The Student Room Group

A2 Biology - Proximal convoluted tube

So...
Why is it that we are having to pump sodium ions against a concentration gradient from the epithelial cells of the proximal convoluted tube into the blood if the concentration of the sodium ions in the blood is the same as the filtrate. Not to mention that when they move into the blood, sodium ions move into the cell because of the concentration gradient, so if anything, isn't their a higher concentration of sodium ions in the cell..

Please helppppp
Original post by sweetescobar
So...
Why is it that we are having to pump sodium ions against a concentration gradient from the epithelial cells of the proximal convoluted tube into the blood if the concentration of the sodium ions in the blood is the same as the filtrate. Not to mention that when they move into the blood, sodium ions move into the cell because of the concentration gradient, so if anything, isn't their a higher concentration of sodium ions in the cell..

Please helppppp

Hello young man - I think you are a boy if my memory from answering your Qs in the past is not letting me down [apologies if you are a girl!],

The physiology of maintenance of sodium [and hence water cos of osmosis] balance involves a highly complex set of mechanisms and feedback controls. I shall try to keep it not too much higher than A level standard for u.

The main mechanism that determines [by promoting sodium retention in exchange for K+ ions] in the kidney is the so-called renin-aldosterone-angiotensin axis [RAAA]. The hormone renin secreted by the juxtaglomerular cells of the kidney promotes the synthesis of aldosterone [an example of a mineralocorticoid hormone - the adrenal cortex [outer layer - inner one is called the medulla] produces two types of hormones: glucocorticoids e.g. cortisol and mineralocorticoids. The latter, via stimulating the conversion of angiotensinogen into angiotensin I then ACE [angiotensin converting enzyme] catalysing the conversion of angiotensin I into angiotensin II, tends to conserve sodium - we cannot just kick out sodium as we please; RATHER we need to maintain serum Na+ within the normal range of 135-150 mmoles/L, one reason [a v important one] being to maintain ECF [extracellular fluid, which includes blood plasma] volume cos if this drops too low, b.p. will drop and perfusion of tissues will suffer, and in severe depletin of fluid, will lead to haemodynamic collapse [called hypovolaemic shock].

[The opposite also holds [tho u r not asking] - if too much sodium is retained it will lead to an increase of blood volume and [as popular health discussions mention] b.p. will rise.]

Another major influence on sodium/water balance is the control of secretion of ADH [antidiuretic hormone] from the pituitary gland [the master endocrine gland], which tends to increase reabsorption of water in the loop of Henle & collecting duct.

All these mechanisms are v finely controlled by feedback mechanisms [google ACTH, Conn's syndrome, Cushing's syndrome, Addison's disease, diabetes insipidus if interested].

Sorry if I have failed in simplifying the above.

M.

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