Mechanisms of adenosine-induced renal vasodilatation in hypertensive patients

Wierema, Thomas K.A.; Houben, A. J. H. M.; Postma, Cornelis T.; Koster, Derk; Engelshoven, Jos M. A. van; Smits, P.; Leeuw, Peter W. de

doi:10.1097/01.hjh.0000180160.89264.9d

Cited by 20 publications

(16 citation statements)

References 28 publications

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“…4b). This would be consistent with other studies showing no direct eff ect of caff eine on resting blood fl ow [37][38][39] and/or induced vascular contractility 40 . Along these lines, there is confl ict- Table 1.…”

Section: Eff Ect Of Caff Eine On Blood Fl Owsupporting

confidence: 93%

Caffeine Does Not Modulate Nutritive Blood Flow to Rat Gastric Submucosa - A Microdialysis Study

Cibíček¹,

Zivna²,

Cibicek³

et al. 2008

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Background and Aims:Coff ee irritates the gastric mucosa disrupting its barrier and increasing the risk of peptic ulcers. However, caff eine's contribution to these eff ects has not yet been elucidated. In this study we looked at the local eff ect of caff eine on the microcirculation and nitric oxide production in rats together with systemic marker of oxidative stress malondialdehyde as possible mechanisms whereby caff eine might participate in mucosal barrier impairment.Materials and Methods: Four groups of rats were anesthetized and administered as a bolus four diff erent intraperitoneal doses of caff eine (0, 1, 10 and 50 mg kg -1 b.wt.). The gastric submucosal microcirculation and nitric oxide production were then recorded for 2.5 hours by in situ microdialysis using the fl ow marker ethanol. At the completion of the experiments, plasma caff eine and malondialdehyde levels as well as morphological mucosal injury were determined.Results: There were no major diff erences in the macro-or microscopic pictures of the mucosa among the groups. Local microcirculatory (ethanol out/in ratio) and nitric oxide monitoring failed to demonstrate statistically signifi cant changes as did measurement of plasma malondialdehyde in response to caff eine injections.Conclusions: Caff eine per se seems unlikely to contribute to the gastric mucosal barrier injury associated with coff ee consumption by alterations in nutritive blood fl ow, nitric oxide production or aggravation of systemic oxidative stress. This information is relevant for better understanding of the mechanisms involved in caff eine-mediated infl uences on gastric physiology in relation to the irritant eff ects of coff ee.

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Section: Eff Ect Of Caff Eine On Blood Fl Owsupporting

confidence: 93%

Caffeine Does Not Modulate Nutritive Blood Flow to Rat Gastric Submucosa - A Microdialysis Study

Cibíček¹,

Zivna²,

Cibicek³

et al. 2008

BIOMED PAP

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“…39,40 In experimental models, caffeine attenuated the endotoxin-induced release of cytokines and augmented endotoxin-induced increases in plasma catecholamines and PRA: caffeine, most likely through the interaction with adenosine receptors and interference with antiinflammatory and/or glomerular hemodynamic effects of adenosine, augments proteinuria and stimulates some of the key proliferative mechanisms involved in glomerular remodeling and sclerosis. 41 Adenosine is an endogenous nucleoside with potent vasodilatory capacities: its mechanisms of action, however, remain elusive. Adenosine induces vasodilatation in the human hypertensive kidney and this effect is mediated by the adenosine receptor.…”

Section: Discussionmentioning

confidence: 99%

Coffee, nutritional status, and renal artery resistive index

et al. 2010

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Background: The relationship between nutrition and atherosclerosis is known, even dissociated from protein malnutrition. Cardiovascular impact of several nutrients is known; among them the action of coffee is still debated and cardiovascular effect of caffeine has been investigated without definite results. Objective: The aim of this study is to investigate whether coffee habits, and/or quantity of coffee consumption, have any relationship with renal resistive index (RRI), a hallmark of arterial stiffness (AS). The relationship of AS with nutritional status assessed by body composition and serum albumin, insulin resistance (assessed by HOMA), and renal function assessed by glomerular filtration rate (GFR) is concurrently investigated. Methods: This study was done with 221 consecutive patients, without diabetes, cancer, liver, renal, and heart disease, referred for clinical noninvasive assessment and nutritional counseling: 124 essential hypertensive and 97 nonhypertensive patients were eligible. Personalized Mediterranean diet, physical activity increase, and smoking withdrawal counseling were provided. Results: By multiple linear regression, fat-free mass (FFM), HOMA (positive relationship), and number of cups of coffee/day (negative relationship) account for 17.2% of the variance to RRI. By odds ratios lower risk to increased RRI is associated with higher serum albumin, higher hemoglobin, and FFM; greater risk is associated with hypertension, insulin resistance (HOMA ≥ 3.0), and renal insufficiency (GFR ≤ 90); coffee, assessed by number of cups/day, reduces risk. Conclusion: Coffee use is inversely associated with RRI. Habitual coffee users have risk protection to higher RRI; lower serum albumin, insulin resistance, and renal insufficiency are associated with greater RRI.

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“…A 2 receptors mediate vasorelaxation in part via the endothelium and release of NO, and Purinergic Signaling and Blood Vessels endothelial dysfunction may cause the attenuation of adenosine receptor-mediated responses seen in aortae of SHR (Fahim et al, 2001;Nejime et al, 2009). However, NO plays, at most, a minor part in adenosine-induced vasodilation in human hypertensive kidney (Wierema et al, 2005). A 2A receptor activation is required for adenosine-induced mesenteric relaxation, and a decreased density of A 2A receptors may contribute to the decreased mesenteric relaxation in portal hypertensive rabbit (de Brito et al, 2002).…”

Section: A Hypertensionmentioning

confidence: 99%

“…Hypertension is a feature of chronic renal disease, and it has been claimed that this is largely due to sympathetic overactivity triggered by afferent signals emanating from the kidney and resetting sympathetic tone by stimulation of hypothalamic centers (Orth et al, 2001). Both essential hypertensive patients and patients with renal artery stenosis show a dose-dependent vasodilation after adenosine infusion (Wierema et al, 1998(Wierema et al, , 2005. In raisedtone perfused kidneys from normal rats ATP elicited constriction at low doses and vasodilatation at higher doses; ATP-mediated vasoconstriction was increased in hyperthyroid kidneys and severely attenuated in kidneys from hypothyroid rats, whereas the vasodilator response in kidneys from hypothyroid rats was abolished (Vargas et al, 1996).…”

Section: Purinergic Signaling and Blood Vesselsmentioning

confidence: 99%