{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T20:48:58Z","timestamp":1770065338058,"version":"3.49.0"},"reference-count":31,"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":[[2000,10]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Hypertension with renal  artery stenosis is associated with both an activated  renin-angiotensin system and elevated sympathetic activity.  Therefore, in this condition it may be favorable to use a therapeutic  modality that does not reflexly increase heart rate, renin secretion,  and sympathetic nervous activity. The purpose of the present study  was to assess overall, renal, and muscle sympathetic activity after  short-term administration of an angiotensin-converting  enzyme inhibitor (enalaprilat) and a nonspecific  vasodilator (dihydralazine) to hypertensive patients with renal  artery stenosis. Forty-eight patients undergoing a clinical  investigation for renovascular hypertension were included in the study.  An isotope dilution technique for assessing norepinephrine  spillover was used to estimate overall and bilateral renal  sympathetic nerve activity. In 11 patients simultaneous  intraneural recordings of efferent muscle sympathetic nerve  activity were performed. Thirty minutes after dihydralazine  administration, mean arterial pressure fell by 15%,  whereas plasma angiotensin II, muscle sympathetic nerve  activity, heart rate, and total body norepinephrine  spillover increased (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05 for all). In contrast,  after enalaprilat administration a fall in arterial  pressure similar to that for dihydralazine was followed by  decreased angiotensin II levels and unchanged muscle  sympathetic nerve activity, heart rate, and total body  norepinephrine spillover, whereas renal  norepinephrine spillover increased by 44%  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Acute blood pressure reduction by an  angiotensin-converting enzyme inhibitor  provokes a differentiated sympathetic response in patients with  hypertension and renal artery stenosis, inasmuch that overall  and muscle sympathetic reflex activation are blunted, whereas the  reflex renal sympathetic response to blood pressure reduction is  preserved.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.4.543","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"543-548","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension"],"prefix":"10.1161","volume":"36","author":[{"given":"Mats","family":"Johansson","sequence":"first","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mikael","family":"Elam","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bengt","family":"Rundqvist","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Graeme","family":"Eisenhofer","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans","family":"Herlitz","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gert","family":"Jensen","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Friberg","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., P.F.), Clinical  Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H., G.J.),  Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg,  Sweden; and National Institutes of Neurological Disorders and Stroke,  Bethesda, Md (G.E.)."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.17.6.1057"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.99.19.2537"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.139.3551.210"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199904293401704"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1968.tb04222.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"crossref","unstructured":"Brody MJ Varner KJ Vasquez EC Lewis SJ. 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