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I am confused about membrane transport and the purpose of Na+ pumps and K+.

What's the importance?

2007-01-17 16:31:55 · 5 answers · asked by An Agent of Chaos 5 in Science & Mathematics Biology

I meant just one "animal"...sorry.

2007-01-17 16:32:38 · update #1

5 answers

The Na+ and K+ pumps are called electrogenic pumps. They create a difference in chemical and electrical gradient between the interior and exterior of the cell. WIthout it cells would not be able to be involved in many functions.

One such cell is the neuron, one the main cells in the nervous system. During an action potential extra sodium accrues within the neuron, and must somehow leave the cell. By having these pumps located throughout the cell membrane, sodium is brought out and potassium brought in, in order to bring the cell back to rest. If the neuron does not maintain this gradient, it will not be able to participate in impulse conduction.

2007-01-17 17:08:01 · answer #1 · answered by Diana M 3 · 1 0

The sodium Na pump is essential for nerve conduction

Sodium and potassium work against eachother within cardiac tissue to potentiate contraction and relaxation through nerve conductions.

Therefore, elevated reduced or imbalanced level of sodium and or potassium will affect the effectiveness of the hearts conduction and muscle system

2007-01-17 16:41:31 · answer #2 · answered by mandy 2 · 2 0

a. Na+ ions ………… K+ ions 3 Na + will be transferred out for 2 K+

2016-05-24 02:26:05 · answer #3 · answered by Anonymous · 0 0

Clausen, Torben. Na+-K+ Pump Regulation and Skeletal Muscle Contractility. Physiol Rev 83: 1269-1324, 2003; 10.1152/physrev.00011.2003.—In skeletal muscle, excitation may cause loss of K+, increased extracellular K+ ([K+]o), intracellular Na+ ([Na+]i), and depolarization. Since these events interfere with excitability, the processes of excitation can be self-limiting. During work, therefore, the impending loss of excitability has to be counterbalanced by prompt restoration of Na+-K+ gradients. Since this is the major function of the Na+-K+ pumps, it is crucial that their activity and capacity are adequate. This is achieved in two ways: 1) by acute activation of the Na+-K+ pumps and 2) by long-term regulation of Na+-K+ pump content or capacity. 1) Depending on frequency of stimulation, excitation may activate up to all of the Na+-K+ pumps available within 10 s, causing up to 22-fold increase in Na+ efflux. Activation of the Na+-K+ pumps by hormones is slower and less pronounced. When muscles are inhibited by high [K+]o or low [Na+]o, acute hormone- or excitation-induced activation of the Na+-K+ pumps can restore excitability and contractile force in 10-20 min. Conversely, inhibition of the Na+-K+ pumps by ouabain leads to progressive loss of contractility and endurance. 2) Na+-K+ pump content is upregulated by training, thyroid hormones, insulin, glucocorticoids, and K+ overload. Downregulation is seen during immobilization, K+ deficiency, hypoxia, heart failure, hypothyroidism, starvation, diabetes, alcoholism, myotonic dystrophy, and McArdle disease. Reduced Na+-K+ pump content leads to loss of contractility and endurance, possibly contributing to the fatigue associated with several of these conditions. Increasing excitation-induced Na+ influx by augmenting the open-time or the content of Na+ channels reduces contractile endurance. Excitability and contractility depend on the ratio between passive Na+-K+ leaks and Na+-K+ pump activity, the passive leaks often playing a dominant role. The Na+-K+ pump is a central target for regulation of Na+-K+ distribution and excitability, essential for second-to-second ongoing maintenance of excitability during work.
The Na+-K+-ATPase mediating the active coupled transport of Na+ and K+ across cell membranes was first identified in 1957 by Skou (392), who in 1997 was awarded the Nobel Prize in chemistry for this discovery. His review defining the role of this transport system, the Na+-K+ pump, as a regulator of the transport and distribution of Na+ and K+ across cell membranes was published in this journal (393). This raised the question whether and how this transport regulator itself was regulated. Later reviews have described the regulation of the Na+-K+ pumps in skeletal muscle (62), kidney (139), and heart (166). Many early or more general references may be found in these reviews. A related area, the K+ homeostasis in skeletal muscle and the heart during exercise, was recently reviewed (384). The detailed molecular mechanisms and specific signaling pathways involved in the regulation of the Na+-K+ pumps in a wide variety of tissues have been reviewed (134, 408). The present review is written with the specific purpose of analyzing how regulation of the activity and the capacity of the Na+-K+ pumps influences excitability and contractile performance in skeletal muscle. With the growing realization that the Na+-K+ pumps undergo large regulatory changes both in their transport activity and capacity (tissue content of Na+-K+-ATPase), the functional implications of such changes are gaining interest; in particular for the understanding of the frequently occurring pathophysiological and pharmacological modifications of Na+-K+ pump function. Therefore, the more general homeostatic role of Na+-K+ pump regulation in skeletal muscle will also be illustrated by some clinical examples

2007-01-17 17:45:54 · answer #4 · answered by veerabhadrasarma m 7 · 0 2

they produce atp, which breaks into adp and give out energy needed by our body...

2007-01-17 16:39:47 · answer #5 · answered by Rogue Bagel 2 · 0 0

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