PMID: 9182246Feb 1, 1996Paper

Cardiac alpha(1)-adrenoceptors that regulate contractile function: subtypes and subcellular signal transduction mechanisms

Neurochemical Research
M Endoh

Abstract

Activation of alpha(1)-adrenoceptors as well as endothelin (ET) and angiotensin II (Ang II) receptors in cardiac muscle is coupled to acceleration of the hydrolysis of phosphoinositide (PI), with resultant production of inositol 1,4,5-trisphosphate (IP(3)) and diacylglycerol. There is an excellent correlation between the extent of acceleration of the PI hydrolysis and the positive inotropic effect (PIE) under most experimental conditions after the administration of a-adrenoceptor agonists, ET and Ang II in the rabbit ventricular muscle. The PIE of the alpha-adrenoceptor agonists, ET and Ang II is associated with a negative lusitropic effect and an increase in the sensitivity of myofilaments to Ca(2)+ ions. The PIE can be selectively inhibited by inhibitors of protein kinase C (PKC) such as staurosporine, NA 0345 and H-7, with little effect on the PI hydrolysis and the PIE of isoproterenol and Bay k 8644. Surprisingly, an activator of PKC, phorbol 12,13-dibutyrate (PDBu), selectively and more completely inhibited the PIE and acceleration of PI hydrolysis induced by the alpha-adrenoceptor agonists as well as by ET and Ang II in the rabbit. These receptor agonists consistently cause intracellular alkalinization by activation of Na...Continue Reading

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Citations

Nov 5, 2008·Circulation Journal : Official Journal of the Japanese Circulation Society·Masao Endoh
Jun 21, 2001·Biochemical and Biophysical Research Communications·A F JamesM J Shattock
Jan 24, 2002·Nature·Donald M Bers
Jan 29, 2002·Journal of Cardiovascular Pharmacology·L Chu, M Endoh
Jun 27, 2006·Journal of Pharmacological Sciences·Masao Endoh
Aug 26, 2006·Journal of Cardiovascular Medicine·Claudia PennaGianni Losano
Sep 1, 2001·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·B Civantos Calzada, A Aleixandre de Artiñano

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