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Magnesium is the second most abundant divalent ion in the body, but the effects of this cation on atrial natriuretic peptide (ANP) release have not been examined. The present study was conducted to determine the effect of magnesium on ANP secretion. Experiments were conducted in six groups of male Wistar rats. Each group was assigned a diet containing a different amount of magnesium. Plasma magnesium was 0.42 +/- 0.01, 0.63 +/- 0.01, 0.75 +/- 0.02, 0.97 +/- 0.03, 1.03 +/- 0.01, and 1.19 +/- 0.01 mM in groups I, II, III, IV, V, and VI, respectively. Plasma ANP concentration was significantly higher in the hypermagnesemic animals and significantly lower in the hypomagnesemic rats. A significant positive correlation was found between plasma magnesium and plasma ANP levels (y = 88 + 23 chi; r = 0.46; P less than 0.01). ANP concentration in the atria was lower in hypomagnesemic rats and higher in hypermagnesemic rats. This suggests that the low concentrations of ANP found in the plasma of hypomagnesemic animals were due to the lack of ANP in the atria. The atria from the various groups were isolated and perfused in a modified Langendorff apparatus to measure the rate of ANP secretion. Our results showed that the hypomagnesemic rats have a lower release rate as opposed to that seen in hypermagnesemic animals. A significant correlation was also seen between ANP secretion and tissue ANP concentration. The higher rate of ANP release from the heart of hypermagnesemic animals was due to the presence of more ANP, which was reduced during hypomagnesemia.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of intracellular signals in the regulation of atrial natriuretic peptide (ANP) release was studied using the isolated left and right atria from a rat. The atria were perfused with Tyrode's solution, equilibrated with 95% O2-5% CO2 at 37 degrees C with a constant flow of 0.5 ml/min. Addition of epinephrine (10(-6) M), an alpha- and beta-agonist, to the perfusate induced the biphasic release of ANP from the right atrium without effect on the left. The initial peak (19.2 +/- 2.6 pg.min-1.ml-1) occurs 2-4 min after the administration of epinephrine, which lasted 4-6 min and returned to base line (10.4 +/- 1.1 pg.min-1.mg-1). The second peak (16.5 +/- 2.0 pg.min-1.ml-1) appeared 30-35 min after epinephrine administration and was sustained for 100 min, at which time the experiment was terminated. The first peak was stimulated by isoproterenol (10(-6) M), a beta-agonist, and blunted by propranolol (10(-6) M), a beta-antagonist. The second peak appeared following methoxamine (10(-6) M), an alpha-agonist, and could be suppressed by phentolamine (10(-6) M), an alpha-antagonist. These studies indirectly suggest that the adenosine 3',5'-cyclic monophosphate system and the inositol triphosphate system are involved in ANP secretion, with the former responsible for the initial rapid release and the latter maintaining the secretion.

The effect of thyroid hormone on circulating levels of atrial natriuretic peptide (ANP) was studied in experimental hyperthyroid and hypothyroid rats. Plasma ANP was 102 +/- 5 pg/ml in euthyroid rats, 82 +/- 4 pg/ml in hypothyroid rats, and 138 +/- 11 pg/ml in hyperthyroid rats. We have also measured immunoreactive ANP in the atria of euthyroid, hypothyroid, and hyperthyroid rats. ANP content and concentration in the atria were lower (546 +/- 32 pg/mg tissue) in hyperthyroid rats than in hypothyroid rats (802 +/- 74 pg/mg tissue). Right atrium from euthyroid, hypothyroid, and hyperthyroid rats was superfused with a modified Langendorff preparation. Spontaneous release of ANP was significantly higher from the hyperthyroid rats (20 +/- 2 pg.min-1.mg-1) than from the hypothyroid rats (5.6 +/- 0.5 pg.min-1.mg-1). ANP release from the euthyroid rats was 9.3 +/- 1.2 pg.min-1.mg-1. These results indicate hyperthyroidism causes an increase in ANP secretion and a decreased release occurs during hypothyroidism.