Potassium Channels in the Cardiovascular System

Potassium works with sodium to regulate the body’s water balance. The kidneys help to control the blood pressure by controlling the amount of fluid stored in the body. Therefore, the more fluid then the higher the blood pressure is. The kidneys do this by filtering out the blood and extracting any extra fluid, which then is stored in the bladder as urine. This is done very delicately as both sodium and potassium pull the water across the wall of the cells from the bloodstream into a collecting channel that leads to the bladder. When eating to much salt, the amount of sodium in the bloodstream will be imbalanced compared to the amount of potassium and thus reducing the ability of the kidneys remove the extra fluid. Eating more fruit and vegetables, the potassium levels increase and can help restore the chemical imbalance. However, there is a possibility of too much potassium, also known as hyperkalemia, which can lead to other issues like renal failure.

The voltage gated potassium-complex are made of single ion pore with subunits. Located in the postsynaptic fold. The voltage gated potassium complex has a significant amount of roles such

Following exposure to epinephrine, the heart was allowed to return to its resting state determined in procedure 1. This same procedure was repeated with the following chemicals: 1) Acetylcholine, 2) Atropine, 3) Calcium solution, 4) Nicotine solution, and 5) Caffeine solution.

The blood glucose level has very limited range for humans to survive and stay healthy. Generally, people are able to remove excess glucose rapidly from the body but this is not the case when they are diagnosed with diabetes and insulin resistant situations. The lack of insulin resistance can also lead to a decrease in glycogen synthesis and storage as it usually converts glucose to energy for cell’s use (Jensen & et al. 2011). When insulin is produced under insulin resistance, the cells are incapable of using them effectively which then leads to high blood sugar level as ketones and ketoacids are produced as an alternative energy source for the body. The rise of ketoacid causes the blood pH acidic and the patient may also be diagnosed with ketoacidosis (Newton & Raskin 2004). There would also be less intake of lipid and more of stored triglycerides as the lipids are effected by the insulin. As the glucose levels increase, the muscle glucose uptake will decrease while the liver glucose production and blood fatty acid concentration will also increase within the body (Lichtenstein & Schwab 2000). Excess glucose within the blood are converted to fat which can lead to Diabetic Dyslipidaemia and furthermore to obesity, hypertension and

4. Why does potassium concentration rise in patients with acidosis? What is this called? What effects does it have?

This experiment seeks to analyze how the resting membrane potential of Orconectes rusticus muscle cells changes in response to increasing [K+]o solution concentrations. By recording the intracellular voltage of the DEM, DEL1, and DEL2 crayfish muscle cells at six concentrations of [K+]o solution, we determined whether the observed resting membrane potentials (Vrest) were significantly different from the predicted Nernst equilibrium potential values. We hypothesized that the Vrest of the crayfish muscles at each concentration would not significantly differ from the Nernst potential, which solely considers the permeability of potassium ions to the cell membrane. However, our findings suggested differently, and results indicated that the Nernst equation did not accurately predict the obtained values of the resting membrane potential. The differences in muscle cell Vrest reveal instead that the membrane is differentially permeable to other ions.

-If the potassium transport pump was blocked the leakage channels would still be open allowing Na+ to

Voltage gated channels are necessary components of life processes, in many organisms. One in particular, is the calcium voltage gated ion channel. Often lodged within the phospholipid bilayer, the imbalance of the calcium, or, the inside vs outside concentration, creates a gradient. The channel proteins often undergo conformations, states that which allow or block calcium ions from passing through. As ions move inside the cell, this creates a depolarization, or surge in the voltage. Clinically, this is associated with the heart and how it allows the heart to contract, which can be read in the

Gluconate is reported to have biological activities that are not related to its function as an anion substitute (Christoffersen and Skibsted, 1975). Therefore, we investigated the effect on electrical activity in mouse jejunal circular smooth muscle of replacing extracellular Cl- with isethionate, a different anion with low permeability through Cl- channels. Replacement of [Cl-]o with isethionate affected both membrane potential and slow wave properties. Application of 13.3 mM [Cl-]o, isethionate Krebs solution did not cause the transient effect on membrane potential in the first 40 s period after the solution change that was observed with the gluconate Krebs solution (Fig 2A). However, unlike gluconate, replacement of extracellular Cl- with isethionate did cause a significant depolarization of the membrane potential after the solution change (4-5 min) (Fig 3A, 4A; ∆Em, 13.3 mM [Cl-]o: 3.73 ± 1.06 mV; N=5; P < 0.05 vs. baseline; paired t test).

(c) Estimate the EC50 values for the effects of acetylcholine and nitroprusside in both types of arterial ring, and present these in a table.

6. The effect on slow wave activity of reducing [Ca2+]o in Krebs to the level of [Ca2+]o obtained by adding gluconate (A) and isethionate (B) (see Fig. 5). Lowering [Ca2+]o did not replicate the effect of replacing [Cl-]o with gluconate or isethionate on electrical activity in mouse jejunal smooth muscle layer. A-B, Representative traces of intracellular recordings upon perfusion with 0.13 mM and 0.54 mM [Ca2+]o. Expanded time scales are shown below the traces.

A major problem is the correlation of many of the features of this syndrome. In prospective studies, fasting plasma glucose (FPG) is linked to development of diabetes and correlated so with coronary artery disease. The predictive utility of the metabolic syndrome as a concept adds little to its constituent risk factors when they are used individually. The long term usefulness of the definition of the metabolic syndrome for intervention and identification in order to prevent diabetes and cardiovascular disease it is due to be

Potassium plays an important role in nerve and muscle function. As a result of this role, abnormalities in serum potassium may trigger membrane excitability and considerable nerve, muscle and cardiac dysfunction leading to ventricular arrhythmias and subsequently sudden cardiac death. It is estimated that between 1% and 10% of patients admitted to a hospital experience hyperkalemia, with a mortality rate of 1 per 1,000 (Raymond & Wazny,2010).

Choice “B” is the best answer. Insulin modulates potassium utilization by skeletal muscles. With this patient, the combination of impaired insulin action and increased osmolality causes a marked decrease in potassium utilization, leading to intracellular potassium depletion. Potassium is also lost via osmotic diuresis. These factors lead to a profound total body potassium deficiency. Therefore, diabetic ketoacidotic (DKA) patients can present with a broad range of serum potassium concentrations. The institution of insulin therapy and correction of hyperglycemia can lead to eventual hypokalemia. Therefore, potassium replacement should be started with initial fluid replacement if potassium levels are normal or low. Potassium should be added to the replacement solution (10–20 mEq/L) once urine output is adequate, and the serum K+ is < 6.0.

Potassium is crucial to heart function, important for normal digestive and muscular function. It is the primary positive ion (cation) found inside body cells that it is essential for normal cell function. The proper function of the body requires 8% electrolytes in the bones,90% in skin intracellular fluid and 2% in extracellular fluid. Buttarro, et. al., (2017) mentioned that the human body average potassium is about 50 mEq/kg and normal blood potassium level is 3.5 - 5.0 milliEquivalents/liter (mEq/L). The decrease in potassium level is known as Hypokalemia; it profoundly affects the nervous system and heart, and when extreme may lead to sever complication or death (Buttarro et. al., 2017). Hypokalemia is a possible life-threatening imbalance that in some cases are acquired through inducing drugs (iatrogenic), genetic, endocrine, vascular and renal disorders (Butarro et. al.,