Expression of proTRH in the heart has already been shown. Recent data (1) indicate important role of TRH in arterial blood pressure in spontaneously hypertensive rats. TRH can also increase cardiac performance in rats with ischemic cardiomyopathy (2). Thus, in addition to catecholamine and angiotensin II, pro-TRH/TRH may be another important axis that affects hemodynamics and cardiac function (2). It was of interest to show if cardiac tissue could secrete TRH and how this secretion could be controlled. For in vivo experiments, arterial (a. carotis) and venous (v. jugularis) canula was inserted under Inactin anesthesia (133 mg kg^-1) on the day of the experiment. One hour later the animals were injected with 0.5 ml of undiluted specific rabbit TRH antiserum or normal rabbit serum intravenously. Mean arterial blood pressure and heart rate were measured 30 and 90 min later. Hemorrhage (30% of circulating blood volume) was induced by opening the arterial canula at a speed 0.3 ml min^-1. Arterial blood pressure and heart rate were than measured immediately after the hemorrhage as well as 60 and 120 min later. For in vitro experiments the heart was rapidly removed after humane killing of intact adult male rats and tissue from the left auricle (LA) and ventricle (LV) dissected. Pieces about 1 mm wide were used for incubations. The incubations were performed in stoppered Eppendorf tubes at 37°C in a 5% CO₂-95% O₂ atmosphere. After a 60 min preincubation period, the septum was incubated for four 15-min periods in basal or stimulating media in a final volume of 150 μl. The amount of secreted TRH was determined by RIA. Immunoneutralization of endogenous TRH with specific antibody results in a deeper decrease of mean arterial pressure (to 22.2 ± 3.7 and 40 ± 10.6 mmHg in experimental and control rats, respectively, p<0.05, n=6, Student's t test) at the end of bleeding of experimental rats. RT PCR revealed two times higher TRH expression in LA than in LV of intact rats. Slices secreted measurable amount of TRH. Angiotensin II (10 nM) added into the medium significantly decreased basal secretion of TRH by 38% (pairwise multiple comparison procedures (Tukey test): p<0.001), and this effect was prevented by addition of Losartan, an inhibitor of AT1 receptors. Hyposmotic medium (202 mOsm) or high KCl significantly (p<0.05) increased the amount of secreted TRH. The effect of hyposmotic stimulation could not be inhibited by angiotensin II (10 or 100 nM). In conclusion, endogenous TRH has a role in regulation of blood pressure in bleeding rats. TRH secretion from heart slices possesses attributes of regulated secretion: it could be either stimulated or inhibited. Angiotensin II inhibits TRH secretion by heart tissue and its effect is mediated by AT1 receptors.