Myogenic responsiveness and autoregulation of renal and cerebral blood flow is altered in hypertension and diabetes. These conditions are the major risk factors for the development of cerebral vascular dysfunction, stroke, and chronic kidney disease. Loss of myogenic tone contributes to increased transmission of pressure to the cerebral capillaries, breakdown of the blood brain barrier, cerebral edema and neurological damage following ischemia or trauma. Impaired auto regulation of renal blood flow leads to glomerulosclerosis, proteinuria and chronic kidney disease. My lab is interested in identifying the role of altered ion-channel activity of vascular smooth muscle (VSM) cells in cerebral and renal vasculature in Fawn Hooded Hypertensive (FHH) rats. The FHH rat is a good genetic model system in which autoregulation of renal and cerebral blood flow is impaired, and we have developed a congenic strain of FHH.1BN rats in which a small region of chromosome 1 from BN rats is transferred into the FHH genome and autoregulation is restored. My lab utilizes enzymatically isolated VSM cells to perform patch clamp and calcium imaging studies (single channel and whole cell current recording), and, we perform vascular reactivity studies both in vivo and in vitro. We study ion-channels such as calcium-activated potassium, voltage-gated calcium, TRP, and ENaC, in the regulation of vascular tone. My lab also studies the role of second messenger signaling molecules such as PKC, DAG, IP3, etc., in the regulation of these ion-channels.
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