Vasonatrin peptide attenuates the enhancement of electrically-induced intracellular calcium transient by isoproterenol in rat cardiac myocytes.
- Author:
Hai-Tao GUO
1
;
Miao-Zhang ZHU
;
Rong-Huai ZHANG
;
Hui BI
;
Bo ZHANG
;
Hai-Feng ZHANG
;
Jun YU
;
Shun-Yan LU
;
Jian-Ming PEI
Author Information
1. Department of Physioloy, Fourth Military Medical University, Xi'an 710032 China.
- Publication Type:Journal Article
- MeSH:
Animals;
Atrial Natriuretic Factor;
pharmacology;
Calcium;
metabolism;
Calcium Channels;
metabolism;
Cyclic GMP;
metabolism;
Depression, Chemical;
Female;
Guanylate Cyclase;
metabolism;
Isoproterenol;
pharmacology;
Male;
Myocytes, Cardiac;
metabolism;
Rats;
Receptors, Atrial Natriuretic Factor;
metabolism
- From:
Acta Physiologica Sinica
2004;56(3):335-340
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the effects of vasonatrin peptide (VNP) on electrically-induced intracellular calcium ([Ca(2+)](i)) transient and mechanism of the effects in the cardiac myocytes. The [Ca(2+)](i) transient was measured with a fluoremetric method. The effects of HS-142-1, 8-Br-cGMP and methylene blue (MB) on [Ca(2+)](i) transient in cardiac myocytes were also determined. Isoproterenol (Iso) at 10(-10)~10(-6) mol/L augmented electrically-induced [Ca(2+)](i) transient dose-dependently, which was (13+/-8)% (P>0.05), (26+/-13)% (P< 0.05), (66+/-10)% (P<0.01), (150+/-10)% (P<0.01) and (300+/-25)% (P<0.01), respectively. These effects were blocked by an beta-adrenergic bloker propranolol (10(-6) mol/L). The effect of Iso (10(-8) mol/L) on [Ca(2+)](i) transient was attenuated in a dose-dependent manner by VNP at 10(-10)~10(-6) mol/L, which was (99+/-3)% (P>0.05), (96+/-2)% (P<0.05), (84+/-6)% (P<0.01), (66+/-3)% (P<0.01) and (62+/-3)% (P<0.01), respectively. 8-Br-cGMP (10(-7)~10(-3) mol/L) aslo attenuated 10(-8) mol/L Iso-induced [Ca(2+)](i) transient dose-dependent. The effect of VNP on [Ca(2+)](i) transient was almost abolished in the presence of HS-142-1 (2x10(-5) mol/L), an antagonist of the natriuretic peptide guanylate cyclase (GC) receptors. MB (10(-5) mol/L), an inhibitor of GC, not only blocked the effect of VNP in myocytes, but also augmented electrically-induced [Ca(2+)](i) transient. VNP and HS-142-1 themselves did not change the [Ca(2+)](i) transient in the cardiac myocytes significantly. But MB augmented the [Ca(2+)](i) transient in the cardiac myocytes significantly. These results suggest that VNP attenuates [Ca(2+)](i) transient induced by Iso. This effect is possibly achieved by binding VNP with the natriuretic peptide GC receptors in the myocytes, leading to an increase in intracellular cGMP.
