Angiotensin II is a multifunctional hormone that exerts its effects by interacting will cell surface receptors. Two major subtypes of receptors (AT1 and AT2) have been distinguished by pharmacological and molecular biological techniques. AT1 receptors have been further subdivided into AT1A and AT1B receptors. Several other isoforms have been found, notably in nonmammalian systems, but further information is necessary before definitive classification can be made. AT1 receptors mediate most known functions of angiotensin II, while AT2 receptors may be important developmentally. The molecular, structural, and biochemical characteristics of these receptors have been described, as well as the factors that regulate their expression. This receptor system has been implicated in several cardiovascular diseases, including hypertension, restenosis after angioplasty, cardiac hypertrophy, heart failure, myocardial infarction, and ventricular remodeling. Structural analysis of AT receptors may provide the basis for the development of new therapeutic agents with enhanced specificity for the treatment of these diseases.

Exposure to particulate matter (PM) can induce the production of reactive oxygen and nitrogen species (ROS/RNS) in biological systems. Secondary organic aerosols (SOA) make up a substantial fraction of ambient fine PM. In this study, the contribution of hydrogen peroxide (H2O2) to intracellular ROS/RNS production upon exposure to naphthalene SOA was investigated using an oxidative stress indicator (carboxy-H2DCFDA) and a H2O2 scavenger (catalase). With the addition of catalase, the ROS/RNS response was substantially suppressed, indicating that H2O2 was the main type of ROS contributing to the measured ROS/RNS. We also found that H2O2 in naphthalene SOA extracts (H2O2[SOA]) could rapidly diffuse into cells and contribute to intracellular ROS/RNS, while another contribution was from H2O2 produced by cells (H2O2[cell]). The contributions from H2O2[SOA] and H2O2[cell] were both determined. The results showed that H2O2[SOA] (3.16–4.20 ng/μg) was substantially higher than H2O2[cell] (1.03–1.27 ng/μg), assuming the production of H2O2 by cells was constant over time. These findings demonstrated that H2O2 was the main ROS accumulated in cells upon exposure to naphthalene SOA and that the diffusion of H2O2[SOA] into the cells could represent one of the main pathways contributing to intracellular ROS/RNS.

Background Previous studies suggest that the migration of adventitial cells into the neointima after balloon angioplasty might have an important role in vascular lesion formation. The current experiments were designed to study the migration of adventitial cells in response to mechanical injury of the rat carotid artery. Methods and Results Adventitial cells were stained in situ with PKH26, a fluorescent dye, after balloon angioplasty of the rat common carotid artery. Animals were killed at different time points, and tissue sections were examined under light and fluorescence microscopy. PKH26-labeled cells were detected exclusively in the adventitia. No labeled cells were present in the media or the neointima at any time point examined. A highly cellular neoadventitial layer composed of myofibroblasts exhibited an extensive proliferative response 3 days after injury over the entire adventitial circumference. Conclusions Despite the prominent role that adventitial myofibroblasts seem to have in the postangioplasty remodeling process, they do not migrate to the medial or intimal layers in the rat carotid artery angioplasty model.

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