title: Adaptations to iron deficiency: cardiac functional responsiveness to norepinephrine, arterial remodeling, and the effect of beta-blockade on cardiac hypertrophy.
abstract: BACKGROUND
  Iron deficiency (ID) results in ventricular hypertrophy, believed to involve sympathetic stimulation. We hypothesized that with ID 1) intravenous norepinephrine would alter heart rate (HR) and contractility, 2) abdominal aorta would be larger and more distensible, and 3) the beta-blocker propanolol would reduce hypertrophy.
  
  
  METHODS
  1) 30 CD rats were fed an ID or replete diet for 1 week or 1 month. Norepinephrine was infused via jugular vein; pressure was monitored at carotid artery. Saline infusions were used as a control. The pressure trace was analyzed for HR, contractility, systolic and diastolic pressures. 2) Abdominal aorta catheters inflated the aorta, while digital microscopic images were recorded at stepwise pressures to measure arterial diameter and distensibility. 3) An additional 10 rats (5 ID, 5 control) were given a daily injection of propanolol or saline. After 1 month, the hearts were excised and weighed.
  
  
  RESULTS
  Enhanced contractility, but not HR, was associated with ID hypertrophic hearts. Systolic and diastolic blood pressures were consistent with an increase in arterial diameter associated with ID. Aortic diameter at 100 mmHg and distensibility were increased with ID. Propanolol was associated with an increase in heart to body mass ratio.
  
  
  CONCLUSIONS
  ID cardiac hypertrophy results in an increased inotropic, but not chronotropic response to the sympathetic neurotransmitter, norepinephrine. Increased aortic diameter is consistent with a flow-dependent vascular remodeling; increased distensibility may reflect decreased vascular collagen content. The failure of propanolol to prevent hypertrophy suggests that ID hypertrophy is not mediated via beta-adrenergic neurotransmission.
authors.affiliation: Department of Biological Sciences R,A, Henson School of Science and Technology Salisbury State University Salisbury, MD 21801, USA. lexssu@hotmail.com
authors.forename: Lexa Rae
authors.initials: LR
authors.lastname: Turner
authors.forename: Daniel Aaron
authors.initials: DA
authors.lastname: Premo
authors.forename: Brett Jason
authors.initials: BJ
authors.lastname: Gibbs
authors.forename: Megan Lesley
authors.initials: ML
authors.lastname: Hearthway
authors.forename: Madelyne
authors.initials: M
authors.lastname: Motsko
authors.forename: Andrea
authors.initials: A
authors.lastname: Sappington
authors.forename: LeeAnn
authors.initials: L
authors.lastname: Walker
authors.forename: Michael Eugene
authors.initials: ME
authors.lastname: Mullendore
authors.forename: Herbert George
authors.initials: HG
authors.lastname: Chew
mesh_terms: D000222:Adaptation, Physiological; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000818:Animals; D001158:Arteries / Q000473:pathology* / Q000503:physiopathology; D001835:Body Weight; D006332:Cardiomegaly / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D004548:Elasticity; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects; D006400:Hematocrit; D006439:Hemodynamics; D000090463:Iron Deficiencies; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000473:pathology; D009638:Norepinephrine / Q000494:pharmacology*; D009929:Organ Size; D011433:Propranolol / Q000627:therapeutic use*; D051381:Rats
chemical_list: D000319:Adrenergic beta-Antagonists; D011433:Propranolol; D009638:Norepinephrine