The roles of cell Ca2+, protein kinase C and the Na(+)-H+ antiport in the development of hypertension and insulin resistance

J Am Soc Nephrol. 1992 Nov;3(5):1049-63. doi: 10.1681/ASN.V351049.

Abstract

There is evidence that the cytosolic free Ca2+, protein kinase C, and the Na(+)-H+ antiport cross-communicate with one another through positive and negative feedback mechanisms, thereby maintaining cellular Ca2+ and pH homeostasis. This triumvirate may play a role in the development of insulin resistance--a common characteristic of both essential hypertension and non-insulin-dependent diabetes mellitus. Circulating cells from patients with essential hypertension and non-insulin-dependent diabetes mellitus demonstrate elevated cytosolic free Ca2+, increased protein kinase C activity, or both, and these perturbations are associated with augmented activity of the Na(+)-H+ antiport. If present in other cells (e.g., striated muscle cells and adipocytes), these alterations could underlie insulin resistance in essential hypertension and non-insulin-dependent diabetes mellitus.

Publication types

  • Editorial
  • Review

MeSH terms

  • Animals
  • Calcium / physiology*
  • Carrier Proteins / physiology*
  • Coronary Disease / etiology
  • Diabetes Mellitus, Type 2 / complications
  • Diabetes Mellitus, Type 2 / epidemiology
  • Diabetes Mellitus, Type 2 / ethnology
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Dogs
  • Down-Regulation
  • Feedback
  • Female
  • Glucose / metabolism
  • Humans
  • Hydrogen-Ion Concentration
  • Hypertension / complications
  • Hypertension / epidemiology
  • Hypertension / ethnology
  • Hypertension / metabolism
  • Hypertension / physiopathology*
  • Insulin / blood
  • Insulin / pharmacology
  • Insulin Resistance / physiology*
  • Male
  • Models, Biological*
  • Muscle, Smooth, Vascular / physiopathology
  • Natriuresis / drug effects
  • Obesity / complications
  • Obesity / ethnology
  • Obesity / physiopathology
  • Protein Kinase C / physiology*
  • Protein-Tyrosine Kinases / physiology
  • Receptor, Insulin / metabolism
  • Signal Transduction* / drug effects
  • Sodium-Hydrogen Exchangers
  • Sympathetic Nervous System / physiopathology

Substances

  • Carrier Proteins
  • Insulin
  • Sodium-Hydrogen Exchangers
  • Protein-Tyrosine Kinases
  • Receptor, Insulin
  • Protein Kinase C
  • Glucose
  • Calcium