{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T14:35:28Z","timestamp":1783953328121,"version":"3.55.0"},"reference-count":11,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2003,10]]},"abstract":"<jats:p>\n            Subpressor doses of angiotensin II (SP-Ang II) cause a slow increase in blood pressure in rats as assessed by tail cuff plethysmography (TCP), reflecting either sustained hypertension or an exaggerated pressor response to diverse stimuli. We examined whether subpressor doses of Ang II enhance blood pressure responses to simple stress (handling of trained rats for TCP). We implanted telemetry in Sprague-Dawley rats. After 10 days of recovery and TCP training, we implanted osmotic minipumps with either SP-Ang II (50 ng\/kg per minute) or vehicle, and then measured systolic blood pressure continuously in unrestrained rats for 13 days. We also recorded telemetry readings while obtaining TCP measurements every 2 days. SP-Ang II increased blood pressure from 134\u00b119 to 159\u00b122 mm Hg by TCP, which matched the simultaneous telemetry readings of 131\u00b120 to 154\u00b125 mm Hg. In contrast, SP-Ang II did not change the blood pressure in the unrestrained rats (measured with continuous telemetry: 124\u00b12 versus 127\u00b11 mm Hg). The blood pressure in the control rats did not change in the unrestrained state (125\u00b13 versus 128\u00b15 mm Hg on days 0 and 12, respectively), and only slightly increased during TCP (11\u00b15 and 6\u00b14 mm Hg by TCP and simultaneous telemetry, respectively;\n            <jats:italic>P<\/jats:italic>\n            =NS). In summary, SP-Ang II, although unable to provoke sustained hypertension, nonetheless magnifies the pressor response to otherwise trivial stimuli. We speculate that even modestly elevated Ang II levels may contribute to hypertensive complications because such levels promote the punctuation of an apparent normotensive state by episodic hypertension occasioned by seemingly innocuous stimuli.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000085782.99773.b6","type":"journal-article","created":{"date-parts":[[2003,7,22]],"date-time":"2003-07-22T00:35:00Z","timestamp":1058834100000},"page":"798-801","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["Low-Dose Angiotensin II Enhances Pressor Responses Without Causing Sustained Hypertension"],"prefix":"10.1161","volume":"42","author":[{"given":"Laura I.","family":"Pelaez","sequence":"first","affiliation":[{"name":"From the Departments of Family Medicine (L.A.P.), and Physiology (M.C.M., J.C.R.), and the Division of Nephrology (K.A.N., L.A.J.), Mayo School of Medicine, Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa C.","family":"Manriquez","sequence":"additional","affiliation":[{"name":"From the Departments of Family Medicine (L.A.P.), and Physiology (M.C.M., J.C.R.), and the Division of Nephrology (K.A.N., L.A.J.), Mayo School of Medicine, Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl A.","family":"Nath","sequence":"additional","affiliation":[{"name":"From the Departments of Family Medicine (L.A.P.), and Physiology (M.C.M., J.C.R.), and the Division of Nephrology (K.A.N., L.A.J.), Mayo School of Medicine, Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan C.","family":"Romero","sequence":"additional","affiliation":[{"name":"From the Departments of Family Medicine (L.A.P.), and Physiology (M.C.M., J.C.R.), and the Division of Nephrology (K.A.N., L.A.J.), Mayo School of Medicine, Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis A.","family":"Juncos","sequence":"additional","affiliation":[{"name":"From the Departments of Family Medicine (L.A.P.), and Physiology (M.C.M., J.C.R.), and the Division of Nephrology (K.A.N., L.A.J.), Mayo School of Medicine, Mayo Clinic, Rochester, Minn."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(63)91929-9"},{"key":"e_1_3_1_2_2","first-page":"H381","volume":"241","year":"1981","unstructured":"Brown AJ, Casals-Stenzel J, Gofford S, Lever AF, Morton JJ. 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