Lobar emphysema due to anomalous aortic origin of the left pulmonary artery.

The unusual case of an infant with aortic origin of the left pulmonary artery is presented. The patient developed a rare complication of lobar emphysema due to bronchial compression from the enlarged right pulmonary artery. Operative anastomosis of the left pulmonary artery to the pulmonary trunk was successful, with subsequent resolution of the lobar emphysema.

Angiotensin-(1-7) binding at angiotensin II receptors in the rat brain.

Angiotensin-(1-7) (Ang-(1-7)) is reported to be equipotent with angiotensin II (AII) in producing some central biological effects but the receptors responsible for these actions have not been defined. Three classes of receptor have been proposed: AT1, AT2, and a putative Ang-(1-7) selective receptor. This study specifically evaluates Ang-(1-7) competition at AII binding sites (AT1 and AT2) in the rat brain. 125I Sar1 Ile8 AII (269-312 pM) was used to conduct receptor autoradiographic binding assays in brain sections. Competition with Ile5 AII and Val5 AII was similar at nuclei in which either AT1 or AT2 receptor subtypes predominate (Ki = 11-18 nM). Ang-(1-7) competed 150-fold less effectively than native AII at AT1 predominant brain nuclei (Ki = 2.4 microM). At brain regions where AT2 receptors predominate, Ang-(1-7) showed a very low affinity (Ki = 104 microM) for the majority of the 125I Sar1 Ile8 AII binding sites (AT2). A small proportion of 125I Sar1 Ile8 AII binding sites showed an affinity of 2.0 microM, presumably AT1 receptors present in those brain regions. For biological responses where Ang-(1-7) is reported to be equipotent with AII, it is unlikely that these actions are mediated by the widely distributed AT1 or AT2 receptor subtypes which recognize 125I Sar1 Ile8 AII.

Angiotensin II binding sites in the hamster brain: localization and subtype distribution.

This study was designed to characterize the distribution of angiotensin II (AII) binding sites in the hamster brain. Brain sections were incubated with [125I][sar1,ile8]-angiotensin II in the absence and presence of angiotensin II receptor subtype selective compounds, losartan (AT1 subtype) and PD123177 (AT2 subtype). Binding was quantified by densitometric analysis of autoradiograms and localized by comparison with adjacent thionein stained sections. The distribution of AII binding sites was similar to that found in the rat, with some exceptions. [125I][sar1,ile8]-angiotensin II binding was not evident in the subthalamic nucleus and thalamic regions, inferior olive, suprachiasmatic nucleus, and piriform cortex of the hamster, regions of prominent binding in the rat brain. However, intense binding was observed in the interpeduncular nucleus and the medial habenula of the hamster, nuclei void of binding in the rat brain. Competition with receptor subtype selective compounds revealed a similar AII receptor subtype profile in brain regions where binding is evident in both species. One notable exception is the medial geniculate nucleus, predominately AT1 binding sites in the hamster but AT2 in the rat. Generally, the AII binding site distribution in the hamster brain parallels that of the other species studied, particularly in brain regions associated with cardiovascular and dipsogenic functions. Functional correlates for AII binding sites have not been elucidated in the majority of brain regions and species mismatches might provide clues in this regard.