The document provides an overview of renal pharmacology. It discusses the structure and function of the renal corpuscle and nephron. It describes the processes of filtration, reabsorption, and secretion that occur along the nephron to produce urine. It also discusses the sites and mechanisms of action of various classes of diuretic drugs, including loop diuretics, thiazide diuretics, and potassium-sparing diuretics.

1. Renal Pharmacology
Bidya Dhar Sahu

2. Introduction:

3. Introduction:

4. The renal corpuscle contains a bundle of capillaries called the glomerulus. The glomerulus receives blood via an
afferent arteriole and blood exits the glomerulus via the efferent arteriole. Ultrafiltrate is forced through the
glomerular capillaries of the glomerulus into Bowman’s space and enters the proximal tubule for ultimate processing
to produce urine.
Introduction:

5. Introduction:

6. Int. J. Mol. Sci. 2021, 22(20), 11182; https://doi.org/10.3390/ijms222011182
A simplified diagram of the renal
corpuscle. Blood flows into a
glomerulus from the afferent
renal arteriole. The filtered
blood goes out through the
efferent arteriole. Mesangial
cells form the center of the
corpuscle and hold the
glomerulus together. (b) The
three components of the
glomerular filtration barrier
(GFB) are endothelial cells
(which have a surface covered
by glycocalyx), the glomerular
basement membrane (GBM),
and podocytes. Blood from the
glomerular capillary is filtered
through these three layers, and
the filtrate escapes out into the
urinary space of Bowman’s
capsule, as indicated by the
yellow arrow. The GFB typically
prevents particles larger than 6–
8 nm in size from passing
through.
Simplified diagram of the renal corpuscle:

7. Kidneys:
o Represent 0.5% of total body weight, but receive ~25% of the
total arterial blood pumped by the heart
o Each contains from one to two million nephrons:
• – The glomerulus
• – The proximal convoluted tubule
• – The loop of Henle
• – The distal convoluted tubule
• – The collecting duct
o Renal Blood Flow-1200ml/min
o Renal Plasma Flow-650 ml/min
o GFR-120 ml/min
Renal Physiology:

8. The nephron functions to maintain balance
Bowman’s
Capsule
Afferent
arteriole
Efferent
arteriole
Renal vein
Glomerulus
Loop of Henle with
capillary network
Tubule
Collecting duct
The functions include:
• Filtration
▪ Glomeruli generate ultrafiltrate of the
plasma.
• Reabsorption
▪ Tubules selectively reabsorb substances
from the ultrafiltrate.
• Secretion
▪ Tubules secrete substances into the urine.
o In 24 hours the kidneys reclaim:
o ~ 1,300 g of NaCl
o ~ 400 g NaHCO3
o ~ 180 g glucose
o almost all of the 180 L of water that
entered the tubules

9. Kidney functions
o Balance of electrolytes, Plasma volume, Acid Base
o Activate 25(OH)D to 1,25 (OH)2D (active vitamin D)
o Synthesis of Erythropoietin to stimulate bone marrow, Urokinase
o Excretion of Urea, Uric acid, Creatinine etc.
o Blood pressure regulation: the kidney is the critical organ in maintaining normal
blood pressure.
▪ (1) homeostasis of sodium and water, maintaining normal extracellular
fluid volume,
▪ (2) control of the renin –angiotensin –aldosterone axis,
▪ (3) production of vasodilatory substances.
o Metabolic function (1) Gluconeogenesis; (2) Metabolize drugs and
endogenous substances (e.g., insulin)

10. Major segments of the nephron and their functions:

11. Major drug transporters expressed in
human renal proximal tubule cells. ADP,
adenosine diphosphate; ATP, adenosine
triphosphate; DC, dicarboxylate; OA,
organic anion; and OC, organic cation.
Major drug transporters
expressed in human renal
proximal tubule cells.
Ref: Wang et al., 2016, Acta Pharmaceutica Sinica B, 6 (5),
363-373. https://doi.org/10.1016/j.apsb.2016.07.013

12. Apical membrane Na+/H+ exchange (via
NHE3) and bicarbonate reabsorption in
the proximal convoluted tubule cell.
Na+/K+-ATPase is present in the basolateral
membrane to maintain intracellular sodium
and potassium levels within the normal
range. Because of rapid equilibration,
concentrations of the solutes are
approximately equal in the interstitial fluid
and the blood. Carbonic anhydrase (CA) is
found in other locations in addition to the
brush border of the luminal membrane.
SGLT2, Na+/glucose transporter.

13. Ion transport pathways across the
luminal and basolateral membranes of
the thick ascending limb cell.
The lumen positive electrical potential
created by K+ back diffusion drives
divalent (and monovalent) cation
reabsorption via the paracellular pathway.
NKCC2 is the primary transporter in the
luminal membrane.

14. Ion transport pathways across the luminal and
basolateral membranes of the distal convoluted
tubule cell.
As in all tubular cells, Na+/K+-ATPase is present in the
basolateral membrane. NCC is the primary sodium and
chloride transporter in the luminal membrane. R,
parathyroid hormone (PTH) receptor.

15. Ion transport pathways across the luminal and basolateral
membranes of collecting tubule and collecting duct cells. Inward
diffusion of Na+ via the epithelial sodium channel (ENaC)
leaves a lumen-negative potential, which drives reabsorption of
Cl− and efflux of K+. R, aldosterone receptor.
Water transport across the luminal and basolateral membranes of
collecting duct cells. Above, low water permeability exists in the absence of
ADH. Below, in the presence of ADH, aquaporins are inserted into the
apical membrane, greatly increasing water permeability. AQP2, apical
aquaporin water channels; AQP3,4, basolateral aquaporin water channels;
V2, vasopressin V2 receptor.

16. Inflammation in acute kidney
diseases:
Under physiologic conditions,
endothelial, epithelial, and immune cells
(around parenchymal structures and/ or
vessels) interact harmonically within the
kidney (left side). Upon an insult by
bacteria or bacterial products, drug
toxicity, or following nonsterile
stimulation, epithelial and endothelial
cells undergo necrosis or apoptosis,
releasing products that can activate Toll-
like receptors (TLR), NOD-like receptors
(NLR), and NLPR3 inflammasome in
immune and kidney cells. This activation
leads to the production of chemokines
and proinflammatory cytokines, which
recruit monocytes and neutrophils to the
organ. Concomitantly, resident immune
cells (mainly dendritic cells) get activated
and induce the proliferation of T cells
(TH1, TH17, and CD8 cytotoxic cells),
which in turn produce cytokines,
exacerbating the inflammation process
Inflammation in acute kidney diseases:
Andrade-Oliveira et al., 2019, Front. Pharmacol. 10:1192. doi: 10.3389/fphar.2019.01192.

17. Actors in the transition from acute
kidney injury (AKI) to chronic kidney
disease (CKD). Inflammation is a
common link between AKI and CKD, and
increased expression and/or activation of
TLR, NLRP3 inflammasome, and NF-ĸB
are present in both scenarios. The
composition of the immune cell
population depends on the context. In
AKI, a large number of TH1/TH17
lymphocytes and neutrophils concentrate
around parenchymal structures and/or
vessels, whereas in CKD TH2
lymphocytes and M2 macrophages
predominate. M1 macrophages, dendritic
cells, and CD8+ T cells are seen in both
processes. In CKD, epithelial– and/or
endothelial–mesenchymal transition, with
fibroblast proliferation, may contribute
substantially to the development of
inflammation and fibrosis. Gut microbiota
composition, along with its subproducts,
can have an important role in both AKI
and CKD.
Transition from AKI to CKD:
Andrade-Oliveira et al., 2019, Front. Pharmacol. 10:1192. doi: 10.3389/fphar.2019.01192.

18. Diuretics

19. Three important features are
noteworthy:
1. Transport of solute across
epithelial cells in all nephron
segments involves highly
specialized proteins, which for
the most part are apical and
basolateral membrane integral
proteins.
2. Diuretics target and block the
action of epithelial proteins
involved in solute transport.
3. The site and mechanism of
action of a given class of
diuretics are determined by the
specific protein inhibited by the
diuretic.
Sites and mechanisms of action of diuretics:

20. Tubule transport systems and sites of action of diuretics:

21. Carbonic Anhydrase Inhibitors
Acetazolamide, Dichlorphenamide,
Methazolamide, Dorzolamide, Brinzolamide
o In PCT epithelial cells, the apical NHE transports H+
into the tubular lumen in exchange for Na+. H+ in the
lumen reacts with HCO3 in the ultrafiltrate to form
H2CO3, which decomposes to CO2 and water.
o Because CO2 is lipophilic, this gas readily diffuses
into epithelial cells and reacts with water to form
H2CO3, a reaction that is facilitated by cytoplasmic
carbonic anhydrase. NHE maintains a low H+
concentration in the cell; thus H2CO3 ionizes to H+
and HCO3, which creates a gradient for HCO3 across
the basolateral membrane.
o Carbonic anhydrase inhibitors potently inhibit both the
membrane-bound and cytoplasmic forms of carbonic
anhydrase, and can cause nearly complete abolition of
NaHCO3 reabsorption in the proximal tubule.

22. Adverse effects:
o Hyperchloremic Metabolic Acidosis
o Renal Stones (Phosphaturia and hypercalciuria occur during the bicarbonaturic response to inhibitors of CA)
o Renal Potassium Wasting
o Drowsiness and paresthesias, Hypersensitivity reactions
USES:
A. Treatment of Glaucoma (The reduction of aqueous humor formation by CA inhibitors decreases the intraocular
pressure. Topically active agents, which reduce intraocular pressure without producing renal or systemic effects, are
available (dorzolamide, brinzolamide).
B. Treatment of Metabolic Alkalosis (Acetazolamide can be useful in correcting the alkalosis as well as producing
a small additional diuresis for correction of volume overload)
C. Treatment of Acute Mountain Sickness (Weakness, dizziness, insomnia, headache, and nausea can occur in
mountain travelers who rapidly ascend above 3000 m. By decreasing CSF formation and by decreasing the pH of the
CSF and brain, acetazolamide can increase ventilation and diminish symptoms of mountain sickness)
D. Other Uses (Carbonic anhydrase inhibitors have been used as adjuvants in the treatment of epilepsy and in some
forms of hypokalemic periodic paralysis)
Carbonic Anhydrase Inhibitors

23. Loop Diuretics
Furosemide, Bumetanide, Ethacrynic Acid,
Torsemide
o N+–K+–2Cl- Symport Inhibitors
o Epithelial cells of the thick ascending limb (TAL) have an
efficient mechanism for cotransporting Na+, K+, and Cl-
from the tubular lumen into the cell interior.
o These drugs act on the TAL, inhibiting the Na+/K+/2Cl−
carrier in the lumenal membrane by combining with its
Cl−binding site.
o Studies demonstrate that there are actually two isoforms of
Na+–K+–2Cl- symporters.
o The ‘absorptive’ symporter (called ENCC2, NKCC2, or
BSC1) is expressed only in the TAL of the kidney where it
is localized to apical membranes and subapical intracellular
vesicles. In contrast, the ‘secretory’ symporter (called
ENCC3, NKCCl, or BSC2) is a ‘housekeeping’ protein that
is expressed in basolateral membranes of many nonrenal
epithelial cells.

24. Adverse effects:
o Excessive Na+ and water loss, especially in elderly patients,
hyponatremia, extracellular fluid volume depletion
(hypovolaemia), hypotension, reduced GFR, circulatory
collapse, thromboembolic episodes, or hepatic
encephalopathy.
o Potassium loss, resulting in low plasma K+ (hypokalaemia),
and metabolic alkalosis.
o Hyperuricaemia is common and can precipitate acute gout.
o Hypomagnesemia or hypocalcemia
o Dose-related hearing loss (compounded by concomitant use
of other ototoxic drugs such as aminoglycoside antibiotics)
can result from impaired ion transport by the basolateral
membrane of the stria vascularis in the inner ear
(experienced as tinnitus, hearing impairment, deafness,
vertigo, and a sense of fullness in the ears).
USES:
Loop diuretics are used (cautiously!), in
conjunction with dietary salt restriction and
often with other classes of diuretic, in the
treatment of salt and water overload
associated with:
o acute pulmonary oedema
o chronic heart failure
o cirrhosis of the liver complicated by
ascites
o nephrotic syndrome
o renal failure
▪ Treatment of hypertension complicated by
renal impairment (thiazides are preferred
if renal function is preserved).
Loop Diuretics

25. Thiazide Diuretics
Chlorothiazide, Hydrochlorothiazide, Hydroflumethiazide,
Methyclothiazide, Trichlormethiazide, Bendroflumethiazide,
Chlorthalidone, Indapamide, Metolazone, Quinethazone)
o Na+/Cl- symport inhibitor
o Thiazides bind the Cl− site of the distal tubular
Na+/Cl− co-transport system, inhibiting its action
and causing natriuresis with loss of sodium and
chloride ions in the urine.
o In DCT, the Na+/Cl- symporter transports Na+
‘downhill’ while cotransporting Cl- ‘uphill’ out of
the tubular lumen into DCT cells; Cl- then exits
the basolateral membrane of DCT cells passively
through Cl channels. The net result is
reabsorption of NaCl.

26. USES:
o Edema associated with diseases of the
heart (congestive heart failure), liver
(hepatic cirrhosis), and kidneys
(nephrotic syndrome, chronic renal
failure, and acute glomerulonephritis).
o Hypertension
o To prevent recurrent stone formation in
idiopathic hypercalciuria.
o Nephrogenic diabetes insipidus.
Adverse Effects:
o Extracellular volume depletion, hypotension,
hypokalemia, hypochloremia, metabolic alkalosis,
and hypomagnesemia.
o Hypercalcemia
o Hyponatraemia is potentially serious, especially in
the elderly.
o In brain (vertigo, headache, paresthesias,
xanthopsia, and weakness),
o In gut (anorexia, nausea, vomiting, cramping,
diarrhea, constipation),
o In gallbladder (cholecystitis),
o In pancreas (pancreatitis), bone marrow (blood
dyscrasias), and skin (photosensitivity and skin
rashes).
o Erectile dysfunction in men,
o Decrease glucose tolerance (thus inducing
diabetes mellitus), and
o Increase plasma levels of LDL cholesterol, total
cholesterol, and triglycerides.
Thiazide Diuretics

27. Epithelial Sodium Channel (ENaC) Inhibitors:
Potassium-Sparing Diuretics
(Examples: Triamterene, Amiloride)
o A particular form of renal epithelial cell, called the
principal cell, resides in late distal tubules and
collecting ducts; and apical ENaCs in the principal
cell permit the ‘downhill’ movement of Na+ into the
cell
o ENaC inhibitors bind to and block epithelial Na+
channels inhibiting Na+ reabsorption in the apical
membrane of principal cells in late distal tubules
and collecting ducts.
o The mechanism probably involves competition of
the ENaC inhibitor with Na+ for negatively charged
regions within the Na+ pore of ENaC.

28. Adverse effects:
o Because of their effects on K+ secretion,
ENaC inhibitors may induce severe, life-
threatening hyperkalemia.
o Triamterene is a weak folic acid antagonist
and therefore may cause megaloblastosis;
o Triamterene also reduces glucose tolerance,
causes photosensitization, and may induce
interstitial nephritis and renal stones.
o Most common adverse effects of triamterene
are nausea, vomiting, leg cramps, and
dizziness;
o Most common adverse effects of amiloride
are nausea, vomiting, diarrhea, and
headache.
USES:
o ENaC inhibitors are often administered in
combination with thiazide and loop diuretics.
o ENaC inhibitors are also very useful for the
management of Liddle syndrome, an autosomal
dominant form of low-renin, volume-expanded
hypertension caused by mutations in ENaC’s
beta or gamma subunits leading to increased
Enaz expression in apical membranes of the
collecting duct.
o Aerosolized ENaC inhibitors improve
mucociliary clearance in patients with cystic
fibrosis.
o Also, because ENaC inhibitors block Li+
transport into collecting duct cells, these
diuretics attenuate lithium-induced nephrogenic
diabetes insipidus.
Epithelial Sodium Channel (ENaC) Inhibitors:

29. Mineralocorticoid Receptor (MR) Antagonists:
Aldosterone Antagonists; Potassium-Sparing
Diuretics
(Examples: Spironolactone, Eplerenone, Canrenone)
o The adrenal cortex releases aldosterone into the circulation, which delivers aldosterone to
the kidney.
o Principal cells in late distal tubules and collecting ducts express a high-affinity cytosolic
receptor for aldosterone called the mineralocorticoid receptor (MR).
o Aldosterone diffuses across the basolateral membrane of principal cells, binds to
intracellular MRs, and triggers the translocation of MR–aldosterone complexes to the
nucleus of these epithelial cells. In the nucleus, the MR– aldosterone complex binds to
hormone-responsive elements in DNA and increases the expression of aldosterone-induced
proteins (AIPs).
o Aldosterone increases the levels of ENaC in apical membranes leading to increased Na+
transport.

30. Overview of aldosterone’s influences on
Na+ retention. Via interaction with the
mineralocorticoid receptor (MR), aldosterone affects
myriad renal pathways that handle Na+.
Key to numbered items influenced by ALDOSTERONE:
1. Activation of membrane-bound Na+ channels
2. Na+ channel (ENaC) removal from the membrane
inhibited
3. De novo synthesis of Na+ channels
4. Activation of membrane-bound Na+, K+-ATPase
5. Redistribution of Na+,K+-ATPase from cytosol to
membrane
6. De novo synthesis of Na+,K+-ATPase
7. Changes in permeability of tight junctions
8. Increased mitochondrial production of ATP
Diuretics that are MR antagonists block the binding of
aldosterone to MRs and thereby prevent initiation of
aldosterone signaling.

31. Details of aldosterone’s
influences on membrane
ENaC:
ERK signaling phosphorylates components of
ENaC, making them susceptible to interaction with
Nedd4-2, a ubiquitin-protein ligase that
ubiquitinates ENaC, leading to its degradation. The
Nedd4-2 interaction with ENaC occurs via several
prolinetyrosine- proline (PY) motifs of ENaC.
ALDO enhances expression of the serum and
glucocorticoid-regulated kinase-1 (SGK1) and the
glucocorticoid-induced leucine zipper protein
(GILZ; TSC22D3). SGK-1 phosphorylates and
inactivates Nedd4-2; 14-3-3 dimers bind to the
phosphorylated sites in Nedd4-2 and stabilize them.
Phosphorylated Nedd4-2 no longer interacts well
with the PY motifs of ENaC. As a result, ENaC is
not ubiquitinated and remains in the membrane,
leading to increased Na+ entry into the cell.

32. Adverse effects:
o Life threatening hyperkalemia
o Induce metabolic acidosis, particularly in
patients with liver cirrhosis.
o ‘off-target’ effects on other steroid
receptors, spironolactone may cause
gynecomastia, impotence, decreased
libido and menstrual irregularities.
o Other adverse effects include diarrhea,
gastritis, gastric bleeding, peptic ulcers,
drowsiness, lethargy, ataxia, confusion,
headache, skin rashes, and blood
dyscrasias.
USES:
o Co-administered with thiazide or loop
diuretics to treat edema and hypertension.
o MR antagonists are particularly effective
when aldosterone levels are greatly
elevated, for example, in patients with
primary hyperaldosteronism.
o MR antagonists are preferred diuretics in
patients with hepatic cirrhosis, and added
to standard therapy, reduce morbidity,
mortality, and ventricular arrhythmias in
patients with heart failure.
o Resistant essential hypertension
(especially low-renin hypertension)
Mineralocorticoid Receptor (MR) Antagonists

33. Cyclic Nucleotide Gated Channel Inhibitors
o The IMCD Na+ transport and its
regulation. Na+ enters the IMCD cell
in one of two ways: via ENaC and
through a CNGC that transports Na+,
K+, and NH4+ and is gated by cGMP.
o Na+ then exits the cell via the Na+,
K+-ATPase.
o The CNGC is the primary pathway for
Na+ entry and is inhibited by
Natriuretic peptides (NPs).

34. Cyclic Nucleotide Gated Channel Inhibitors
(Examples: Nesiritide, Carperitide, Ularitide)
o The deepest part of the collecting duct is called the inner medullary collecting duct (IMCD), and
this nephron segment is the last site for reabsorption of Na+.
o Although the IMCD expresses ENaC, Na+ reabsorption in the IMCD is mediated in part by a
cyclic nucleotide gated (CNG) channel that has equal permeability for Na+ and K+ and is
inhibited by cGMP.
o Diuretics that are CNG channel inhibitors belong to a family of endogenous natriuretic factors
that include atrial natriuretic peptide (ANP; carperitide), brain natriuretic peptide (BNP;
nesiritide), urodilatin (ularitide), and C-type natriuretic peptide (CNP).
o Presently, CNG channel inhibitors have limited use, mostly to treat patients with acutely
decompensated heart failure with shortness of breath at rest. However, CNG channel inhibitors
do not appear to reduce either short- or long-term mortality in patients with acute
decompensated congestive heart failure.

35. Osmotic Diuretics
(Examples: Mannitol, Glycerin, Isosorbide, Urea)
o These are inert substances; they do not directly interact with renal transport
systems.
o They filtered into the renal tubules, undergo minimal reabsorption and
accomplish diuresis in part due to their physical presence in the tubular lumen.
o Because osmotic diuretics have limited cellular permeability, their presence in the
blood causes osmotic extraction of water from cells; a process that expands the
extracellular fluid volume, decreases blood viscosity, inhibits renin release, and
increases renal blood flow. Probably these changes contribute to cause diuresis.
o Osmotic diuretics act both in the PCT and loop of Henle, with the loop of Henle
probably being the main site of action; and they increase urinary excretion of
most electrolytes, including Na+, K+, Ca2+, Mg2+, Cl-, HCO3
-, and phosphate.

36. Adverse effects:
o The extracellular fluid volume by osmotic
diuretics may cause heart failure, pulmonary
congestion, and pulmonary edema.
o Also dilution of the plasma may result in
hyponatremia leading to headache, nausea,
and vomiting.
o Renal loss of water in excess of sodium can
cause hypernatremia and dehydration.
USES:
o Osmotic diuretics have several
important uses including treatment of
dialysis disequilibrium syndrome,
reducing intraocular pressure, and
managing cerebral edema.
Osmotic Diuretics:

37. Anti-diuretics

38. ❖An antidiuretic is a substance that helps the body retains water.
❖It prevents the kidneys and bladder from removing and eliminating water from
the body too quickly.
❖Antidiuretic medicines are used to treat bed-wetting, incontinence and similar
conditions.
❖These are drugs that reduce urine volume, particularly in diabetes INSIPIDUS
(DI).
❖Diabetes Insipidus (Drinker’s disease): Hypo-secretion of ADH
(Antidiuretic hormone or Vasopressin) causes a disorder known as diabetes
insipidus (Excretion of large quantity of dilute urine).
Anti-diuretics

39. Difference between DM and DI:

40. Vasopressin
Synthesis and structure

41. - ADH synthesized in the cell bodies of hypothalamic neurons in the supraoptic nucleus.
- ADH is stored in the neurohypophysis (posterior pituitary)-forms the most readily released ADH pool
Release

42. Vasopressin receptors

43. Vasopressin receptors

44. V2 Receptor Antagonists
(Examples: Conivaptan, Lixivaptan, Mozavaptan,
Satavaptan Tolvaptan)
V2 Receptor Agonists
(Example: Desmopressin)

45. Mechanism of action of Vasopressin

46. Mechanisms regulating AVP release

47. Functions of Vasopressin:
1. Kidney:
o Increasing the water
permeability of distal
convoluted tubule and
collecting duct cells in the
kidney, thus allowing water
reabsorption and excretion of
more concentrated urine, i.e.,
antidiuresis.
o Acute increase of sodium
absorption across the
ascending loop of henle.
o Vasopressin also increases the
concentration of calcium in the
collecting duct cells.
2. Cardiovascular system
o Vasopressin increases
peripheral vascular resistance
(vasoconstriction) and thus
increases arterial blood
pressure.
o Act as an important
compensatory mechanism for
restoring blood pressure in
hypovolemic shock such as that
which occurs during
hemorrhage.
3. Central nervous system
o Vasopressin is released into the
brain in a circadian rhythm by
neurons of the suprachiasmatic
nucleus.
o Vasopressin released from
centrally projecting
hypothalamic neurons is
involved in aggression, blood
pressure regulation, and
temperature regulation.
o Recent evidence suggests that
vasopressin may have
analgesic effects.

48. ❑ To treat neurogenic (central) diabetes insipidus.
❑ Reduction in bleeding and blood transfusions during burn wound
excision.
❑ Treatment of upper gastrointestinal haemorrhage secondary to
haemorrhagic gastritis.
❑ Treatment of severe haematuria.
❑ Reduction of blood loss and prevention of intraoperative hypotension
during liver transplant.
❑ Treatment of refractory bleeding after uterine myoma resection.
❑ Use of vasopressin in cardiac arrest.
❑ Uterus is contracted by AVP acting on oxytocin receptors. In the
nonpregnant and early pregnancy uterus, AVP is equipotent to oxytocin.
❑ Von Willebrand's Disease (a lifelong bleeding disorder in which your blood doesn't clot
properly)
USE of Vasopressin

49. Vasopressin Analogues
1. Arginine Vasopressin
(AVP)
2. Desmopressin
3. Terlipressin
4. Lypressin

50. Thank You