Contrary to public perception, hypertension remains one of the most important public health problems in the United States, affecting 46% of adults with increased risk for heart attack, stroke, and kidney diseases. The mechanisms underlying poorly controlled hypertension remain incompletely understood. Recent development in the Cre/LoxP approach to study gain or loss of function of a particular gene has significantly helped advance our new insights into the role of proximal tubule angiotensin II (Ang II) and its AT₁ (AT_1a) receptors in basal blood pressure control and the development of Ang II-induced hypertension. This novel approach has provided us and others with an important tool to generate novel mouse models with proximal tubule-specific loss (deletion) or gain of the function (overexpression). The objective of this invited review article is to review and discuss recent findings using novel genetically modifying proximal tubule-specific mouse models. These new studies have consistently demonstrated that deletion of AT₁ (AT_1a) receptors or its direct downstream target Na⁺/H⁺ exchanger 3 (NHE3) selectively in the proximal tubules of the kidney lowers basal blood pressure, increases the pressure-natriuresis response, and induces natriuretic responses, whereas overexpression of an intracellular Ang II fusion protein or AT₁ (AT_1a) receptors selectively in the proximal tubules increases proximal tubule Na⁺ reabsorption, impairs the pressure-natriuresis response, and elevates blood pressure. Furthermore, the development of Ang II-induced hypertension by systemic Ang II infusion or by proximal tubule-specific overexpression of an intracellular Ang II fusion protein was attenuated in mutant mice with proximal tubule-specific deletion of AT₁ (AT_1a) receptors or NHE3. Thus, these recent studies provide evidence for and new insights into the important roles of intratubular Ang II via AT₁ (AT_1a) receptors and NHE3 in the proximal tubules in maintaining basal blood pressure homeostasis and the development of Ang II-induced hypertension.

We report a case of descending necrotizing mediastinitis (DNM) in a 68-year-old male who presented in acute respiratory distress accompanied with anterior cervical neck swelling and pain with swallowing. Contrast enhanced computed tomography (CECT) of the neck demonstrated a large, peripherally enhancing retropharyngeal fluid and air collection that appeared to communicate with a fluid and air collection within the mediastinum. CECT of the chest demonstrated punctate foci of air and fat stranding along the anterior and superior mediastinum. Radiological evidence and the presence of necrosis on surgical debridement of the retropharyngeal abscess established the diagnosis of DNM. This case emphasizes the role of computed tomography (CT) in the diagnosis of DNM and demonstrates the utility of chest imaging in a high-risk patient who presents with a retropharyngeal abscess.