Kidney and endocrine processes Flashcards
4 main roles of the kidney
- regulating blood vol
- regulation BP
- regulating pH of the blood
- production of RBC
- synthesis of calcitrol - VitD
- excretion of waste products and foreign bodies
blood pressure (Pa)
cardiac output x total peripheral resistance
BP=
CO x TRP
quick BP control
baroreceptor reflex
slow BP control
RAAS - long term
Baroreceptor reflex
-neural- fast
Parasympathetic- vagus nerve on SA node- M2AchR
Sympathetic- cardiac SA node and myocardium- B1A
Arterioles- A1AR= vaso/venoconstirction
Parasympathetic control of BP
Vagus nerve- M2ACHr
- decreases CO= decrease BP
Sympathetic control
1) SAN and myocardium B2AR (adrenoreceptor)- via Gs= increase CO
2) arteriole A1AR- vaso/venoconstriction= increase TPR
arteriole A1AR- vaso/venoconstriction=
increase TPR
which cells in the kidney detect a decrease in BP
Juxtagolermular= mechanoreceptors
Macula densa= sense decrees ein tubular NaCl
Macula densa cells release
RENIN
RAAS
1) juxtaglomerular apparatus (juxtflomerular cells/ macula densa), detect a decrease in BP and tubular NaCl
2) macho densa releases renin
3) renin is the enzyme for the zymogen of angiotensinogen
4) angiotensinogen converted to angiotensin 1
5) ACE (released for vascular tissue- lungs) converts angiotensin 1 to angiotensin 2
6) angiotensin 2 is a strong vasoconstrictor, stimulates thirst and causes the adrenal medulla to release aldosterone
7) aldosterone opens Na+ channels, so more water is reabsorbed
8) increase in blood volume= increase in BP
what sort of stimulation causes renin release
B1 adrenoreceptors
zymogen
n inactive precuroser- large than active form
angiotensin II provide negative feedback to
ANP system
angiotensin also stipulates ADH release from the
also known as vasopressin ADH is released by the p.pituitary (made in the hypothalamus) in response to low BP. Causes aquaporins (2) to be added to principle cells, increase water reabsorption
- increase BP
- decrease diuresis
ANP/BNP are released in response to
cardiac destination
sympathetic stimulation (beta adrenergic)
angiotensin II
mechanism of action of ANP/BNP
binds to natriuretic peptide receptors (NPRs) and stimulates guanlyly cycle to produce cGMP
- cGMP causes s.muscle relaxation
- due to is activation MLCP
- vasodilation- increase in GFR
- decrease in renin release
- therefore increased soda conc and in urine and more of it
ANP/BNP feedback cyle
1) ANP/BNp released int espouse to high BP
2) causes decreased renin release in the kidney, decreasing the release of ANG and ALDO
3) increase diuresis
4) decreased blood volume and therefore blood pressure
5) vasodilation
the thyroid
an endocrine gland in the enc consisting of two lobes.
- thyroid romones ar released here- which primarily influence metabolic rate and protein synthesis
hormonal output of the thyroid is regulated by
TSH- released from the a.pituitary
thyroid hormones
- building blocks are tyrosine and iodide
- T3 and T4
- cells producing thyroid hormone car arrange din follicles
much more of…. is released than…
much more T4 is released than T3
- however T4 is converted to T3 in target cells
T4 has a longer
half-life than T3
T3 is responsible
for almost all thyroid activity
action of T3/T4
Basal/metabolic rate (generates heat/consume O2) Cardiac muscle activity Sympathetic NS activity Protein synthesis/growth Cerebral activity Action of GH
where ar most receptors for T3/T4 found
in the brain
hormone cellular mechanism of T3/T4
- stimulates nuclear receptors to activate DNA transcription
- increases adaptive phosphorylation in the mitochondria, as well as mitochondrial DNA transcription
- GPCR receptor- stimulates nuclear DNA transcription
T3/T4 provide negative feedback to
hypothalamus and a.pituitary
TRH (thyroid releasing hormone) stimulates the
anterior pituitary to release TSH
TSH stimulates
the thyroid to release T3/T4
GFR
the amount of filta=rate produced by both kidneys in a minute
normal GFR
105 ml/min
analysis of renal function can
be used to asses renal fucntion
low GFR
waste product not excreted
high GFR
filtrate passes through the tubules too quickly and can be reabsorbed
affects of angiotensin 2
1) smooth muscle contraction ( AT1R)
2) kidney nephron (PCT) –> increase in sodium and HCO3– reabsorption- acid base balance
3) hypothlamus- increase thirst
4) adrenal glands- aldosterone release –> increases sodium and fluid retention in DCT and CD
5) ANP is released as negative feedback
overall affect of angiotensin 2
sodium reabsorption, water reabsorption, increase in blood volume
angiotensin 2 also causes the release of
ADH
release Posterior Pituitary.
↑ fluid retention- aquaporin’s (V2R-Gs).
Stimulates Na+-K+2Cl- cotransport TAL
the menstrual cycle
1) GnrH produce and released from he hypothalamus
2) stimulates the a.pituitary to release FSH and LH
3) FSH causing maturation of the follicles int he ovaries
4) as the follicles grow, the y produce more oestrogen
5) when oestrogen meets is reaching threshold, negative feedback is sent o the a.pituitary
6) when threshold is met- oestrogen causes a surge in FSH and LH
7) surge in LH causes ovulation
8) empty follicle becomes corps luteum - which releases progesterone
9) progesterone causes endometrium to develop
10) high levels of progesterone inhibits FSH and LH - so only one pregnancy
if not pregnant
CL will deteriorate and less progesterone produced- FSH and LH produced from A.pituitary
