Potassium Channels in the Cardiovascular System
Research & Methods
Concerning
Potassium Channels in the Cardiovascular System Response to Diabetes Mellitus and Hypertension
ABSTRACT
Research concerning the functional role of potassium ions in the cardiovascular system with respect to hypertension and diabetes mellitus has boomed in the past decade. Through a series of experiments, data has been gathered which shows the diverse response of K+ channels in the cardiovascular system when exposed to these diseases.
In elevated glucose levels, diabetes mellitus, the potassium ion channels in vascular smooth muscle cells produced increased superoxides and decreased responsiveness of normal stimulation from 4-aminopyridine. Essentially, they became During hypertension, however, K+ channels adapted to the harsh environment, attempting to maintain normal function.
These experiments were conducted using a wide array of modern biological techniques. The studies for elevated glucose levels utilized patch-clamp, hydroethidine dying, and videomicroscopy. For hypertension, patch-clamp, Western immunoblotting, and ribonuclease protection assay were the methods by which information was gathered on K+ channels.
All of these experiments were performed on rats in an academic setting.
Introduction The potassium ion channels are a main component on the anatomy and physiology in animals, as they are, in part, responsible for the depolarization and hyperpolarization of neurons, especially in the cardiovascular system (Moyes and Schulte 2006). K+ channels are voltage-gated ion channels, though certain types of these channels need accessory ions to open properly (Shier et al. 2004). Four types of potassium ion channels will be discussed in this paper. According to Moyes and Schulte (2006), delayed rectifier channels open in response to a change in membrane potential, repolarizing after an axon potential. The A channel (KA channel) makes the neuron more excitable as it opens when the neuron is depolarized. Inward
Concerning
Potassium Channels in the Cardiovascular System Response to Diabetes Mellitus and Hypertension
ABSTRACT
Research concerning the functional role of potassium ions in the cardiovascular system with respect to hypertension and diabetes mellitus has boomed in the past decade. Through a series of experiments, data has been gathered which shows the diverse response of K+ channels in the cardiovascular system when exposed to these diseases.
In elevated glucose levels, diabetes mellitus, the potassium ion channels in vascular smooth muscle cells produced increased superoxides and decreased responsiveness of normal stimulation from 4-aminopyridine. Essentially, they became During hypertension, however, K+ channels adapted to the harsh environment, attempting to maintain normal function.
These experiments were conducted using a wide array of modern biological techniques. The studies for elevated glucose levels utilized patch-clamp, hydroethidine dying, and videomicroscopy. For hypertension, patch-clamp, Western immunoblotting, and ribonuclease protection assay were the methods by which information was gathered on K+ channels.
All of these experiments were performed on rats in an academic setting.
Introduction The potassium ion channels are a main component on the anatomy and physiology in animals, as they are, in part, responsible for the depolarization and hyperpolarization of neurons, especially in the cardiovascular system (Moyes and Schulte 2006). K+ channels are voltage-gated ion channels, though certain types of these channels need accessory ions to open properly (Shier et al. 2004). Four types of potassium ion channels will be discussed in this paper. According to Moyes and Schulte (2006), delayed rectifier channels open in response to a change in membrane potential, repolarizing after an axon potential. The A channel (KA channel) makes the neuron more excitable as it opens when the neuron is depolarized. Inward
Cited: Beech, D., A. Cheong, and N. Rusch, 2005. Regulation of Arterial Tone by KV1 Potassium Channels Berger, M., C. Vandier, P. Bonnet, W. Jackson, and N. Rusch, 1998. Intracellular acidosis differentially regulates KV channels in coronary and pulmonary vascular muscle Cox, R. and N. Rusch, 2002. New expression profiles of voltage-gated ion channels in arteries exposed to high blood pressure Gauthier, K. and N. Rusch, 2001. Rat coronary endothelial cell membrane potential responses during hypertension Li, H., D. Gutterman, N. Rusch, A. Bubolz, and Y. Liu, 2004. Nitration and functional loss of voltage-gated K+ channels in rat coronary microvessels exposed to high glucose Liu Y, Hudetz AG, Knaus HG, Rusch N., 1998. Increased expression of Ca2+-sensitive K+ channels in the cerebral microcirculation of genetically hypertensive rats: evidence for their protection against cerebral vasospasm Liu, Y., K. Pleyte, H. Knaus, and N. Rusch, 1997. Increased expression of Ca2+-sensitive K+ channels in aorta of hypertensive rats Liu, Y., K. Terata, N. Rusch, and D. Gutterman, 2001. High glucose impairs voltage- gated K+ channel current in rat small coronary arteries Moyes, C. and P. Schulte, 2006. Principles of Animal Physiology. Benjamin Cummings. Rusch, N. and A. Runnells, 1994. Remission of high blood pressure reverses arterial potassium channel alterations Shier, D., J. Butler, and R. Lewis, 2004. Hole’s Human Anatomy and Physiology. McGraw-Hill.