Abstract-In the present study we tested the hypothesis whether an anglotensm AT, receptor-mediated stlmulatlon of the bradykmm (BK)/mtnc oxide (NO) system can account for the effects of AT1 receptor antagonism on aortlc cGMP described previously m SHRSP Adult SHRSP were treated for 4 hours with anglotensm II (ANG II) (30 rig/kg per mm IV) or vehicle (0 9% NaCl IV) Animals were pretreated with vehicle, losartan (100 mg/kg PO), PD 123319 (30 mg/kg IV), losartan plus PD 123319, lcatlbant (500 @g/kg IV), NG-mtro-L-argmme methyl ester (L-NAME, 1 mg/kg IV), or mmoxldll (3 mg/kg IV) Mean arterial blood pressure (MAP) was contmuouqly monitored over the 4-hour experlmental period, and plasma ANG II and aortlc cGMP were measured by RIA at the end of the study ANG II infusion over 4 hours raised MAP by about 20 mm Hg. Losartan alone or losartan plus ANG II '1s well as mmoxldll plus ANG II markedly reduced blood pressure when compared to vehicle-treated or ANG II-treated ammals, respectively Plasma levels of ANG II were increased 2-fold by ANG II mfuslon alone or by ANG II m combmallon with lcatlbant, L-NAME, or mmoxldll The increase m plasma ANG II levels was even more pronounced after losartan treatment Aortlc cGMP content was slgmficantly increased by ANG II, losartan, losartan plus ANG II, and mmoxldll plus ANG II by 60%, 45%, 68%, and 52%, respectively (P< 05) The effects of ANG II and of losartan plus ANG II on aortlc cGMP content were both blocked by cotreatment with the AT2 receptor antagonist PD 123319 Icatlbant and L-NAME abohshed the effects of ANG II on aortlc cGMP Our results demonstrate the followmg (1) ANG II increases aortlc cGMP by an AT, receptor-medlated action because the effect could be prevented by an AT1 receptor antagonist, (2) the effect of ANG II was not secondary to blood pressure increase because it remained under reduction of MAP with mmoxldll, (3) losartan increased aortlc cGMP most likely by increasing plasma ANG II levels with a subsequent stlmulatlon of AT, receptors, and (4) the effects of AT1 receptor stlmulatlon are mediated by BK and, subsequently, NO because they were abolished by B, receptor blockade as well as by NO synthase mhlbltlon of ANG II generation, but, m addition, also potentlate the effects of bradykmm (BK) by mhlbltlon of BK degradation ' Two major tools have been introduced m recent years to study the contnbutlon of BK to the cardiovascular actlons of ACE inhibitors first, the combined treatment with an ACE mhlbltor and with a specific BK B2 receptor antagonist such as lcatlbant, and second, the comparison of the effects of an ACE inhibitor with those of an AT, receptor antagonist which block the RAS without an interaction with kmm metabolism. With these approaches, several mvestlgators have demonstrated that a number of actions of ACE mhlbltors IS related to cardiovascular control can be blocked by B2 receptor antagonism and thus be related to kuuns ' For example, m a series of expenrnents our laboratory demonstrated that longterm treatment with ACE inhibitors improved ca...

Most of the cardiac tumours in children are benign. Spontaneous regression is possible not only in rhabdomyoma. Surgical intervention is only required for children who develop relevant clinical symptoms. Total resection of the tumour is not the only therapeutic aim; more important is the restoration of the best possible heart function.

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The aortic velocity time integral (VTI) is an echocardiographic tool used to estimate cardiac output (CO) by multiplying it with the aortic valve (AV) area and heart rate (HR). Inaccurate measurement of AV diameter will lead to squared miscalculation of CO. The aortic VTI itself can serve as a left-ventricular (LV) output parameter. The normal range of aortic VTI in adulthood is relatively stable, compared with childhood, but reference data are lacking. The aim of this study was to establish reference values of VTI in infants, children, and adolescents. A retrospective analysis of 1223 echocardiographic examinations of healthy children (age 0-20 years, body surface area [BSA] 0.11-2.23 m(2)) was performed. Data were correlated with age, BSA, and HR, and age subgroups with normal distribution were determined. Interobserver and intraobserver variability was calculated. Aortic VTI ranged from mean 13.8 cm (10.0-18.4 cm 5-95th percentile) in neonates to 25.1 cm (19.6-32.8 cm 5-95th percentile) in children >17 years of age and had a positive correlation with age (r = 0.685, p < 0.001), BSA (r = 0.645, p < 0.001) and a negative correlation with HR (r = -0.710, p < 0.001). Interobserver and intraobserver variability were excellent (3.9 ± 3.1 and 4.6 ± 3.7 %, respectively). Calculated mean values and percentile charts for the different age groups can serve as reference data to easily judge LV output in patients with or without congenital heart disease without enlargement or dysfunction of the AV.