Species Differences in Renal Vascular Effects of Dipyridamole and in the Potentiation of Adenosine Action by Dipyridamole

Sakai, Kazushige; Aono, Junichiro; Haruta, Koichi

doi:10.1097/00005344-198105000-00002

Cited by 13 publications

(5 citation statements)

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“…In the heart, dipyridamole enhances the coronary vasodilation produced by adenosine (Feigl, 1983). likewise, the renal vasoconstriction produced by the intrarenal injection of adenosine is augmented in the presence of dipyridamole (Sakai et al, 1981). In the present study, bolus injections of adenosine produced transient vasoconstrictions which were enhanced during the infusion of dipyridamole.…”

Section: Discussionsupporting

confidence: 57%

Dipyridamole decreases glomerular filtration in the sodium-depleted dog. Evidence for mediation by intrarenal adenosine.

Arend

Thompson

Spielman

1985

Circulation Research

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SUMMARY. To determine the renal effects of inhibiting the uptake and subsequent metabolism of endogenous adenosine, dipyridamole, a nucleoside transport inhibitor, was infused intrarenally into anesthetized dogs. Dipyridamole (24 MgAg per min) inhibited the cellular extraction of [ 14 C]adenosine (72 ± 3% vs. 9 ± 3%) and elevated the excretion of endogenous adenosine (0.60 ± 0.08 to 1.70 ± 0.21 nmol/min, P < 0.05). The action of exogenous adenosine to decrease glomerular filtration rate is known to be enhanced by sodium depletion, and is minimal or absent in sodium-loaded animals. To ascertain whether dietary sodium intake alters the renal effects of elevated endogenous adenosine, dipyridamole was infused into sodium-depleted and sodiumloaded dogs. In the sodium-depleted dogs (n = 9), dipyridamole infusion decreased the glomerular filtration rate by 59 ± 7% (20 ± 1 to 8 ± 2 ml/min, P < 0.05) which returned to control levels within 30 minutes after stopping infusion of dipyridamole. Renal vascular resistance was unchanged during dipyridamole infusion. In the sodium-loaded dogs (n = 5), dipyridamole had no effect on glomerular filtration rate (22 ± 4 vs. 25 ± 3 ml/min) or renal vascular resistance. In a separate series of sodium-depleted dogs (n = 8), the dipyridamole-induced decrease in glomerular filtration rate was completely reversed or inhibited by theophylline, an adenosine receptor antagonist. These experiments demonstrate that inhibition of cellular uptake of adenosine elevates adenosine levels, that dipyridamole decreases glomerular filtration rate in sodium-depleted but not sodium-loaded dogs, and that the decrease in glomerular filtration rate is inhibited by theophylline. We conclude that the decrease in glomerular filtration rate during dipyridamole administration is mediated by increased endogenous adenosine. (Circ Res 56: 242-251, 1985)

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Section: Discussionsupporting

confidence: 57%

Dipyridamole decreases glomerular filtration in the sodium-depleted dog. Evidence for mediation by intrarenal adenosine.

Arend

Thompson

Spielman

1985

Circulation Research

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“…Microcirculation. Adenosine was shown early to increase vascular resistance in the kidneys of pigs, dogs, rabbits, and rats, whereas it vasodilates most other nonrenal blood vessels (Thurau, 1964;Scott et al, 1965;Osswald, 1975;Sakai et al, 1981). Sympathetic nerve-mediated vasoconstriction results in release of adenosine into the perfusate of the kidney vascular bed (Fredholm and Hedqvist, 1978), in retrospect probably released from endothelial cells in response to shear stress induced by changes in blood flow.…”

Section: N Human Umbilical and Placental Vesselsmentioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…In particular, adenosine mediates vasoconstriction of afferent arterioles (Hansen et al, 2007). Infusion of adenosine into the renal artery of pigs, rabbits, rats and dogs, induced vasoconstriction in the cortex (Osswald, 1975;Sakai et al, 1981) followed by vasodilation (Hansen and Schnermann, 2003;Macias et al, 1983), probably mediated via different P1 purinoceptor subtypes.…”

Section: Sympathetic Innervation Of Kidney: Generalmentioning

confidence: 99%

Sympathetic innervation of the kidney in health and disease: Emphasis on the role of purinergic cotransmission

Burnstock

Loesch

2017

Autonomic Neuroscience

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There is introductory information about non-synaptic transmission at sympathetic neuroeffector junctions and sympathetic nerve cotransmission utilizing noradrenaline and ATP as cotransmitters. Then the organzation and location of sympathetic nerves in different sites in the kidney are described, including renal arteries, juxtaglomerular arterioles and renal tubules. Sympathetic nervous control of glomerular filtration rate and of renin secretion are discussed. Evidence, obtained largely from experiments on animals, for sympathetic nerve modulation of the transport of water, sodium and other ions in the collecting duct of the nephron is described. Finally, there is coverage of the roles of sympathetic nerves in renal diseases, including hypertension, diabetes, hypothyroidism and ischaemia.

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Species Differences in Renal Vascular Effects of Dipyridamole and in the Potentiation of Adenosine Action by Dipyridamole

Cited by 13 publications

References 0 publications

Dipyridamole decreases glomerular filtration in the sodium-depleted dog. Evidence for mediation by intrarenal adenosine.

Dipyridamole decreases glomerular filtration in the sodium-depleted dog. Evidence for mediation by intrarenal adenosine.

Purinergic Signaling and Blood Vessels in Health and Disease

Sympathetic innervation of the kidney in health and disease: Emphasis on the role of purinergic cotransmission

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