Agnoletti G, Cornacchiari A, Panzali A F, Ghielmi S, De Giuli F, Ferrari R
Cattedra di Cardiologia, Università degli Studi di Brescia, Italy.
Cardiovasc Res. 1990 Nov;24(11):938-45. doi: 10.1093/cvr/24.11.938.
The aim was to investigate the pattern of release of atrial natriuretic factor induced by mechanical and adrenergic stimulation from atria of rats with or without congestive heart failure.
Monocrotaline, a pyrrolizidine alkaloid, was given to rats to cause severe pulmonary hypertension, leading to a marked degree of right ventricular hypertrophy and failure. Measurements of noradrenaline and atrial natriuretic factor were performed in each cardiac chamber and in plasma. Right and left atria of control rats and rats with congestive heart failure were isolated and subjected to mechanical or adrenergic stimulation to study the in vitro release of atrial natriuretic factor.
Studies were performed on plasma, ventricles, and isolated right and left atria of 276 male Wistar rats, 80-100 g weight, with or without congestive heart failure.
In monocrotaline rats right and left ventricular concentrations of noradrenaline were significantly reduced. In the same rats concentrations of atrial natriuretic factor fell to 15.2% in the right atria and to 65.5% in the left atria. Whole heart content of atrial natriuretic factor was diminished, while plasma concentrations were increased sevenfold. Isolated hypertrophied right atria of failing hearts did not release atrial natriuretic factor in response to stretch or to isoprenaline (10(-9)M) and they were insensitive to the inotropic action of isoprenaline. On the other hand, non-hypertrophied left atria from the same animals released increased amounts of atrial natriuretic factor under basal conditions and after both stimuli, despite reduced tissue stores of the peptide.
Heart failure may deplete cardiac stores of noradrenaline and atrial natriuretic factor, especially in hypertrophied chambers, and can result in a decrease in the release of atrial natriuretic factor from atrial tissue in response to mechanical and adrenergic stimulation.
旨在研究有无充血性心力衰竭的大鼠心房，在机械和肾上腺素能刺激下利钠肽的释放模式。
给大鼠注射吡咯里西啶生物碱野百合碱，以引起严重的肺动脉高压，导致明显程度的右心室肥厚和衰竭。对每个心腔和血浆中的去甲肾上腺素和利钠肽进行测量。分离对照大鼠和充血性心力衰竭大鼠的右心房和左心房，进行机械或肾上腺素能刺激，以研究利钠肽的体外释放。
对276只体重80 - 100克、有无充血性心力衰竭的雄性Wistar大鼠的血浆、心室以及分离的右心房和左心房进行研究。
在野百合碱处理的大鼠中，右心室和左心室的去甲肾上腺素浓度显著降低。在同组大鼠中，右心房利钠肽浓度降至15.2%，左心房降至65.5%。全心利钠肽含量减少，而血浆浓度增加了7倍。衰竭心脏分离出的肥厚右心房对拉伸或异丙肾上腺素（10⁻⁹M）无利钠肽释放反应，且对异丙肾上腺素的变力作用不敏感。另一方面，同一动物未肥厚的左心房在基础状态和两种刺激后，尽管肽的组织储存减少，但利钠肽释放量增加。
心力衰竭可能会耗尽心脏中的去甲肾上腺素和利钠肽储备，尤其是在肥厚的心腔中，并可能导致心房组织在机械和肾上腺素能刺激下利钠肽释放减少。
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