title: Possible mechanisms of salt-induced hypertension in Dahl salt-sensitive rats.
abstract: Genetic factors, diet, and salt sensitivity have all been implicated in hypertension. To further understand the mechanisms involved in salt-induced hypertension, cardiovascular, hemodynamics, and biochemical parameters in Dahl salt-sensitive rats were evaluated in animals on high- and low-sodium diets. During a 4-week treatment period, blood pressure was significantly elevated in the high (8.0%) salt group compared to the low (0.3%) salt group (p< or =0.05 for weeks 2 and 4, respectively). No significant changes were observed in heart rate. The increase in blood pressure was associated with significant increases in lower abdominal aortic and renal vascular resistance, along with a reduction in blood flow. A fourfold increase in arginine vasopressin was observed in animals on the high-salt diet. In contrast, there was no effect on plasma sodium, potassium, or aldosterone levels during the treatment period. As measured in isolated aortic rings, the high-salt diet also caused a significant elevation in stimulated norepinephrine release and a reduction in cyclic GMP levels. These data suggest that salt-induced elevation in blood pressure is due to activation of both the sympathetic and arginine vasopressin systems via mechanisms involving decreased cyclic GMP generation in vascular smooth muscle.
authors.affiliation: Department of Pharmacology/Toxicology, Morehouse School of Medicine, Atlanta, GA 30310, USA.
authors.forename: M A
authors.initials: MA
authors.lastname: Bayorh
authors.forename: E C
authors.initials: EC
authors.lastname: Ogbolu
authors.forename: E
authors.initials: E
authors.lastname: Williams
authors.forename: M
authors.initials: M
authors.lastname: Thierry-Palmer
authors.forename: G
authors.initials: G
authors.lastname: Sanford
authors.forename: N
authors.initials: N
authors.lastname: Emmett
authors.forename: S
authors.initials: S
authors.lastname: Harris-Hooker
authors.forename: R R
authors.initials: RR
authors.lastname: Socci
authors.forename: T C
authors.initials: TC
authors.lastname: Chu
authors.forename: V M
authors.initials: VM
authors.lastname: Chenault
mesh_terms: D000450:Aldosterone / Q000097:blood; D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000503:physiopathology; D001127:Arginine Vasopressin / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D006152:Cyclic GMP / Q000378:metabolism; D004039:Diet, Sodium-Restricted; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000503:physiopathology; D009638:Norepinephrine / Q000378:metabolism; D011188:Potassium / Q000097:blood; D051381:Rats; D020303:Rats, Inbred Dahl; D012039:Regional Blood Flow / Q000187:drug effects; D012964:Sodium / Q000097:blood; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D017673:Sodium Chloride, Dietary; D001127:Arginine Vasopressin; D000450:Aldosterone; D012964:Sodium; D006152:Cyclic GMP; D011188:Potassium; D009638:Norepinephrine