Low pH (acidosis) --> impaired growth, decreased cardiac output and blood pressure, insulin resistance, hyperkalemia (low potassium can also cause acidosis). Can be caused by drinking too much coffee and not breathing well (increased CO2). Can also be caused by diarrhea (losing HCO3), diabetes mellitus, renal failure, lactic acid from exercise. Compensation: breathe more and piss out acid.
High pH (alkalosis)--> heart arrhythmias, tetany (due to low calcium levels). Can be caused by excess angiotensin II and aldosterone (in hypertension or response to drop in BP or blood volume). Can also be caused by hyperventilation, vomiting gastric acids, hypokalemia. Compensation: breathe less and piss out HCO3.
BICARBONATE BUFFER CYCLING
H20 + CO2 <--> H2CO3 <--> H+ + CO3-
enzyme: carbonic anhydrase
In the tubule cells of the kidney, H20 and C02 recombine via enzyme carbonic anhydrase to form H2CO3, which then decomposes into H+ (acid) and HCO3- (bicarbonate), the primary systemic chemical buffer in humans. The acid is secreted into the proximal convoluted tubule. Any bicarbonate that has been filtered into the PROXIMAL tubule buffers the acid until it is again reabsorbed into a tubule cell. The acid is pumped into the lumen of the kidney tubule, where eventually (in the DISTAL tubule) it is buffered by ammonia and phosphate (instead of bicarbonate) and then excreted. This is how we keep our phosphate levels lower than our calcium levels.
Confusing. Another pass:
CO2 can pass through membranes easily. So it goes into the tubular cell, combines with water, forms acid and bicarbonate. The acid is actively excreted. Once in the lumen, the acid combines with any filtered bicarbonate, splits into CO2 and water again, and comes back into the tubule cell to make acid and bicarbonate again. Notice that the acid keeps going back out, grabbing some carbons, coming back in, then splitting up such that the bicarbonate stays in and the acid keeps cycling out. This is how we hang onto our buffers.
Normal urine pH is around 4.5, even after buffering with ammonium and phosphate. Any lose acid that doesn't get buffered by ammonium or phosphate makes more bicarbonate which is reabsorbed as above.
Ammonia (NH3) is the major buffer for excess acid excretion. Ammonium is produced from glutamine in PROXIMAL tubule. Glutamine (from liver) --> NH3/NH4 (buffer) and glutamate. Ammonium buffer is first secreted into PROXIMAL tubule, then reabosorbed in thick ASCENDING LOOP. NH3 (but not NH4) is secreted into the DISTAL tubule and COLLECTING tubules/ducts, which are more permeable to NH3. Intercalated cells in COLLECTING tubules secrete acid, which is buffered by the NH3 and excreted.
If there is more potassium in the interstitium, there is more acid in the body, because the two are antiported in the COLLECTING duct. Decreased potassium causes withdrawal of cellular potassium and entry of acid via potassium-acid antiporter.
Angiotensin II and Aldosterone can cause excessive acid secretion and HCO3 reabsorption: alkalosis.
A-II stimulates PCT Na/H co-transporters, increasint acid secretion and sodium reabsorption.
ALD increases sodium reabsorption and enhances secondary transport of acid via sodium-acid antiporter, stimlutaion of potassium ATPase, and stimulation of intercalated cell secretion of acid.
Calcium oxalate stones form due to intestinal hyperabsorption of calcium, or defective renal reabsorption of calcium, or from excess intake of purine from meat/fish/poultry, or from intestinal overabsorption of oxalates due to fat malabsorption or dietary excess of oxalate, ascorbic acid loading, or hereditary conditions.
Struvite stones MgNH4PO4 precipitates out caused by urease enzyme produced by bacterial infection such as Proteus. The urease converts urea to NH3 and CO2, then NH3 becomes NH4+, raising the pH of urine to 8-9 and binding PO4- and Mg to form crystals.
Filling is mediated by sympathetic nervous system, sensory baroreceptors in bladder stimulate sympathetic activity (L1,2) to relax detrusor muscle and constrict internal urethral sphrincter, allowing filling.
The MICTURITION REFLEX is parasympathetic (S2,3,4) that alternates detrusor contraction alternating with relaxation (muscarinic). As bladder fills this reflex may be triggered several times and subside. Eventually one must void.
Voluntary micturition is a combo of the parasympathetic (above) and the voluntary (somatic, pudendal nerve S2,3,4) control of the external urethral sphrincter and also abdominal muscles, which contract to press out urine.