Schiebinger R J, Linden J
Circ Res. 1986 Jul;59(1):105-9. doi: 10.1161/01.res.59.1.105.
Atrial natriuretic peptide is a potent diuretic hormone secreted by the atria in response to volume expansion. We examined the effect of resting tension on atrial natriuretic peptide secretion by rat atria superfused in vitro. Left atria were hooked between an electrode and force transducer and superfused with medium 199. The atria were studied at a pacing frequency of 0 or 3 Hz. Atrial natriuretic peptide content of the superfusate was measured by radioimmunoassay. In nonpaced and paced atria, increasing resting tension three- to five-fold caused immunoreactive atrial natriuretic peptide secretion to increase by 35 +/- 5% (mean +/- SEM, n = 6, p less than 0.01) and 30 +/- 3% (n = 4, p less than 0.01), respectively. Lowering resting tension by 50% in nonpaced and paced atria lowered immunoreactive atrial natriuretic peptide secretion by 30 +/- 3% (n = 7, p less than 0.01) and 24 +/- 3% (n = 6, p less than 0.01), respectively. To exclude the possibility that release of norepinephrine or acetylcholine from endogenous nerve endings was mediating this effect, the atria were superfused with the combination of propranolol 0.1 microM, phentolamine 1.0 microM, and atropine 10 microM. These concentrations of the antagonists were 125-fold or higher than their Kd for binding to their respective receptors. The antagonists did not block the rise in immunoreactive atrial natriuretic peptide secretion; neither did they inhibit an established rise in immunoreactive atrial natriuretic peptide secretion induced by increasing the resting tension.(ABSTRACT TRUNCATED AT 250 WORDS)
心房利钠肽是心房在容量扩张时分泌的一种强效利尿激素。我们研究了静息张力对体外灌流的大鼠心房分泌心房利钠肽的影响。将左心房钩在电极和力传感器之间，并用199培养基灌流。以0或3Hz的起搏频率研究心房。通过放射免疫测定法测量灌流液中的心房利钠肽含量。在非起搏和起搏的心房中，将静息张力增加三至五倍分别导致免疫反应性心房利钠肽分泌增加35±5%（平均值±标准误，n = 6，p<0.01）和30±3%（n = 4，p<0.01）。在非起搏和起搏的心房中，将静息张力降低50%分别使免疫反应性心房利钠肽分泌降低30±3%（n = 7，p<0.01）和24±3%（n = 6，p<0.01）。为了排除内源性神经末梢释放去甲肾上腺素或乙酰胆碱介导这种效应的可能性，用0.1μM普萘洛尔、1.0μM酚妥拉明和10μM阿托品的组合灌流心房。这些拮抗剂的浓度比它们与各自受体结合的Kd高125倍或更高。拮抗剂并未阻断免疫反应性心房利钠肽分泌的增加；它们也没有抑制因增加静息张力而导致的免疫反应性心房利钠肽分泌的既定增加。（摘要截断于250字）
