{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T23:58:01Z","timestamp":1793145481154,"version":"4.5.0"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"19","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1999,5,18]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            \u2014Increased sympathetic nerve activity may contribute to the progression of renovascular hypertension. Because previous results have been inconclusive, we investigated whether renovascular hypertensives show increased total and regional sympathetic nerve activity.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            \u2014Sixty-five patients underwent renal angiography and measurements of plasma renin activity and angiotensin II in conjunction with estimation of sympathetic nerve activity by means of radiotracer dilution and intraneural recordings of muscle sympathetic nerve activity (MSNA). Age-matched healthy subjects (n=15) were examined for comparison. Total body norepinephrine (NE) spillover, an index of overall sympathetic nerve activity, was increased by 100% and MSNA by 60% in the hypertensive patients compared with healthy subjects (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01 for both). A subgroup of 24 patients with well-defined renovascular hypertension (cured or improved hypertension after renal angioplasty) showed similar increases in total body NE spillover compared with the group at large. Patients with arterial plasma renin activity and angiotensin II levels above median had higher values for total body NE spillover than patients below median (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014This study unequivocally demonstrates elevated sympathetic nerve activity in patients with renovascular hypertension. The adrenergic overactivity may contribute to the blood pressure elevation and perhaps also to the high cardiovascular mortality in renovascular hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.cir.99.19.2537","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:42:29Z","timestamp":1339461749000},"page":"2537-2542","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":145,"title":["Increased Sympathetic Nerve Activity in Renovascular Hypertension"],"prefix":"10.1161","volume":"99","author":[{"given":"Mats","family":"Johansson","sequence":"first","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mikael","family":"Elam","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bengt","family":"Rundqvist","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graeme","family":"Eisenhofer","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans","family":"Herlitz","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gavin","family":"Lambert","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Friberg","sequence":"additional","affiliation":[{"name":"From the Departments of Clinical Physiology (M.J., G.L., P.F.), Clinical Neurophysiology (M.E.), Cardiology (B.R.), and Nephrology (H.H.), Go\u0308teborg University, Sahlgrenska University Hospital, Go\u0308teborg, Sweden, and National Institutes of Neurological Disorders and Stroke (G.E.), Bethesda, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","unstructured":"Swales J. 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