title: Telmisartan improves survival and ventricular function in SHR rats with extensive cardiovascular damage induced by dietary salt excess.
abstract: Excessive dietary salt intake induces extensive cardiovascular and renal damage in spontaneously hypertensive rats (SHR) that may be prevented by antihypertensive agents. This study examines whether salt-induced cardiac damage may be reversed by angiotensin II (type 1) receptor blockade (telmisartan). Eight-week-old male SHRs were divided into four groups; Group 1 (NS) was fed regular rat chow, and Group 2 (HS) received high-salt diet (HS; 8% NaCl). After 8 weeks on their respective diets, systemic hemodynamics and indices of left ventricular (LV) function were determined. Group 3 (HSnoT) was given HS for 8 weeks and then switched to a regular chow (0.6% NaCl) diet with no other treatment, and Group 4 (HSArb) received HS for 8 weeks and was then given regular diet plus telmisartan. Rats from these latter two groups were monitored for the ensuing 30 days. Compared with the NS group, rats in the HS group exhibited increased mean arterial pressure (161 ± 7 vs. 184 ± 8 mm Hg) and LV diastolic dysfunction, as evidenced by a decreased rate of LV pressure decline (-8754 ± 747 vs. -4234 ± 754 mmHg/sec) at the end of the 8 weeks of their respective treatment. After switching to regular chow, only one of 11 rats in the HSnoT group survived for the 30 days, whereas 10 died within 18 days; in the HSArb group only one of nine rats died; eight survived 30 days (P < .01). Telmisartan significantly improved LV function and survival in those SHR rats having extensive cardiovascular damage induced by dietary salt excess.
authors.affiliation: Hypertension Research Laboratory, Institute for Translational Research, Ochsner Clinic Foundation, New Orleans, LA.
authors.forename: Dinko
authors.initials: D
authors.lastname: Susic
authors.affiliation: Hypertension Research Laboratory, Institute for Translational Research, Ochsner Clinic Foundation, New Orleans, LA. Electronic address: efrohlich@ochsner.org.
authors.forename: Edward D
authors.initials: ED
authors.lastname: Frohlich
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology*; D001565:Benzoates / Q000494:pharmacology*; D001835:Body Weight; D003971:Diastole / Q000187:drug effects; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000188:drug therapy; D008297:Male; D011897:Random Allocation; D011918:Rats, Inbred SHR; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000009:adverse effects*; D000077333:Telmisartan; D018754:Ventricular Dysfunction / Q000139:chemically induced / Q000188:drug therapy*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D012982:Sodium, Dietary; D000077333:Telmisartan
keywords: Dietary salt excess; angiotensin receptor blockers; left ventricular dysfunction; reversal of cardiovascular damage; survival