URI S4 - L1 ( Renal Physiology )
- baroreceptor reflex is important in short term regulation of BP by - ACE works to degrade bradykinin.
controlling peripheral resistance , HR and contractillity - Bradykinin has good vasodilator effects,
- closely intertwined with homeostasis of body fluid volume - ACE inhibitors cause dry cough due to bradykinin .
- determined by balance between fluid intake and output.
- Kidney : Atrial Natriuretic Peptide(ANP) :-
a. regulate BFV and determine circulatory volume and CO - Decreas Na and Water Reabsorption.
b. have endocrine function - controlling periphral resistance - When specific cells of cardiac atria stretched because of plasma
through secretion of rennin from JGA volume expansion and increased atrial blood pressure secrete ANP.
c. control BP and CO is natriuresis (enhance Na excretion in urine) - Increased ANP directly inhibit reabsorption of Na & water by renal
tubules, especially in collecting ducts.
Role of kidney in regulation of BP :-
-
RAAS- - ANP inhibits renin secretion which helps to return blood volume back
1. RAAS toward normal.
2. Sympathtic When BP
- ANP levels are greatly elevated in CHF when cardiac atria are
3. ADH either acts on ATL stretched because of impaired pumping of ventricles.
-> or AT2
[Link] recent
- The increased ANP helps to attenuate Na and water retention in HF.
5. Others….. eg. Prostaglandin & bradykinin
SYMPATHETIC ACTIVATION “SA” INCREASES Na REABSORPTION :-
- Activation if severe decrease Na and water excretion by constricting
- Ang II return BP and ECF volume to normal by increasing Na and renal arterioles &reducing GFR.
water reabsorption - low levels of SA increasing Na reabsorption in proximal tubule, thick
- through 3 effects: ascending loop of Henle, by activating α adrenergic receptors on renal
1. Ang II directly stimulates Na reabsorption in proximal tubules, tubular epithelial cells.
loops of Henle, distal tubules & collecting tubules. - SNS stimulation —> increases renin release and Ang II formation,
which adds to overall effect to increase tubular reabsorption and
2. Ang II stimulates aldosterone secretion, which in turn increases decrease renal excretion of sodium.
sodium reabsorption.
Prostaglandins :-
3. Ang II constricts efferent arterioles, - kidney produce PGE2, PGI2
- GFR to normal - vasodilators increase blood flow and filtration .
- has 2 effects on peritubular capillary dynamics that increase - protection by buffer excessive vasoconstriction by SNS & RAAS.
sodium and water reabsorption. - NSAIDs inhibit formation of PG.
- if NSAIDs given ; renal perfusion is compromised (e.g. in renal
A) First , efferent arteriolar constriction raises filtration fraction in disease) …. GFR decreased —> acute renal failure.
glomerulus & increases con. of proteins and colloid OP in - In HF or HTN , NSAIDs can exacerbate condition by increasing NaCl
peritubular & water retention.
capillaries.
- increases reabsorptive force at peritubular capillaries and raises ADH antidiuretic hormone [ AVP (arginine vasopressin) ] :-
tubular reabsorption of sodium and water. - synthesis by hypothalmus ; secreted by posterior pitutary .
- increase water permeability of distal tubule, collecting tubule, and
B) Second, efferent arteriolar constriction reduces peritubular collecting duct .
capillary HP. - controlling dilution or con. of urine
- which increases net tubular reabsorption, especially from the - affect urea reabsorption .
proximal tubules. - In absence of ADH, the permeability of distal tubules & collecting
ducts to water is low, causing kidneys to excrete large amounts of
Aldosterone dilute urine, a condition called diabetes insipidus .
- secreted by adrenal cortex - ADH binds to V2 receptors —> stimulates movement of intracellular
- important regulator of Na reabsorption and secretion of k and protein, called aquaporin-2 (AQP-2), to luminal side of cell membranes.
hydrogen by the renal tubules. - AQP-2 molecules cluster and fuse with cell membrane by exocytosis
- renal tubular site of aldosterone action is on the principal cells to form water channels that permit rapid diffusion of water.
of the cortical collecting tubule. - AQP-3 & AQP-4, in basolateral side of cell membrane provide a path
for water to rapidly exit cells not regulated by ADH.
- When ADH con. decreases —> AQP-2 molecules are shuttled back to
cell cytoplasm —> removing water channels from luminal membrane
and reducing water permeability.
