Characteristics of hypoxia-induced ANP Secretion in Perfused Beating Atria.
- Author:
Kong Soo KIM
1
;
Min Ho KIM
;
Chang Gon KIM
;
Suk Gee KIM
;
Gyung Woo JO
;
Hoon CHOI
Author Information
1. Department of Thoracic and Cardiovascular Surgery, Chonbuk University Medical school.
- Publication Type:Original Article
- Keywords:
Heart atrium;
Natriureitc peptide;
atrial;
Hypoxia;
Radioimmuroasy
- MeSH:
Anoxia;
Atrial Natriuretic Factor*;
Endocrine Glands;
Glyburide;
Heart Atria;
Humans;
Natriuretic Peptides;
Nitrogen;
Oxygen;
Radioimmunoassay;
Stroke Volume
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2000;33(5):398-406
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Cardiac atrium is an endocrine gland secreting a family of natriuretic peptides. The secretion of atrial natriuretic peptide(ANP) had been shown to be controlled by variable factors. The change in atrial dynamics have been considered as one of the most prominent stimuli for the stimulation of ANP secretion. Hypoxic stress has been shown to increase cardiac ANP secretion. However, the mechanism by which hypoxia increases ANP secretion cardiac ANP secretions. However, the mechanism by which hypoxia increases ANP secretion has not to be defined. Therefore, the purpose of the present study was tow-fold: to develop a protocol to defined the effect of hypoxia on ANP secretion in perfused beating rabbit atria and to clarify the mechanism responsible for the accentuation by hypoxia of ANP secretion. MATERIAL AND METHOD: Experiments have been done in perfused beating rabbit atria. ANP was measured by radioimmunoassay. RESULT: Hypoxic stimulus with nitrogen decreased atrial stroke volume. The decrease in atrial stroke volume recovered basal level during the period of recovery with oxygen. ANP secretion and the concentration of perfusate ANP in terms of extracellular fluid(ECF) translocation which reflects the rate of myocytic release of ANP were increased by hypoxia and returned to basal levels during the recovery. Changes in ECF translocation paralleled by hypoxia and returned to basal levels during the recovery. Changes in ECF translocation paralleled to that of atrial stroke volume. At the start of recovery in atrial storke volume, ECF tranalocation incrased for several minutes. The above responses were stable and reproducible. Glibenclamide treatment prevented the recovery in atrial stroke volume. Increments by hypoxia of ANP secretion and ANP concentration were suppressed by glibenclamide. CONCLUSIONS: These results indicate that hypoxia incrased atrial myocytic ANP release and that the mechanism responsible for the accentuation is partially related to the change in K+ATP channel activity.
