Na/K ATPase (sodium-potassium adenosine triphosphate) is an enzyme found in the plasma membrane of all animal cells and has a key role in performing varied functions in cell physiology. The enzyme is a solute pump pumping sodium out of cells and potassium into the cells, against the concentration gradient. Na/K ATPase is found in large volume in the kidney that acts as a major source for the purification of the enzyme. In the kidney, the enzyme is located on the basolateral aspect of tubule cells, and has a significant role in the active translocation of K and Na across the membrane. Further, the enzyme has an active role in the secondary active transport of other solutes as well. The activity of this enzyme in the renal system changes in parallel with changes in the transport of K and Na, implying that the enzyme has a role in the chronic adaptation of the renal system to altered Na reabsorption or K secretory load. The concentrations of the Na-K pump sites and metabolic energy is integral to the determination of the capacity of transcellular transport. The direction and nature of the solute transport in different segments are dependent on the membrane conductances and Na+-coupled carriers. It is to be noted that the Na-K pump supplies a strong driving force to ensure significantly different active transport processes in different nephron segments. The noted variation in the processes of transport does not exist in within the pump as such. It is noteworthy that the function of the pump is similar in the different segments of the nephron for maintaining electrochemical gradients for Na (Xie et al., 2015).
The different mechanisms that are responsible for maintaining appropriate blood pressure in the human body can be classified into short-term mechanisms (baroreceptor reflexes), intermediate-term mechanisms (stress-relaxation and capillary fluid shift mechanism) and long-term mechanisms (pressure diuresis/natriuresis and Tenin-angiotensin mechanism).
Baroreceptor reflex is supposed to prevent erratic fluctuations noticed in blood pressure. In case of rapid change in blood pressure, the baroreceptor reflex is responsible for bringing about a negative feedback that corrects the initial change in the blood pressure. In case there is no reflex, there would be wild fluctuations in the blood pressure at the time of postural changes or emotional changes. The baroreceptor reflex cannot function if the change in the blood pressure is sustained and gradual. This is due to the fact that baroreceptor resetting occurs, adjusting itself to the resting blood pressure. The reset reflex then attempts to maintain blood pressure at the new resting pressure. Due to such resetting the reflex is not useful for the long term regulation. The capillary fluid shift mechanism is supposed to regulate the blood pressure through filtering of more fluid into the interstitial spaces in case of rise in blood pressure. On a converse manner, in case the blood pressure falls, the fluid moves into the capillaries. The stress-relaxation mechanism relies on the plasticity of smooth muscle in the vascular system. In case of slow increase in blood pressure, the arteriolar smooth muscle leads to dilation of the vessels. The result is the fall in blood pressure.
In case of increase of blood pressure, it is noticed that there is an increased output of salt and water in the urine. The reduction in the body fluid is known to restore the blood pressure to normal. The sympathetic discharge activates the renin-angiotensin mechanism. The sympathetic discharge to the kidneys causes renin-degranulation. Renin catalyzes the formation of angiotensin I that eventually converts into angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a .powerful vasoconstrictor and has a function in the restoration of blood pressure through increase in the peripheral resistance (Rizzo 2015).
Pressure-natriuresis is defined as the association between mean arterial pressure (MAP) and sodium excretion. In this system, increase in renal perfusion pressure is the reason behind decreases in sodium reabsorption and increases in sodium excretion. Blood pressure homeostasis is the key element of the regulation of extracellular fluid volume by excretion of renal sodium. Regulation of sodium reabsorption in the proximal tubule can be done by renal perfusion pressure. The pressure natriuresis response acts as an important powerful tool for achieving stabilization of long-term blood pressure around a set point.
Pressure natriuresis is found to be highly impaired in individuals suffering from hypertension and understanding of the dysfunction arises from genetic analysis. In hypertensive patients, the high blood pressure leads to a fast decline in the re-absorption of salt and water, an important process linked to ubuloglomerular feedback regulation of renal blood flow and glomerular filtration rate, and causes pressure natriuresis. When there is elevation of blood pressure, there is redistribution of apical proximal tubule to intermicrovillar clefts and eventually to endosomal pools. This is followed by suppression of Na/K-ATPase activity. Decline in both Na/K-ATPase activity and surface distribution of NHE3 in a coordinated manner is the response to hypertension. The increased volume flow of salt and water to the loop of Henle is the driving force behind Na/K-ATPase activity, providing evidence for a downstream shift in sodium transport at the time of acute hypertension. It is therefore suggested that hypertension results due to a imperfection in the association existing between sodium secretion and renal perfusion (Ivy and Bailey 2014).
Ivy, J. R., and Bailey, M. A. 2014. Pressure natriuresis and the renal control of arterial blood pressure. The Journal of Physiology, 592(18), pp. 3955–3967. https://doi.org/10.1113/jphysiol.2014.271676.
Rizzo, D.C., 2015. Fundamentals of anatomy and physiology. Cengage Learning.
Xie, J., Ye, Q., Cui, X., Madan, N., Yi, Q., Pierre, S.V. and Xie, Z., 2015. Expression of rat Na-K-ATPase α2 enables ion pumping but not ouabain-induced signaling in α1-deficient porcine renal epithelial cells. American Journal of Physiology-Cell Physiology, 309(6), pp.C373-C382.