Dietary manganese suppresses alpha1 adrenergic receptor-mediated vascular contraction

Anastasia Z Kalea1, Patrick D Harris, Dorothy J Klimis-Zacas

  • 1Department of Food Science and Human Nutrition, College of Natural Sciences, Forestry and Agriculture, University of Maine, Orono, ME 04469, USA.

Insights

Dietary manganese (Mn) impacts rat aorta function. High manganese levels reduced maximal contraction force, while deficiency increased vascular sensitivity to alpha(1) adrenergic receptors, affecting smooth muscle cells.

Area of Science:

  • Cardiovascular Physiology
  • Nutritional Biochemistry
  • Vascular Pharmacology

Background:

  • Dietary manganese (Mn) is essential for various physiological processes.
  • The specific effects of dietary manganese on vascular smooth muscle contractility are not fully understood.

Purpose of the Study:

  • To investigate the impact of varying dietary manganese levels on the contractile machinery of rat thoracic aortas.
  • To determine how manganese influences vascular smooth muscle cell response to alpha(1) adrenergic receptor stimulation.

Main Methods:

  • Weanling male Sprague-Dawley rats were fed manganese-deficient, adequate, or supplemented diets for 15 weeks.
  • Aortic rings were contracted with L-phenylephrine (alpha(1) adrenergic agonist) and relaxed with acetylcholine.
  • Maximal contraction force (Fmax) and sensitivity (pD2) to L-phenylephrine were measured.

Main Results:

  • Manganese-supplemented diet (45-50 ppm) resulted in lower maximal contraction force (Fmax) compared to deficient and adequate groups.
  • Manganese deficiency significantly increased vascular sensitivity (pD2) to L-phenylephrine.
  • Hepatic manganese content indicated successful dietary manipulation and affected animal growth rates.

Conclusions:

  • Dietary manganese levels significantly influence the contractile machinery of vascular smooth muscle.
  • High dietary manganese reduces maximal contractile responses to alpha(1) adrenergic agonists.
  • Manganese deficiency enhances vascular sensitivity to alpha(1) adrenergic receptor stimulation, impacting signaling pathways.

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