pituitrin and nickel-chloride

Despite the importance of brain-mediated sympathetic activation in the morbidity and mortality of patients with high blood pressure, the precise cellular mechanisms involved remain largely unknown. We show that an imbalanced interaction between two opposing currents mediated by potassium (I(A)) and calcium (I(T)) channels occurs in sympathetic-related hypothalamic neurons in hypertensive rats. We show that this imbalance contributes to enhanced membrane excitability and firing activity in this neuronal population. Knowledge of how these opposing ion channels interact in normal and disease states increases our understanding of underlying brain mechanisms contributing to the high blood pressure condition.

Topics: 4-Aminopyridine; Action Potentials; Animals; Calcium Channel Blockers; Calcium Channels, T-Type; Calcium Signaling; Dendrites; Electrophysiological Phenomena; Gene Expression; Hypertension, Renovascular; Hypothalamus; Male; Medulla Oblongata; Membrane Potentials; Neurons; Nickel; Oxytocin; Paraventricular Hypothalamic Nucleus; Patch-Clamp Techniques; Rats; Rats, Wistar; Shal Potassium Channels; Sympathetic Nervous System; Vasopressins