Potassium Channels in the Cardiovascular System

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  • Topic: Ion channel, Action potential, Potassium channel
  • Pages : 7 (2064 words )
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  • Published : September 28, 2008
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Research & Methods
Potassium Channels in the Cardiovascular System Response
to Diabetes Mellitus and Hypertension


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.

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 rectifier channels hyperpolarize the neuron, resulting in a longer action potential. Ca2+ activated channels (KCa) opens in the presence of calcium ions. For regulating the heartbeat, there are Ach channels (KAch) which opens when exposed to acytlcholine. These channels are important to bodily functions, and their failure can result in a host of diseases.

Potassium channels have been linked with a disease called Long-QT syndrome, faulty potassium ions in the heart and inner ear. This disorder often results in deafness and fatal arrhythmia. In the case cited by Shier, Butler, and Lewis (2004), a Norwegian family had four children. The offspring were all deaf, and three died before the age of ten. While it cannot be cured, as it is a genetic disorder, long-QT syndrome may be treated with drugs, pacemakers, and surgery.

Potassium ions, particularly KCa (Liu et al. 1998) and KAch, (Liu et al. 2001) have crucial roles in the cardiovascular system, the target of this report. Both have been linked with hypertension and diabetes mellitus. Many studies have been performed to more fully understand the role which potassium ion channels play to these ends. Two specific experiments were reviewed in this paper to isolate and to comprehend the functional role of K+ channels. The first concerns elevated glucose levels; the latter, hypertension. Glucose Concentration and K+ Channels

In experiments by Liu, Terata, Rusch, and Gutterman (2001), the affects of glucose levels were tested on voltage-gated K+ channels in small coronary arteries. The test animals in these experiments were rats. After a series of tests, it was found that high glucose levels in the coronary arteries have three deleterious effects. First, they increase the production of superoxide. Second, elevated glucose levels decrease the sensitivity of K+ channels to 4-aminopyridine, a Kv channel blocker. Lastly, they reduce contractions induced by 4-aminopyridine. Coronary arteries were incubated in three...
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