Osteomyelitis of the central skull base poses significant challenges for timely and accurate diagnosis. Aggressive management with antimicrobials, coupled with surgical debridement in select cases, may avoid serious neurologic morbidity and mortality.

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Abstract-In moderate sodium-replete states, dopamine 1-like receptors (D 1 R/D 5 R) are responsible for regulating Ͼ50% of renal sodium excretion. This is partly mediated by internalization and inactivation of NaKATPase, when associated with adapter protein 2. We used dopaminergic stimulation via fenoldopam (D 1 -like receptor agonist) to study the interaction among D 1 -like receptors, caveolin-1 (CAV1), and the G protein-coupled receptor kinase type 4 in cultured human renal proximal tubule cells (RPTCs). We compared 2 groups of RPTCs, 1 of cell lines that were isolated from normal subjects (nRPTCs) and a second group of cell lines that have D 1 -like receptors that are uncoupled (uncoupled RPTCs) from adenylyl cyclase second messengers. In nRPTCs, fenoldopam increased the plasma membrane expression of D 1 R (10.0-fold) and CAV1 (1.3-fold) and markedly decreased G protein-coupled receptor kinase type 4 by 94Ϯ8%; no effects were seen in uncoupled RPTCs. Fenoldopam also increased the association of adapter protein 2 and NaKATPase by 53Ϯ9% in nRPTCs but not in uncoupled RPTCs. When CAV1 expression was reduced by 86.0Ϯ8.5% using small interfering RNA, restimulation of the D 1 -like receptors with fenoldopam in nRPTCs resulted in only a 7Ϯ9% increase in association between adapter protein 2 and NaKATPase. Basal CAV1 expression and association with G protein-coupled receptor kinase type 4 was decreased in uncoupled RPTCs (58Ϯ5% decrease in association) relative to nRPTCs. We conclude that the scaffolding protein CAV1 is necessary for the association of D 1 -like receptors with G protein-coupled receptor kinase type 4 and the adapter protein 2-associated reduction in plasma membrane NaKATPase.