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Titolo:
Handling (NaCl)-Na-22 by the blood-brain barrier and kidney - Its relevance to salt-induced hypertension in Dahl rats
Autore:
Simchon, S; Manger, W; Golanov, E; Kamen, J; Sommer, G; Marshall, CH;
Indirizzi:
Columbia Univ, Dept Med, New York, NY USA Columbia Univ New York NY USAColumbia Univ, Dept Med, New York, NY USA NYU, Med Ctr, New York, NY 10016 USA NYU New York NY USA 10016NYU, Med Ctr, New York, NY 10016 USA
Titolo Testata:
HYPERTENSION
fascicolo: 1, volume: 33, anno: 1999,
parte:, 2 supplemento:, S
pagine: 517 - 523
SICI:
0194-911X(199901)33:1<517:H(BTBB>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC CEREBROVENTRICULAR INFUSION; HYPERTONIC SODIUM-CHLORIDE; SENSITIVE RATS; DEPENDENT HYPERTENSION; DIETARY CHLORIDE; PRESSURE; ETIOLOGY; HEMODYNAMICS; FLOW;
Keywords:
brain; cerebrospinal fluid; hemodynamics; ventricles, cerebral; kidney; rats, Dahl;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Simchon, S Natl Hypertens Assoc, 324 E 30th St, New York, NY 10016 USA Natl Hypertens Assoc 324 E 30th St New York NY USA 10016 16 USA
Citazione:
S. Simchon et al., "Handling (NaCl)-Na-22 by the blood-brain barrier and kidney - Its relevance to salt-induced hypertension in Dahl rats", HYPERTENSIO, 33(1), 1999, pp. 517-523

Abstract

We previously reported that inappropriate renal vasoconstriction in Dahl salt-sensitive (DS) rats fed high NaCl diets may cause sodium retention. Thepresent study examined the distribution and elimination of Na-22 in DS andDahl salt-resistant (DR) rats, and we determined whether an abnormality inrenal function might also cause sodium retention in DS rats. Following an intravenous bolus of 4 mu Ci (NaCl)-Na-22 in prehypertensive DS and DR ratswith similar blood pressures on low (0.23%) or high (8% for 4 days) NaCl diets, urinary clearance of Na-22 in 1 hour was about 4 times less in DS than DR rats, and renal retention of Na-22 was up to 8 times greater in DS than DR rats (P<0.01), suggesting that a renal functional defect may contribute to salt retention in DS rats; however, its uptake in tail artery, heart, lungs, liver, and spleen was similar in DS and DR rats. Uptake in brain wasup to 5 times greater in DS than DR rats (P<0.01). Cerebrospinal fluid Na-22 radioactivity (in counts per minute) revealed that the blood-brain barrier is 5 to 8 times more permeable to sodium in DS than DR rats (P<0.01). Cerebrospinal fluid volume and brain water content increased significantly (P<0.01) in DS but not DR rats on an 8% NaCl diet. Intracerebroventricular bolus injection of 0.06 mL of 4.5 mol/L NaCl acutely and transiently induced the same degree of hypertension in DR and DS rats, whereas similar volume injections of isotonic saline, 4.5 mol/L Na-acetate, or 4.5 mol/L NaBr did not produce hypertension in either strain. We conclude that functional abnormalities in DS rat kidneys may cause retention of NaCl and that an increased blood-brain barrier permeability to NaCl may enhance its access to sites in the brain that are then activated and induce hypertension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 10:25:28