L38. Renal (4) Flashcards
(12 cards)
What is the regulation of low plasma volume - Na+?
- Dehydration, blood loss, vomiting or diarrhoea cause low plasma volume
- Arterial (blood) pressure goes down, GFR goes down (mainly dependent on blood pressure)
- Sympathetic nerve activity goes up (receptors)
- Low NaCl concentration at macula densa cells and high sympathetic nerve activity triggers release of renin from the juxtaglomerular cells
- Renin helps to produce angiotensin II
- Angiotensin II (vasoconstrictor) facilitates synthesis of aldosterone
- Aldosterone increases Na+ and water re-absorption in the collecting duct
What is the regulation of high plasma volume - Na+?
- High plasma volume results from hyperhydration
- High plasma volume triggers receptors (distension from the heart)
- The distension leads to a release of atro-natriuretic factor/peptide (ANF, ANP) in the atria
- High plasma ANP levels reduce plasma aldosterone
- High plasma ANP levels dilate afferent and constrict efferent arterioles increasing GFR
- High plasma ANP levels reduce Na+ reabsorption and increase Na+ excretion
What is the role of the kidney in water homeostasis?
The kidney is responsible for the excretion of 2/3 of the water from the diet (food and liquids) and metabolism
What is water reabsorption in the kidney?
Three important places within the nephron, where water is reabsorbed:
1. PCT (66%)
2. tDLH (25%)
3. CCT (2-8%)
What happens with water reabsorption at the PCT?
- In leaky epithelium the consequence of the paracellular chloride and sodium absorption is a huge water gradient over the epithelium; this drives the trans and paracellular absorption of water
What happens with water reabsorption at the tDLH?
- The TAL reabsorbs Na+ into the intersitium via NKCC2; the tDLH is leaky epithelium facilitating water reabsorption via aquaporins and the paracellular pathway
What is the osmolarity of urine along the nephron?
- The primary urine coming from the PCT is isotonic (300mosmol/L); it becomes hypertonic due to water reabsorption in tDLH; turns into hypotonic urine due to sodium reabsorption via NKCC2 in TAL and becomes hypertonic again in medullary collecting duct (only under anti-diuretic condition/low water intake)
Tell me about water homeostasis in regards to vasopressin release?
- Vasopressin or ADH is secreted from the posterior pituitary gland
- The stimulus for ADH release is low blood pressure (sensed by baroreceptors) or high blood osmolarity sensed by osmoreceptors
- The target organ of vasopressin is the principal cell in the collecting duct of the kidneys
What happens with water reabsorption at the CCT?
- The collecting duct is a tight epithelium facilitating 2-8% of water reabsorption
- Water reabsorption in the principal cells of the CCT is regulated by vasopressin (ADH)
What are the definition of acid-base disturbances?
Acidosis: increase of arterial H+: arterial pH < 7.4
Alkalosis: decrease of arterial H+: arterial pH < 7.4
What are the acid-base disturbances with respiratory problems?
Respiratory acidosis: increase of Co2, hypoventilation
Compensation: increase of HCO3- reabsorption, kidney
Respiratory alkalosis: decrease of CO2, hyperventilation
Compensation: secretion of HCO3- in CCT, kidney
What are the acid-base disturbances with metabolic problems?
Metabolic acidosis: diabetes mellitus, diarrhea
Compensation: increase of ventilation, lung
Metabolic alkalosis: vomiting
Compensation: decrease of ventilation/none if not renal: secretion of HCO3- in CCT, kidney
