What we still do not know about adrenal vein sampling for primary aldosteronism.

During the last two decades, primary aldosteronism has emerged as the most common cause of secondary hypertension, and advances in the diagnosis and treatment of this condition have improved patient care substantially. A major stumbling block in the evaluation and management of these patients, which ultimately guides treatment and prognosis, is answering the question, "Which adrenal gland(s) produce aldosterone?" Adrenal vein sampling has emerged as the only reliable method to determine the answer to this question; however, the methodology and criteria for lateralization have been determined empirically with little prospective data. The major remaining controversies surrounding adrenal vein sampling include: who should perform and who should undergo the procedure; what criteria should be used to define a successful study and lateralization of aldosterone production; whether cosyntropin should be infused during the procedure and how; and what to do when results are ambiguous? This article reviews some of the advances in the execution of this procedure, the variations in procedure, the data that fuel the controversies, and the issues that need to be resolved in the future.

Motor responses of autoimmune NZB/B1NJ and C57BL/6Nnia mice to arecoline and nicotine.

In 11-13 month C57BL/6Nnia mice, arecoline produced a dose-dependent decrease in motor activity at doses of 0.64-2.5 mg/kg, whereas at doses of 5.0-20.0 mg/kg arecoline produced a dose-dependent increase in motor activity. In marked contrast, age-matched NZB/B1NJ (New Zealand Black) mice failed to exhibit the first phase of the response, but showed a greater dose-dependent increase in motor activity following the doses of 10 and 20 mg/kg. Nicotine, 0.64-2.5 mg/kg, produced a dose-dependent decrease in motor activity in both strains. The effects of arecoline and nicotine were antagonized by scopolamine (2.5 mg/kg) and mecamylamine (1.0 mg/kg), respectively. These findings suggest that muscarinic neurotransmission may be altered in NZB/B1NJ mice, which produce brain-reactive autoantibodies, exhibit learning/memory dysfunctions, and also exhibit a loss of neurons staining positive for choline acetyltransferase.