ArticleBritish journal of pharmacology2005
Noradrenaline and extracellular nucleotide cotransmission involves activation of vasoconstrictive P2X(1,3)- and P2Y6-like receptors in mouse perfused kidney.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 36 citations in OpenAlex.
- UDP-induced relaxation is enhanced in aorta from female obese Otsuka Long-Evans Tokushima Fatty rats.Purinergic signalling · 2018Article
- ATP acting through P2Y receptors causes activation of podocyte TRPC6 channels: role of podocin and reactive oxygen species.American journal of physiology. Renal physiology · 2014Article
- P2Y2 receptor deficiency aggravates chronic kidney disease progression.Frontiers in physiology · 2013Article
- Endogenous adenosine contributes to renal sympathetic neurotransmission via postjunctional A1 receptor-mediated coincident signaling.American journal of physiology. Renal physiology · 2012Article
- Regulation of renal sympathetic neurotransmission by renal α(2A)-adrenoceptors is impaired in chronic renal failure.British journal of pharmacology · 2011Article
- NTPDase1 (CD39) controls nucleotide-dependent vasoconstriction in mouse.Cardiovascular research · 2010Article
- Intestinal ischemia-reperfusion injury alters purinergic receptor expression in clinically relevant extraintestinal organs.The Journal of surgical research · 2008Article
- P2Y1 receptor switches to neurons from glia in juvenile versus neonatal rat cerebellar cortex.BMC developmental biology · 2007Article
- Evidence for the expression of multiple uracil nucleotide-stimulated P2 receptors coupled to smooth muscle contraction in porcine isolated arteries.British journal of pharmacology · 2007Article
- Alpha(2A)-adrenoceptors regulate sympathetic transmitter release in mice kidneys.British journal of pharmacology · 2007Article
- Endothelium-dependent relaxation evoked by ATP and UTP in the aorta of P2Y2-deficient mice.British journal of pharmacology · 2006Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotides like ATP and UTP act as potent extracellular signalling molecules. Released from sympathetic nerve endings as cotransmitters of noradrenaline or paracrine from nonexcitatory cells, they activate specific receptors (ion-gated P2X(1-7) and G-protein-coupled P2Y(1,2,4,6,11-15)). Which of these subtypes, however, are able to modulate vasoconstriction in the kidney is unclear. Wild-type- and P2Y4-receptor-deficient mice kidneys were isolated and perfused with Krebs-Henseleit solution. Pressor responses to renal nerve stimulations (RNS) and added drugs were recorded. Release of endogenous noradrenaline was measured by HPLC. RNS (1-15 Hz) induced a frequency-dependent increase in the perfusion pressor (14.2+/-5.1-67.3+/-6.9 mmHg) and noradrenaline release (1.4+/-0.3-24.2+/-3.4 ng g(-1) kidney). Pressor responses to RNS were not (1-2 Hz) or only partially (5-15 Hz) blocked by the alpha-adrenoceptor antagonist phentolamine (1 microM). Combination of phentolamine and the P2-receptor blocker PPADS (5 microM) prevented RNS-induced pressor responses. The P2X(1,3)-receptor selective antagonist NF279 (10 microM) reduced RNS-induced pressor responses in a frequency-dependent manner. Perfusion of ATP, ADP, UTP, UDP and alpha,beta-meATP concentration dependently increased perfusion pressor with the following rank order of potency alpha,beta-meATP>ADP approximately ATP approximately UDP > or = UTP. NF279 (10 microM) reduced alpha,beta-meATP- (0.1 microM) (21.7+/-3.9% of control) but not UTP- (0.3 microM) (102.6+/-15.3% of control) induced pressor responses. No differences in nucleotide-induced effects were detected among wild-type and P2Y4-receptor knockout mice. Continuous perfusion of alpha,beta-meATP (0.01 microM) potentiated UTP-, UDP- and ATP-gamma S-induced pressor responses. Neuronally and paracrine-released nucleotides evoked renal vasoconstriction by activation of P2X(1,3)- and P2Y6-like receptors in mice. Pretreatment with the P2X(1,3)-receptor agonist alpha,beta-meATP potentiated P2Y6-like receptor-mediated vasoconstrictions.
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