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Updated: Feb 8, 2026

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
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Reduced secretion of parathyroid hormone and hypocalcemia in systemic heterozygous ATP2B1-null hypertensive mice

Yosuke Ehara1, Nobuhito Hirawa2, Kouichiro Sumida1

  • 1Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.

Hypertension Research : Official Journal of the Japanese Society of Hypertension
|June 29, 2018
PubMed

Insights

The ATP2B1 gene impacts blood pressure by affecting calcium homeostasis. ATP2B1 deficiency causes hypocalcemia and impaired nitric oxide production, contributing to hypertension.

Area of Science:

  • Genetics
  • Cardiovascular Biology
  • Endocrinology

Background:

  • The ATP2B1 gene encodes plasma membrane calcium ATPase 1 (PMCA1), traditionally linked to intracellular calcium regulation.
  • Previous studies linked systemic heterozygous ATP2B1-null (ATP2B1+/-) mice to hypertension via impaired endothelial nitric oxide synthase (eNOS) activity and reduced nitric oxide (NO) production.
  • Emerging evidence suggests ATP2B1's role extends beyond cellular levels to whole-body calcium metabolism.

Purpose of the Study:

  • To elucidate the systemic roles of ATP2B1 in calcium homeostasis.
  • To investigate the impact of ATP2B1 deficiency on blood pressure regulation.
  • To examine alterations in calcium-related factors in ATP2B1+/- mice.

Main Methods:

  • Analysis of calcium-related factors in systemic heterozygous ATP2B1-null (ATP2B1+/-) mice.
  • Assessment of ATP2B1 expression in the kidney and small intestine.
  • Measurement of intact parathyroid hormone (PTH) levels and bone mineral density.

Main Results:

  • ATP2B1+/- mice exhibited hypocalcemia and decreased ATP2B1 expression in the kidney and small intestine.
  • Hypercalciuria and lower intact-PTH levels were observed in ATP2B1+/- mice.
  • Increased bone mineral density was noted, suggesting inhibited bone resorption without PTH compensation.

Conclusions:

  • ATP2B1 plays a crucial role in maintaining calcium homeostasis and controlling blood pressure.
  • Hypocalcemia in ATP2B1 deficiency may stem from reduced bone resorption and impaired PTH secretion.
  • Altered NO production due to reduced PTH may contribute to increased vascular contractility and hypertension.

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