Tubuloglomerular feedback: Increase in renal arterial pressure increases the renal blood flow and GFR which leads to increased delivery of filtered Na+. Increased distal tubular Na+ concentration causes the macula densa cells to swell by activation of the N+K+2Cl- (NKCC) transporter. These cells release ATP, that either directly activates arteriolar cells through purinergic receptors or is converted to adenosine by extracellular nucleotidases. The resulting adenosine can activate adenosine A1 receptors that cause afferent arteriolar constriction. Constriction of the afferent arteriole reduces the amount of blood delivered to the glomerulus thus reducing the renal blood flow and GFR.
Myogenic hypothesis: Increased blood pressure stretches the smooth muscle in the arterial wall hence opening up stretch-activated calcium channels. This causes constriction of the blood vessel. This response is seen at the afferent arteriole which constricts in response to raised arterial pressure.
Liddle Syndrome: This autosomal dominant disease is caused due to gain-of-function mutations of ENaC leading to excessive Na+ reabsorption in the distal tubule and collecting ducts. It presents with early onset of hypertension, hypokalemia, metabolic alkalosis, low aldosterone levels and volume expansion.
| Causes of hypokalemia | Causes of hyperkalemia |
| Gastrointestinal losses like diarrhea, vomiting, fistulas etc; diuretics,laxatives and enemas, osmotic diuresis, mineralocorticoid excess, Types I and II RTA, polydipsia, hypomagnesemia, dialysis, plasmapheresis, Anorexia, alkalosis, insulin, beta 2 agonist, decongestants, amphotericin B, alpha blockers | Renal failure; ACE inhibitors, ARBs, NSAIDs, Potassium sparing diuretics, heparin, lithium, hypoaldosteronism, amyloidosis, acidosis, hyperglycemia, mannitol, beta blockers, alpha agonists, type 1 DM, digoxin toxicity, succinylcholine, cell lysis e.g. tumor lysis syndrome |
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