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.
Subject(s)
Humans , Hypoxia , Atrial Natriuretic Factor , Endocrine Glands , Glyburide , Heart Atria , Natriuretic Peptides , Nitrogen , Oxygen , Radioimmunoassay , Stroke VolumeABSTRACT
It was well known that atrial myocytes systhesize atrial natriuretic peptide[ANP], and secrete it into the atrial lumen through the atrial endocardium. But the mechanism for regulation of ANP secretion has not been clearly elucidated, because there was little information of the atrial morphology concerning basal lamina. Basal lamina is surmised as one of barriers that control the movement of ANP, a large molecule. This study was attempted to elucidate the morphological characteristics of basal lamina and connective tissue fibers of atrial endocardial layer by scanning electron microscopy. Basal lamina was exposed by removal of the overlying endothelium. This was achieved by using OsO4 maceration, immersion in aqueous boric acid or EDTA treatment. After removal of the endothelial cell, the specimens were exposed to ultrasonic vibration in case of need. The external surface of basal lamina showed a fairly smooth appearance on the whole, although a few irregular folds are often encountered. Fenestrations, 0.1-1 micrometer in diameter, were randomly observed on the basal lamina, and they were circular to oval in shape. Margin of fenestrations was somewhat distinct and some was divided into two parts by linear structures. The structural differences of fenestrations between right and left atria were not found. The fibroreticular lamina under the basal lamina was revealed by removal of the endothelial cells and their basal lamina. This layer was consisted of interwoven fine fibers. These fine fibers were repeatedly divided and fused, forming reticular network. Some fine fibers connected with basal lamina. Some connective tissue fibers below fibroreticular layer were collected into thick bundles running parallel to myocytes. Above results may serve as a basis for the physiological and morphological studies of atrium.