These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Direct binding of atrial natriuretic factor to adrenocortical mitochondria. Author: Heisler S. Journal: Eur J Pharmacol; 1989 Mar 21; 162(2):281-8. PubMed ID: 2524398. Abstract: Atrial natriuretic factor (ANF) is a known antagonist of adrenocortical aldosterone synthesis and secretion. Immunocytochemical and ultrastructural autoradiographic evidence suggests that ANF may bind to mitochondria of a number of target tissues including adrenal cortex. Consequently, the ability of [125I]ANF to bind directly to isolated bovine adrenocortical mitochondria was assessed. Mitochondrial-enriched subfractions of adrenocortical homogenates were prepared by differential and sucrose gradient centrifugation. Mitochondrial membranes specifically bound [125I]ANF. At 20 degrees C equilibrium was achieved between 90 and 120 min. [125I]ANF binding was inhibited in a concentration-dependent manner by unlabelled ANF (IC50 about 5 x 10(-10) M); other substances with biological actions on glomerulosa cells (arginine vasopressin, angiotensin II) did not alter [125I]ANF binding. Similarly shorter ANF fragments including ANF-(103-125), ANF-(99-109) and ANF-(111-126) had no significant competitive effect on binding of the labelled ligand. While Ca2+ and Mg2+ had little effect on ANF binding, the divalent cation Ni2+ inhibited binding of radiolabelled ANF by 90% (IC50 about 8.3 x 10(-5) M). Scatchard analysis revealed both high and low affinity binding sites for [125I]ANF with respective KDs of 4.7 +/- 7 pM and 0.3 +/- 0.02 nM and receptor densities of 1.1 +/- 0.2 and 8.6 +/- 0.1 pmol/mg protein. At 0.2 nM, Ni2+ caused a 5-fold and 100-fold decrease in high and low affinity [125I]ANF binding, respectively. The data demonstrate that ANF binds directly to mitochondria and perhaps it is at this site that the atrial peptide negatively modulates agonist-induced aldosterone biosynthesis.[Abstract] [Full Text] [Related] [New Search]