Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats.

Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Research Abstract Details 

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Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Abstract Text:

Ming-Guo Feng,L Gabriel Navar,

Adenosine is an important paracrine agent regulating renal hemodynamics via adenosine A1 and A2 receptors. To determine the interactions between adenosine A1 and A2 receptors and the possible role of adenosine as a modulator of afferent arteriolar autoregulatory responses, videomicroscopic measurements of afferent arteriolar dimensions were performed at different perfusion pressures (from 100 to 125 and 150 mm Hg) using the isolated-blood-perfused rat juxtamedullary nephron preparation. Single afferent arterioles were visualized and superfused with low or high concentrations of adenosine, either alone or with the adenosine A1 receptor antagonist 8-noradamantan-3-yl-1,3-dipropylxanthine (10 micromol/L) or the adenosine A2 receptor antagonist dimethyl-1-propargylxanthine (10 micromol/L). Adenosine (20 micromol/L) decreased afferent arteriolar diameter by -9.0+/-0.9%, and this effect was enhanced by dimethyl-1-propargylxanthine (10 micromol/L) to -16.1+/-1.2%. However, autoregulatory capability was maintained. Adenosine-induced vasoconstriction was prevented by 8-noradamantan-3-yl-1,3-dipropylxanthine (10 micromol/L) with diameter increasing by 9.6+/-1.2%. Adenosine receptor saturation with a high concentration of adenosine (120 micromol/L) or blocking A1 receptors with 8-noradamantan-3-yl-1,3-dipropylxanthine in the presence of adenosine resulted in marked vasodilation and marked impairment of autoregulatory responses to increases in perfusion pressure (-1.5+/-1.1% and -3.5+/-0.9%). However, afferent arteriolar autoregulatory responses to elevations in perfusion pressure were restored after blockade of A2 receptors alone or in combination with A1 receptor blockade. During treatment with dimethyl-1-propargylxanthine in the presence of adenosine receptor saturation (120 micromol/L), afferent arteriolar autoregulatory responses were intact (-16.5+/-1.6% and -26.4+/-2.1%). These results indicate that the interactions between adenosine A1 and A2 receptors exert important modulatory influences on afferent arteriolar tone and autoregulatory capability. Activation of A2 receptors abrogates the counteracting influences of A1 receptors leading to marked vasodilation and decreased afferent arteriolar autoregulatory efficiency.

Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Publishing Authors By Initials

MG Feng,LG Navar,

For similar heterocyclic compounds: alkaloids: xanthines research abstracts see: heterocyclic compounds: alkaloids: xanthines research

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Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Hypertension

VOLUME: 50

Page Numbers: 744-9

Journal Abbreviation: Hypertension

ISSN: 1524-4563

DAY: 30

MONTH: 07

YEAR: 2007

Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Information

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LANGUAGE: eng

NlmUniqueID: 7906255

Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Keywords Mesh Terms:

KEYWORDS: Xanthines

MESH TERMS: pharmacology

Chemical & Substance for Abstract: Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats. Information

Substance Name: Theobromine

Registry Number: 83-67-0

Grant and Affiliation Information for Adenosine A2 receptor activation attenuates afferent arteriolar autoregulation during adenosine receptor saturation in rats.

AFFILIATION: Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, LA 70112, USA. mfeng@tulane.edu

Country: United States

AGENCY: United States NCRR

GRANT: P20RR017659

ACRONYM: RR

MEDLINETA: Hypertension

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