Influence of thyroid state on cardiac and renal capillary density and glomerular morphology in rats

J Endocrinol. 2013 Jan 2;216(1):43-51. doi: 10.1530/JOE-12-0208. Print 2013 Jan.

Abstract

The purpose was to analyse the cardiac and renal capillary density and glomerular morphology resulting from a chronic excess or deficiency of thyroid hormones (THs) in rats. We performed histopathological, morphometrical and immunohistochemical analyses in hypothyroid and hyperthyroid rats to evaluate the density of mesenteric, renal and cardiac vessels at 4 weeks after induction of thyroid disorders. The main angiogenic factors in plasma, heart and kidney were measured as possible mediators of vascular changes. Mesenteric vessel branching was augmented and decreased in hyper- and hypothyroid rats respectively. The numerical density of CD31-positive capillaries was higher in left and right ventricles and in cortical and medullary kidney from both hyper- and hypothyroid rats vs controls. Numbers of podocytes and glomeruli per square millimetre were similar among groups. Glomerular area and percentage mesangium were greater in the hyperthyroid vs control or hypothyroid groups. No morphological renal lesions were observed in any group. Vascularisation of the mesenteric bed is related to TH levels, but an increased capillarity was observed in heart and kidney in both thyroid disorders. This increase may be produced by higher tissue levels of angiogenic factors in hypothyroid rats, whereas haemodynamic factors would predominate in hyperthyroid rats. Our results also indicate that the renal dysfunctions of thyroid disorders are not related to cortical or medullary microvascular rarefaction and that the proteinuria of hyperthyroidism is not secondary to a podocyte deficit. Finally, TH or its analogues may be useful to increase capillarity in renal diseases associated with microvascular rarefaction.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Coronary Vessels / metabolism
  • Coronary Vessels / pathology*
  • Fibroblast Growth Factor 2 / blood
  • Fibroblast Growth Factor 2 / metabolism
  • Glomerular Mesangium / blood supply
  • Glomerular Mesangium / metabolism
  • Glomerular Mesangium / pathology
  • Heart Ventricles / metabolism
  • Heart Ventricles / pathology
  • Hyperthyroidism / blood
  • Hyperthyroidism / metabolism
  • Hyperthyroidism / pathology*
  • Hyperthyroidism / physiopathology
  • Hypothyroidism / blood
  • Hypothyroidism / metabolism
  • Hypothyroidism / pathology*
  • Hypothyroidism / physiopathology
  • Hypoxia-Inducible Factor 1, alpha Subunit / blood
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Kidney / blood supply*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney / physiopathology
  • Kidney Glomerulus / blood supply
  • Kidney Glomerulus / metabolism
  • Kidney Glomerulus / pathology*
  • Kidney Glomerulus / physiopathology
  • Male
  • Microvessels / metabolism
  • Microvessels / pathology*
  • Platelet Endothelial Cell Adhesion Molecule-1 / metabolism
  • Podocytes / metabolism
  • Podocytes / pathology
  • Proteinuria / etiology
  • Rats
  • Rats, Wistar
  • Ribonuclease, Pancreatic / blood
  • Ribonuclease, Pancreatic / metabolism
  • Thyroid Hormones / blood
  • Thyroid Hormones / metabolism
  • Vascular Endothelial Growth Factor A / blood
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Hif1a protein, rat
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Thyroid Hormones
  • Vascular Endothelial Growth Factor A
  • vascular endothelial growth factor A, rat
  • Fibroblast Growth Factor 2
  • angiogenin
  • Ribonuclease, Pancreatic