{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:46:59Z","timestamp":1791996419609,"version":"4.4.0"},"reference-count":70,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","funder":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases","award":["DK137329"],"award-info":[{"award-number":["DK137329"]}],"id":[{"id":"https:\/\/ror.org\/00adh9b73","id-type":"ROR","asserted-by":"crossref"}]},{"name":"National Heart, Lung, and Blood Institute","award":["HL109002"],"award-info":[{"award-number":["HL109002"]}],"id":[{"id":"https:\/\/ror.org\/012pb6c26","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"published-print":{"date-parts":[[2026,6]]},"abstract":"\n Key Points<\/jats:title>\n \n \n \n 2\u2032-AMP is endogenous and causes renal vasoconstriction in part by allosteric modulation of P2X1 receptors that enhances ATP-induced opening of P2X1 receptor channels.<\/jats:p>\n <\/jats:list-item>\n \n Kidney tissue nonspecific alkaline phosphatase (TNAP) by metabolizing 2\u2032-AMP protects against 2\u2032-AMP\u2013induced renal vasoconstriction, a protection lost when kidney TNAP activity is reduced.<\/jats:p>\n <\/jats:list-item>\n \n Drugs with off-target effects that reduce kidney TNAP activity should be avoided in patients at risk of kidney injury.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n Knockout of 2\u2032,3\u2032-cyclic-nucleotide 3\u2032-phosphodiesterse (an enzyme that converts 2\u2032,3\u2032-cAMP to 2\u2032-AMP) reduces 2\u2032-AMP production and improves renal perfusion in renal ischemia-reperfusion injury (R-IRI). These findings motivated our hypothesis, herein tested, that 2\u2032-AMP causes renal vasoconstriction.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n The effect of 2\u2032-AMP on renal vascular resistance (RVR) was investigated in rat kidneys, both\n in vitro<\/jats:italic>\n and\n in vivo<\/jats:italic>\n . 2\u2032-AMP interactions with P2X1 receptors (P2X1Rs) were investigated in membrane preparations and HEK cells. Urinary 2\u2032-AMP levels were assessed in cardiac surgery\/cardiopulmonary bypass (CS-CPB) patients using mass spectrometry.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n In vitro<\/jats:italic>\n , intra-renal-artery\u2013infused 2\u2032-AMP was rapidly metabolized to adenosine and did not increase RVR. Coadministration of a tissue nonspecific alkaline phosphatase inhibitor (TNAPI) reduced 2\u2032-AMP metabolism, thus enabling 2\u2032-AMP to trigger renal vasoconstriction.\n In vivo<\/jats:italic>\n , kidneys rapidly metabolized intra-renal-artery\u2013infused 2\u2032-AMP to adenosine; this was blocked with a TNAPI.\n In vivo<\/jats:italic>\n , intra-renal-artery\u2013infused 2\u2032-AMP decreased RVR, as did adenosine. By contrast, when coadministered with a TNAPI, 2\u2032-AMP increased RVR, and this response was inhibited by NF449 (P2X1R antagonist). In membranes, 2\u2032-AMP enhanced\n 3<\/jats:sup>\n H-\n \u03b1\u03b2<\/jats:italic>\n -methylene-ATP (P2X1R agonist) binding to P2X1Rs, and in HEK cells, 2\u2032-AMP doubled\n \u03b1\u03b2<\/jats:italic>\n -methylene-ATP\u2013induced (and P2X1R-mediated) calcium influx. In TNAPI+2\u2032-AMP\u2013pretreated, but not na\u00efve, rats,\n \u03b2\u03b3<\/jats:italic>\n -methylene-ATP (P2X1R agonist) caused renal vasoconstriction. In rats, R-IRI reduced kidney tissue nonspecific alkaline phosphatase (TNAP) activity, and TNAP inhibition worsened R-IRI. In CS-CPB patients, urinary 2\u2032-AMP levels were elevated 169% during CS-CPB and were associated with a 45% increase in peak 24-hour postprocedure serum creatinine.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n 2\u2032-AMP is a renal vasoconstrictor; however, TNAP, by metabolizing 2\u2032-AMP to adenosine, protects against 2\u2032-AMP\u2013induced renal vasoconstriction. This protection is lost when TNAP activity is reduced. 2\u2032-AMP\u2013induced renal vasoconstriction involves positive allosteric modulation of P2X1Rs that enhances ATP-induced opening of P2X1R channels. R-IRI reduces kidney TNAP activity, and TNAP inhibition worsens R-IRI outcomes.<\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.0000000954","type":"journal-article","created":{"date-parts":[[2025,12,2]],"date-time":"2025-12-02T21:00:21Z","timestamp":1764709221000},"page":"1127-1142","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Effects and Mechanism of 2\u2032-AMP on Renal Vascular Resistance"],"prefix":"10.1681","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8101-6009","authenticated-orcid":false,"given":"Edwin K.","family":"Jackson","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongmei","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Delbert G.","family":"Gillespie","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zaichuan","family":"Mi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stevan P.","family":"Tofovic","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth V.","family":"Menshikova","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vladimir B.","family":"Ritov","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5826-0388","authenticated-orcid":false,"given":"Nahmah A.","family":"Kim-Campbell","sequence":"additional","affiliation":[{"name":"Department of Critical Care Medicine and Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,12,2]]},"reference":[{"issue":"3","key":"B1-20261014","doi-asserted-by":"crossref","first-page":"855","DOI":"10.1124\/jpet.108.146712","article-title":"Identification 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