Slowing of shortening velocity of rat cardiac myocytes by adenosine receptor stimulation regardless of beta‐adrenergic stimulation.

Autor: Strang, K T, Mentzer, R M, Moss, R L
Zdroj: Journal of Physiology; August 1995, Vol. 486 Issue: 3 p679-688, 10p
Abstrakt: 1. Single ventricular myocytes were enzymatically isolated, incubated with the A1‐purinergic and beta‐adrenergic receptor‐specific agonists N6‐cyclopentyladenosine (CPA) and isoprenaline (Iso), and then rapidly skinned. Ca2+ sensitivity of isometric tension and unloaded shortening velocity (Vo) were measured, and protein kinase A (PKA)‐specific phosphorylations of troponin I (TnI) and C‐protein were assessed by back‐phosphorylation of cell suspensions with [gamma‐32P]‐ATP. 2. Isoprenaline treatment decreased the Ca2+ sensitivity of isometric tension relative to propranolol‐treated controls, as did simultaneous stimulation with Iso and CPA (Iso + CPA). CPA alone had no effect on Ca2+ sensitivity. Vo was greater in Iso‐treated cells than in paired controls, while Vo was significantly less than control in both Iso + CPA‐treated and CPA‐treated cells. 3. Phosphorylation of TnI and C‐protein was increased by Iso treatment and also when Iso and CPA were simultaneously applied. CPA alone caused a significant decrease in the phosphorylation state of these two proteins. 4. From these results we conclude that A1‐purinergic receptor stimulation does not inhibit beta‐adrenergic receptor‐mediated phosphorylation of myofilament proteins, nor does it alter the Ca2+ sensitivity of isometric tension at the level of the myofilaments. However, A1‐receptor stimulation does decrease Vo at the level of the myofilaments by a mechanism that is independent of beta‐adrenergically mediated phosphorylation of TnI and C‐protein.
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