Stimulation of phosphoinositide hydrolysis and inhibition of cyclic AMP formation by muscarinic agonists in developing chick heart.

  title={Stimulation of phosphoinositide hydrolysis and inhibition of cyclic AMP formation by muscarinic agonists in developing chick heart.},
  author={Stephanie A. Orellana and J. H. U. Brown},
  journal={Biochemical pharmacology},
  volume={34 8},

Changes in expression of a functional Gi protein in cultured rat heart cells.

Findings support the view that, although Gi is expressed, it is nonfunctional in 4-day-old cultured neonatal rat heart myocytes and acquisition of functional Gi is dependent on culture conditions and the ANG II receptor can couple to Gi in heart.

Enhanced Coupling of Neonatal Muscarinic Receptors in Rat Brain to Phosphoinositide Turnover

It is indicated that muscarinic receptors in fetal and newborn rat cerebral cortex are more efficiently coupled to stimulation of phosphoinositide turnover than in the adult.

Guanine Nucleotide‐Dependent Inositol Trisphosphate Formation in Chick Heart Cells

A saponin-permeabilized cell preparation that would allow external manipulation of the intracellular guanosine triphosphate (GTP) concentration is developed and evidence that a guanine nucleotide-binding protein is involved in the regulation of the polyphosphoinositide-specific phospholipase C in the heart is provided.

Subtype-specific Regulation of Muscarinic Receptor Expression and Function by Heterologous Receptor Activation (*)

Extended activation of β-adrenergic receptors results in an increase in mAChR number and muscarinic responsiveness in chick heart cells due to a cAMP-dependent protein kinase mediated increase in cm2 mRNA levels.

Visualization of muscarinic cholinergic receptors on chick cardiomyocytes and their involvement in phosphatidylcholine hydrolysis

Phosphatidylcholine hydrolysis induced by mACh-R stimulation may be a signal transduction pathway for mA cholinergic receptor in the cardiomyocyte, operating through inhibitory G proteins sensitive to pertussis toxin.

Pertussis Toxin‐Insensitive Phosphoinositide Hydrolysis, Membrane Depolarization, and Positive Inotropic Effect of Carbachol in Chick Atria

It is suggested that muscarinic agonist-induced PI turnover may be responsible for the membrane depolarization and positive inotropic effects of carbachol and acetylcholine, and that an increase in Na+ conductance underlies these responses.

Muscarinic control of the hyperpolarization‐activated current (if) in rabbit sino‐atrial node myocytes.

The results indicate that the inhibitory effect of ACh on if is mediated by G‐proteins activated by muscarinic receptors, and rule against the ACh action being mediated by PDE or by phosphoinositide turnover.



Ontogenesis of physiological responsiveness and guanine nucleotide sensitivity of cardiac muscarinic receptors during chick embryonic development.

The mAChR in hearts from 4-day embryos were significantly less susceptible to regulation of receptor number by in vivo agonist treatment and required a 2-5-fold greater dose of the muscarinic agonist carbachol to achieve a decrease in receptor number equivalent to that observed in 5- or 8-day embryonic hearts.

Phospholipid metabolism in embryonic rat fibroblasts following stimulation by a combination of the serum proteins S1 and S2.

Phospholipid metabolism has been investigated in embryonic rat fibroblasts which have been incubated in serum-free medium and subsequently stimulated by the growth-stimulating serum proteins S1 and S2 and it is shown that phosphatidylcholine biosynthesis is not influenced significantly during this time period.

Dual Mechanism for Inhibition of Calcium‐ Dependent Action Potentials by Acetylcholine in Avian Ventricular Muscle: Relationship to Cyclic AMP

These results are interpreted in a model in which cyclic AMP modulates the permeability of the membrane to Ca2+ and in which GTP regulates the β-adrenergic receptor and adenylate cyclase, and speculated that "indirect" muscarinic inhibition results from interference with GTP-dependent regu- lation of β- adrenergic receptors/adenylate Cyclase interaction.