{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,3]],"date-time":"2025-07-03T04:24:22Z","timestamp":1751516662188},"reference-count":45,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2012,9,15]]},"abstract":"<jats:p>Adenosine, acting on A<jats:sub>1<\/jats:sub>-receptors (A<jats:sub>1<\/jats:sub>-AR) in the nephron, increases sodium reabsorption, and also increases renal vascular resistance (RVR), via A<jats:sub>1<\/jats:sub>-ARs in the afferent arteriole. ANG II increases blood pressure and RVR, and it stimulates adenosine release in the kidney. We tested the hypothesis that ANG II-infused hypertension is potentiated by A<jats:sub>1<\/jats:sub>-ARs' influence on Na<jats:sup>+<\/jats:sup>reabsorption. Mean arterial pressure (MAP) was measured by radiotelemetry in A<jats:sub>1<\/jats:sub>-AR knockout mice (KO) and their wild-type (WT) controls, before and during ANG II (400 ng\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>) infusion. Baseline MAP was not different between groups. ANG II increased MAP in both groups, but on day 12, MAP was lower in A<jats:sub>1<\/jats:sub>-AR KO mice (KO: 128 \u00b1 3 vs. 139 \u00b1 3 mmHg, P &lt; 0.01). Heart rates were significantly different during days 11\u201314 of ANG II. Basal sodium excretion was not different (KO: 0.15 \u00b1 0.03 vs. WT: 0.13 \u00b1 0.04 mmol\/day, not significant) but was higher in KO mice 12 days after ANG II despite a lower MAP (KO: 0.22 \u00b1 0.03 vs. WT: 0.11 \u00b1 0.02 mmol\/day, P &lt; 0.05). Phosphate excretion was also higher in A<jats:sub>1<\/jats:sub>-AR KO mice on day 12. Renal expression of the sodium-dependent phosphate transporter and the Na<jats:sup>+<\/jats:sup>\/glucose cotransporter were lower in the KO mice during ANG II treatment, but the expression of the sodium hydrogen exchanger isoform 3 was not different. These results indicate that the increase in blood pressure seen in A<jats:sub>1<\/jats:sub>-AR KO mice is lower than that seen in WT mice but was increased by ANG II nonetheless. The presence of A<jats:sub>1<\/jats:sub>-ARs during a low dose of ANG II-infusion limits Na<jats:sup>+<\/jats:sup>and phosphate excretion. This study suggests that A<jats:sub>1<\/jats:sub>-AR antagonists might be an effective antihypertensive agent during ANG II and volume-dependent hypertension.<\/jats:p>","DOI":"10.1152\/ajpregu.00116.2012","type":"journal-article","created":{"date-parts":[[2012,8,9]],"date-time":"2012-08-09T06:19:56Z","timestamp":1344493196000},"page":"R683-R688","source":"Crossref","is-referenced-by-count":17,"title":["Adenosine A<sub>1<\/sub>-receptor knockout mice have a decreased blood pressure response to low-dose ANG II infusion"],"prefix":"10.1152","volume":"303","author":[{"given":"Dexter L.","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, Howard University, Washington, D.C.; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tracy D.","family":"Bell","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Nephrology and Hypertension, Georgetown University, Washington, 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