techniques, such as the norepinephrine (NE) spillover method 1 and microneurographic quantification of nerve traffic. 2 SNS activation, which is already present in normotensive offspring of hypertensive patients, 3 is peculiar to the essential hypertensive state 2 and parallels the degree of blood pressure (BP) increase. 2 In addition, it may exert deleterious metabolic and cardiovascular effects, accelerating progression of the target organ damage associated with hypertension. 4 Endothelin 1 (ET-1) is a vasoconstrictor and mitogenic peptide produced by endothelial cells. Its important role in regulation of vascular tone and structure is well established. 5 Essential hypertension is characterized by increased ET-1 vasoconstrictor tone, 6,7 which seems to be a consequence of reduced NO availability. 7 Endothelin receptor antagonists, particularly those acting on endothelin A (ET A ) receptors, are a promising therapeutic option in patients with resistant 8 and renoparechimal 9 hypertension. The role of the endothelin system in cardiovascular homeostasis is not limited to its direct vascular effects but also involves neural regulation of vasomotor tone. 10 Experimental evidence suggests that ET-1 can stimulate central and peripheral SNS activity through ET A receptors. 11,12 Although intracerebral administration of ET-1 can increase BP and SNS activity mainly through ET A receptors in hypertensive as well normotensive animals, 11,12 administration of an ET A receptor antagonist induces the opposite effect in hypertensive animals only, suggesting a specific sympathoexcitatory role for the endothelin system in...

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Coffee Blunts Mental Stress–Induced Blood Pressure Increase in Habitual but Not in Nonhabitual Coffee Drinkers

Cited by 51 publications

References 23 publications

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

Endothelial dysfunction in cardiovascular disease and Flammer syndrome—similarities and differences

Energy Drinks and Their Impact on the Cardiovascular System: Potential Mechanisms

Interactions Between Sympathetic Nervous System and Endogenous Endothelin in Patients With Essential Hypertension

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