Plasma Adenosine Concentrations Are Elevated in Conscious Spontaneously Hypertensive Rats

Yamada, Kaoru; Goto, Akitoshi; Ishii, Masaaki; Yoshioka, Masanori; Matsuoka, Hiroaki; Sugimoto, Tsuneaki

doi:10.1111/j.1440-1681.1992.tb00505.x

Cited by 13 publications

(8 citation statements)

References 17 publications

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“…during restraint stress or during stimulation in the in vitro experiments) at a significantly lower concentration than in Wistar rats. Other possible mechanisms underlying the strain-dependent actions of capadenoson on the stress response and NE release of SHR could be differences in the density or the molecular architecture of adenosine A1 receptors [31], or higher plasma concentrations of adenosine in SHR [32]. In a previous study, a similar effect of a different partial adenosine-A 1 agonist, CVT-2759, was noted for the effects of adrenergic stimulation by isoproterenol in guinea pig myocytes.…”

Section: Discussionmentioning

confidence: 69%

Selective Attenuation of Norepinephrine Release and Stress-Induced Heart Rate Increase by Partial Adenosine A1 Agonism

et al. 2011

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The release of the neurotransmitter norepinephrine (NE) is modulated by presynaptic adenosine receptors. In the present study we investigated the effect of a partial activation of this feedback mechanism. We hypothesized that partial agonism would have differential effects on NE release in isolated hearts as well as on heart rate in vivo depending on the genetic background and baseline sympathetic activity. In isolated perfused hearts of Wistar and Spontaneously Hypertensive Rats (SHR), NE release was induced by electrical stimulation under control conditions (S1), and with capadenoson 6 · 10−8 M (30 µg/l), 6 · 10−7 M (300 µg/l) or 2-chloro-N6-cyclopentyladenosine (CCPA) 10−6 M (S2). Under control conditions (S1), NE release was significantly higher in SHR hearts compared to Wistar (766+/−87 pmol/g vs. 173+/−18 pmol/g, p<0.01). Capadenoson led to a concentration-dependent decrease of the stimulation–induced NE release in SHR (S2/S1 = 0.90±0.08 with capadenoson 6 · 10−8 M, 0.54±0.02 with 6 · 10−7 M), but not in Wistar hearts (S2/S1 = 1.05±0.12 with 6 · 10−8 M, 1.03±0.09 with 6 · 10−7 M). CCPA reduced NE release to a similar degree in hearts from both strains. In vivo capadenoson did not alter resting heart rate in Wistar rats or SHR. Restraint stress induced a significantly greater increase of heart rate in SHR than in Wistar rats. Capadenoson blunted this stress-induced tachycardia by 45% in SHR, but not in Wistar rats. Using a [35S]GTPγS assay we demonstrated that capadenoson is a partial agonist compared to the full agonist CCPA (74+/−2% A1-receptor stimulation). These results suggest that partial adenosine A1-agonism dampens stress-induced tachycardia selectively in rats susceptible to strong increases in sympathetic activity, most likely due to a presynaptic attenuation of NE release.

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Section: Discussionmentioning

confidence: 69%

Selective Attenuation of Norepinephrine Release and Stress-Induced Heart Rate Increase by Partial Adenosine A1 Agonism

et al. 2011

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“…Caffeine interferes with the local action of adenosine in the blood vessel wall. Because of the importance of adenosine regulation, caffeine use should be considered in relation to hypertension and stress 28 …”

Section: Caffeine Pharmacologymentioning

confidence: 99%

Caffeine and Stress: Implications for Risk, Assessment, and Management of Hypertension

Hartley

Lovallo

Whitsett

et al. 2001

J of Clinical Hypertension

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Caffeine use is widespread, and its consumption increases during periods of stress. Caffeine raises blood pressure by elevating vascular resistance, and this effect is larger and more prolonged in hypertensive patients than in normotensive. The pressor response to caffeine occurs equally in persons at rest and under stress. The elevated baseline pressures of the hypertensive patient are therefore increased by both caffeine and stress, potentially leading to undesirably high pressures. Such combined effects on blood pressure may potentially confound the evaluation of hypertension, and possibly reduce the effectiveness of antihypertensive therapy. These effects are not abolished by pharmacologic tolerance to caffeine, as tolerance may not be complete with daily intake. The contribution of caffeine's effects to the development of hypertension warrants continued study, and caffeine use by patients merits consideration in terms of assessment and management of this disorder.

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“…Plasma adenosine concentrations are elevated in conscious SHR (Yamada et al, 1992) and in Dahl saltsensitive rats (Yamada et al, 1995). Adenosine has been claimed to activate the vascular renin-angiotensin system in hypertensive subjects (Taddei et al, 1992).…”

Section: A Hypertensionmentioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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Plasma Adenosine Concentrations Are Elevated in Conscious Spontaneously Hypertensive Rats

Cited by 13 publications

References 17 publications

Selective Attenuation of Norepinephrine Release and Stress-Induced Heart Rate Increase by Partial Adenosine A1 Agonism

Selective Attenuation of Norepinephrine Release and Stress-Induced Heart Rate Increase by Partial Adenosine A1 Agonism

Caffeine and Stress: Implications for Risk, Assessment, and Management of Hypertension

Purinergic Signaling and Blood Vessels in Health and Disease

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