title: Plasma and renal prorenin/renin, renin mRNA, and blood pressure in Dahl salt-sensitive and salt-resistant rats.
abstract: We measured plasma prorenin and renin levels, renal renin mRNA, renal anti-renin and anti-prorenin-prosequence immunoreactivity, and blood pressure in maturing Brookhaven Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats during 14 days of low (0%), medium (0.4%), or high 4%) NaCl diets. Blood pressure was higher in Dahl S rats and did not increase with high NaCl. Seven-week-old Dahl R rats had twofold and sixfold higher levels of plasma prorenin and renal prosequence immunoreactivity, respectively, which by 9 weeks were the same as in Dahl S rats. The anti-renin antiserum, BR1-5, was found to detect prorenin better than renin; Dahl S rats had suppressed renal anti-renin immunoreactivity relative to Dahl-R rats. Dahl R rats were unresponsive to high NaCl, whereas in Dahl S rats, plasma renin and renal prosequence immunoreactivity fell by 90% (P < .01), renal anti-renin immunoreactivity and renal renin MRNA fell by 35% (P < .05 for both), and plasma prorenin fell by 30% (P = NS). NaCl depletion increased prorenin/renin parameters similarly in both strains. There were direct relationships among all of the prorenin/renin parameters. Between low and high salt diets in Dahl S rats, plasma renin increased 20-fold, plasma total renin (renin plus prorenin) and renal renin mRNA both increased threefold, and plasma prorenin increased twofold. The results indicate that under steady-state conditions, plasma and renal renin/prorenin parameters change concordantly and that plasma total renin (renin plus prorenin) reflects changes in renal renin mRNA. The lower blood pressure of Dahl R rats is associated with later maturation-related declines in plasma and renal prorenin. Suppression of plasma renin may delay the salt-induced blood pressure rise in Dahl S rats. Finally, the renin system and blood pressure of Dahl R rats have remarkable disregard for a high salt diet.
authors.affiliation: Cardiovascular Center, Cornell University Medical College, New York, NY, USA.
authors.forename: W G
authors.initials: WG
authors.lastname: Campbell
authors.forename: F
authors.initials: F
authors.lastname: Gahnem
authors.forename: D F
authors.initials: DF
authors.lastname: Catanzaro
authors.forename: G D
authors.initials: GD
authors.lastname: James
authors.forename: M J
authors.initials: MJ
authors.lastname: Camargo
authors.forename: J H
authors.initials: JH
authors.lastname: Laragh
authors.forename: J E
authors.initials: JE
authors.lastname: Sealey
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004039:Diet, Sodium-Restricted; D004351:Drug Resistance / Q000235:genetics; D004792:Enzyme Precursors / Q000097:blood*; D007106:Immune Sera; D007150:Immunohistochemistry; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains / Q000235:genetics; D012083:Renin / Q000097:blood* / Q000235:genetics*; D012965:Sodium Chloride / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D004792:Enzyme Precursors; D007106:Immune Sera; D012333:RNA, Messenger; D012965:Sodium Chloride; D012083:Renin