Tubuloglomerular feedback: An increase in renal arterial pressure increases renal blood flow and GFR, which increases delivery of filtered Na+. A higher distal tubular Na+ concentration activates the Na+K+2Cl- (NKCC) transporter, causing macula densa cells to swell. These cells release ATP, which either directly activates arteriolar cells through purinergic receptors or is converted to adenosine by extracellular nucleotidases. Adenosine then activates adenosine A1 receptors, causing afferent arteriolar constriction. Constriction of the afferent arteriole reduces blood delivery to the glomerulus, lowering renal blood flow and GFR.
Myogenic hypothesis: Increased blood pressure stretches smooth muscle in the arterial wall, opening stretch-activated calcium channels. Calcium entry triggers vasoconstriction. In the kidney, this response occurs in the afferent arteriole, which constricts in response to increased arterial pressure.
Liddle Syndrome: This autosomal dominant disease is caused by gain-of-function mutations of ENaC, leading to excessive Na+ reabsorption in the distal tubule and collecting ducts. It presents with early onset 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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