Indapamide alters the cyclic AMP signal transduction pathway in cardiomyocytes in culture

Rabkin, Simon W.

doi:10.1016/0922-4106(94)90100-7

Cited by 5 publications

(2 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cells were scraped from Petri dishes and centrifuged for 2 min at 10 000 × g, the supernatants were saved, the pellets were washed in 95% ethanol and centrifuged at 10 000 × g, and the supernatants were combined. The supernatants were dried under a stream of N 2 at 55°C and cAMP was analyzed using a competitive protein binding assay method that utilized competitive binding between unlabelled cAMP and a fixed quantity of 3 H-labelled cAMP to a protein with high binding specificity for cAMP, as previously described (Rabkin 1994). The materials were purchased freeze dried from Amersham Canada (Oakville, Ont.).…”

Section: Cyclic Ampmentioning

confidence: 99%

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

Goutsouliak¹,

Wang²,

Cynader³

et al. 1997

Biochem. Cell Biol.

View full text Add to dashboard Cite

The purpose of this study was to visualize muscarinic receptors and their distribution on cardiomyocytes and to examine the effects of muscarinic cholinergic receptor (mACh-R) stimulation with carbachol on phosphatidylcholine hydrolysis. Cardiomyocytes were prepared as primary culture from 7-day-old chick embryo hearts. Cardiomyocytes, grown on cover slips, were labelled with BODIPY PZ, a fluorescent analog of the muscarinic receptor antagonist pirenzepine, and examined with a laser scanning confocal microscope, mACh-R clusters were visualized and were fairly homogeneous in size with diameters ranging from 0.5 to 1.0 micron. The number of receptor clusters per cell was 83.5 +/- 6.8 (mean +/- SEM) and clusters were found at the periphery of the cell. Cardiomyocytes, grown as a monolayer in dishes, were treated with the 10(-4) M carbachol, a mACh-R agonist, and the effects on phosphatidylcholine hydrolysis were ascertained in cells preincubated with [methyl-3H]choline for 18 h. Cells were washed, lysed, and subjected to thin-layer chromatography to separate [3H]choline in various metabolites of phosphatidylcholine. Carbachol significantly (p < 0.05) increased intracellular free choline and decreased cellular phospholipid consistent with phosphatidylcholine hydrolysis. Carbachol increased the amount of [3H]choline that effluxed out of the cardiomyocyte into the medium. Carbachol-induced choline efflux was not prevented by pretreatment with n-butanol, a phospholipase D inhibitor, suggesting that other lipases such as phospholipase C are the major enzyme involved in phosphatidylcholine hydrolysis. Pertussis toxin prevented carbachol-induced choline efflux and the changes in intracellular free choline and phospholipid. An action of carbachol through G proteins was supported by the ability of pertussis toxin to antagonize the carbachol-induced reduction in cAMP generation from isoproterenol. In summary, mACh-Rs, visualized in living cardiomyocytes, were peripheral to the nucleus. Phosphatidylcholine hydrolysis induced by mACh-R stimulation may be a signal transduction pathway for mACh-R in the cardiomyocyte, operating through inhibitory G proteins sensitive to pertussis toxin.

show abstract

Section: Cyclic Ampmentioning

confidence: 99%

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

Goutsouliak¹,

Wang²,

Cynader³

et al. 1997

Biochem. Cell Biol.

View full text Add to dashboard Cite

show abstract

“…Furthermore, a decrease in cAMP levels was detectable after brain microvascular endothelial cells were exposed to hypoxic conditions for 3 h (14). Moreover, indapamide was shown to augment cAMP production induced by forskolin, an adenylyl cyclase activator, but did not alter basal cAMP levels in cardiomyocytes alone (15). Therefore, indapamide may protect cerebral microvascular endothelial cells from ischemic dysfunction by increasing intracellular cAMP levels.…”

mentioning

confidence: 95%

Protective Action of Indapamide, a Thiazide-Like Diuretic, on Ischemia-Induced Injury and Barrier Dysfunction in Mouse Brain Microvascular Endothelial Cells

et al. 2007

View full text Add to dashboard Cite

Abstract. The aim of the present study was to elucidate the effects of indapamide on ischemic damage to the blood-brain barrier (BBB) in vitro. The ischemia / reperfusion conditions employed here significantly decreased the viability of mouse brain capillary endothelial (MBEC4) cells, an effect ameliorated by indapamide. Ischemia increased the permeability of MBEC4 cells to two cellular transport markers, sodium fluorescein and Evan's blue-albumin. Indapamide reduced the ischemia-induced hyperpermeability of cells. These results suggest that indapamide may have a protective role against ischemia-induced injury and dysfunction of the BBB.

show abstract

Comparison of Angiotensin II Type-1 and Type-2 Receptor Antagonists on Angiotensin II– Induced IP3 Generation in Cardiomyocytes

Goutsouliak

Rabkin

1998

General Pharmacology: The Vascular System

View full text Add to dashboard Cite

Indapamide alters the cyclic AMP signal transduction pathway in cardiomyocytes in culture

Cited by 5 publications

References 32 publications

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

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

Protective Action of Indapamide, a Thiazide-Like Diuretic, on Ischemia-Induced Injury and Barrier Dysfunction in Mouse Brain Microvascular Endothelial Cells

Comparison of Angiotensin II Type-1 and Type-2 Receptor Antagonists on Angiotensin II– Induced IP3 Generation in Cardiomyocytes

Contact Info

Product

Resources

About