title: The implication of renin-angiotensin system on renal injury seen in Dahl salt-sensitive rats.
abstract: Angiotensin II (Ang II) progresses to remodeling of the cardiovascular system through nonhemodynamic as well as hemodynamic effects. There have been few data in vivo on whether subpressor concentration of Ang II is exerted to injure directly the cardiovascular system in hypertension. To test this hypothesis, we investigated, using Dahl salt-sensitive (Dahl S) rats, whether subpressor dose of Ang II progresses to cardiovascular injury observed in salt-induced hypertension. Recent studies have provided evidence that renin-angiotensin inhibition protects against renovascular injury in human hypertension as well as in experimental animals. Particularly in the case of Dahl salt-sensitive rats, a genetic model of volume-dependent hypertension in humans, they are likely to develop more severe arterial and renal injuries than those seen in spontaneously hypertensive rats with similar blood pressure levels. The mechanism of the susceptibility to hypertensive injuries is uncertain; however, renin-angiotensin inhibition significantly improved morphologic and functional injuries in the kidney of Dahl S rats. Conversely, subpressor dose of Ang II infusion exacerbated renal function and progressed to glomerulosclerotic lesions. Alterations of Ang II concentration in physiologic range influenced morphologic and functional injuries in Dahl S rats. Multivariate analysis revealed that activity of the renin-angiotensin system is an independent risk factor to glomerular injury in salt-induced hypertension. These data are in favor of the therapeutic strategy in human hypertension that inhibition of renin-angiotensin system is of value to produce beneficial effects of blood pressure reduction on organ injuries.
authors.affiliation: Division of Nephrology, Kohsaikai Asahi Hospital, Yokohama, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Hirawa
authors.forename: Y
authors.initials: Y
authors.lastname: Uehara
authors.forename: A
authors.initials: A
authors.lastname: Numabe
authors.forename: Y
authors.initials: Y
authors.lastname: Kawabata
authors.forename: T
authors.initials: T
authors.lastname: Gomi
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: T
authors.initials: T
authors.lastname: Ohnishi
authors.forename: M
authors.initials: M
authors.lastname: Ishii
authors.forename: M
authors.initials: M
authors.lastname: Omata
mesh_terms: D000818:Animals; D004351:Drug Resistance / Q000235:genetics; D006973:Hypertension / Q000139:chemically induced* / Q000235:genetics* / Q000503:physiopathology; D007668:Kidney / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains / Q000033:anatomy & histology / Q000235:genetics* / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology*
chemical_list: D012965:Sodium Chloride