{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T01:24:12Z","timestamp":1776734652457,"version":"3.51.2"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1991,12]]},"abstract":"<jats:p>African-Americans with essential hypertension are more prone to the development of renal failure and are frequently salt-sensitive as well. Because alterations of intrarenal hemodynamics are important in the progression of renal disease and because salt-sensitive animal models with hypertension manifest a greater propensity to develop glomerulosclerosis in association with a rise in glomerular capillary pressure, we tested whether the renal hemodynamic adaptation to high dietary Na+ intake differs in salt-sensitive and salt-resistant hypertensive patients. We studied 17 black and nine white patients with essential hypertension who were placed on a low Na+ diet (20 meq\/day) for 9 days, followed by a high Na+ diet (200 meq\/day) for 14 days. During the last 4 days of each diet regimen, they received 30 mg\/day of slow-release nifedipine. Eleven blacks were salt-sensitive, and all whites were salt-resistant. During the low Na+ diet period, salt-sensitive and salt-resistant patients had similar mean arterial pressure, glomerular filtration rate, effective renal plasma flow, and filtration fraction.(ABSTRACT TRUNCATED AT 250 WORDS)<\/jats:p>","DOI":"10.1161\/01.hyp.18.6.805","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:24:03Z","timestamp":1339460643000},"page":"805-812","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":143,"title":["Abnormal renal hemodynamics in black salt-sensitive patients with hypertension."],"prefix":"10.1161","volume":"18","author":[{"given":"V M","family":"Campese","sequence":"first","affiliation":[{"name":"Department of Medicine, University of Southern California Medical Center, Los Angeles 90033."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Parise","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California Medical Center, Los Angeles 90033."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F","family":"Karubian","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California Medical Center, Los Angeles 90033."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R","family":"Bigazzi","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Southern California Medical Center, Los Angeles 90033."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","container-title":["Hypertension"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.HYP.18.6.805","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:30:02Z","timestamp":1715535002000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.HYP.18.6.805"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1991,12]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1991,12]]}},"alternative-id":["10.1161\/01.HYP.18.6.805"],"URL":"https:\/\/doi.org\/10.1161\/01.hyp.18.6.805","relation":{},"ISSN":["0194-911X","1524-4563"],"issn-type":[{"value":"0194-911X","type":"print"},{"value":"1524-4563","type":"electronic"}],"subject":[],"published":{"date-parts":[[1991,12]]},"assertion":[{"value":"1991-12-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}