lecture 30/31 Flashcards
how do kidneys maintain water balance
- kidneys can conserve or remove body fluid by regulating the amount of H20 reabsorbed
- remove: is default out with urine
- conserve: vasopressin causes the insertion of water channels for water reabsorption as needed
filtrate osmolarity changes through the nephron
- when plasma is filtered in glomerulus and leaks in bowman’s space it will be isosmotic
- fluid leave proximal tubule down the descending limb become more and more concentrated (hyperosmotic)
- ions will be reabsorbed but not water therefore fluid will be very dilute (hyposmotic)
- vasopressin causes insertion of aquaporins 2 to pull water back in distal tubule and collecting duct as needed
- final urine osmolarity depends on reabsorption in collecting duct
vasopressin
- neurohormone that is released by posterior pituitary gland
- stimuli: high osmolarity (too salty, needs to be diluted), low blood pressure, low blood volume
- controls insertion of aquaporin 2 into the apical membrane of the distal tubule and collecting duct as needed
aldosterone regulates what?
reabsorption of Na+ and secretion of K+
aldosterone
- steroid hormone
- synthesized in and released from adrenal cortex and acts on p cells of the distal tubule and collecting duct
- increase reabsorption of Na+
- stimulus: low blood pressure/low blood volume (RAS pathway) and hyperkalemia (increase K+ in ECF)
List 3 routes low blood pressure stimulates renin secretion
Low blood pressure/low blood volume
1. GFR will decrease because flow of blood into glomerulus decrease therefore Ph decreases. Macula densa cells of distal tubule will detect low flow and result in release of other paracrines on the granular cells of the afferent arteriole. The granular cells will then secrete renin
2. There is a direct affect between decrease in blood pressure and granular cells because granular cells are tiny baroreceptors therefore they can detect a fall in pressure and will secrete renin
3. Afferent arterioles and granular cells receive sympathetic input which trigger the release of renin
The renin-angiotensin-aldosterone system
- When renin is secreted it will go back into circulation and act on angiotensinogen which is produced by the liver and is inactive to produce angiotensin 1 which is still inactive (safety mechanism)
- ANG 1 is concerted to ANG 2 by angiotensin converting enzyme
- First thing ANG 2 is going to do is target the adrenal cortex to release aldosterone to increase Na+ absorption
What are other targets of ANG 2
- Act on cardiovascular system to increase sympathetic input which causes an increase in HR, contractility, SV, CO and blood pressure
- ANG 2 is a powerful vasoconstrictor which will increase blood pressure
- Increase vasopressin release therefore more insertion of water channels
- Induce thirst and salt appetite
maintaining pH homeostasis
- buffers: plasma proteins, hemoglobin, phosphates and HCO3- (pull protons out of solution)
- regulation of ventilation: this is shifting equation one way or another to regulate pH (ex. blowing out more CO2)
- kidneys regulate H+ or HCO3- reabsorption or secretion. kidneys will secret H+ into urine to regulate blood pH
maintaining pH homeostasis-renal compensation
- H+ is secreted and HCO3- reabsorbed at the proximal tubule
- fine regulation of acid and base occurs at collecting duct
- I cells are interspaced between P cells and will either secrete protons or bicarbonate depending on if your in a state of acidosis and alkalosis
bone is always being _______ throughout life. and why?
remodeled because bone is always being made and broken down
calcified extracellular matrix is called
hydroxyapatite
when bond is more likely to break what condition does this lead to?
osteoporosis
osteablasts
synthesize bone
osteoclasts
resorb bone
