Paraxial (somite) mesoderm
The excretory portion of the mesonephros begins to degenerate during the first year of life.
It serves as a transient excretory organ during the development of the definitive kidneys metanephros.
During the early development, the mesonephros lies medial to the developing mullerian ducts.
Development of the nephric ducts (also called wolffian ducts) precedes that of the mesonephric tubules.
Certain elements of the mesonephros persist as part of the reproductive tract.
In humans, although renal maturation continues postnatally, nephrogenesis is completed by birth.
It requires the reciprocal inductive interaction between müllerian duct and metanephric mesenchyme.
The metanephric development requires the inductive effect of the urogenital sinus.
Older, more differentiated nephrons are located at the periphery of the developing kidney, whereas newer, less differentiated nephrons are found near the juxtamedullary region.
The calyces, pelvis, and ureter derive from the differentiation of the metanephric mesenchyme.
Superior mesenteric artery
Common iliac artery
Inferior mesenteric artery
Glial cell line–derived neurotrophic factor (GDNF)
It is expressed in the metanephric mesenchyme but not in the ureteric bud.
GDNF gene knockout mice demonstrate an abnormal renal development.
GDNF arrests the ureteric bud growth in vitro.
It is a ligand for the RET receptor tyrosine kinase.
GDNF expression is restricted by FoxC1 and FoxC2 transcription factors.
Both subtypes of angiotensin II receptor, AT1 and AT2, are expressed in the developing metanephros.
At1 knockout mice demonstrate a spectrum of congenital urinary tract abnormalities, including ureteropelvic junction obstruction and vesicoureteral reflux.
The embryonic kidney is able to produce all components of the renin-angiotensin system.
Infants born to mothers treated with angiotensinconverting enzyme inhibitors during pregnancy have increased rates of oligohydramnios, hypotension, and anuria.
Pharmacologic inhibition of angiotensin-converting enzyme in the neonatal rat produces irreversible abnormalities in renal function and morphology.
median umbilical ligament.
Bladder compliance seems to be low during early gestation, and it gradually increases thereafter.
Histologic evidence of smooth muscle differentiation begins near the bladder neck and proceeds toward the bladder dome.
The bladder body is derived from the urogenital sinus whereas the trigone develops from the terminal portion of the mesonephric ducts.
By the 12th week the urachus involutes to become a fibrous cord, which becomes the median umbilical ligament.
Epithelial-mesenchymal inductive interactions appear to be necessary for proper bladder development.
In male embryos the paramesonephric ducts become the appendix testis and the prostatic utricle.
Both male and female embryos form paramesonephric (müllerian) ducts.
In female embryos the paramesonephric ducts form the female reproductive tract, including fallopian tubes, uterus, and upper vagina.
In male embryos the paramesonephric ducts degenerate under the influence of the müllerian-inhibiting substance (MIS) produced by the Leydig cells.
The paramesonephric duct derivatives are absent in patients with complete androgen insensitivity syndrome.
It requires the conversion of testosterone into dihydrotestosterone by 5α-reductase.
It requires the effects of müllerian-inhibiting substance.
It is first seen at the 10th to 12th week of gestation.
It is dependent on epithelial-mesenchymal interactions under the influence of androgens.
Androgen receptors in the urogenital sinus mesenchyme are required for prostate specification and differentiation.
Gartner duct cysts.
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