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.
Certain elements of the mesonephros persist as part of the reproductive tract.
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.
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.
The calyces, pelvis, and ureter derive from the differentiation of the metanephric mesenchyme.
Older, more differentiated nephrons are located at the periphery of the developing kidney, whereas newer, less differentiated nephrons are found near the juxtamedullary region.
Common iliac artery
Inferior mesenteric artery
Superior mesenteric artery
Glial cell line–derived neurotrophic factor (GDNF)
GDNF expression is restricted by FoxC1 and FoxC2 transcription factors.
It is a ligand for the RET receptor tyrosine kinase.
It is expressed in the metanephric mesenchyme but not in the ureteric bud.
GDNF arrests the ureteric bud growth in vitro.
GDNF gene knockout mice demonstrate an abnormal renal development.
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.
At1 knockout mice demonstrate a spectrum of congenital urinary tract abnormalities, including ureteropelvic junction obstruction and vesicoureteral reflux.
Both subtypes of angiotensin II receptor, AT1 and AT2, are expressed in the developing metanephros.
Pharmacologic inhibition of angiotensin-converting enzyme in the neonatal rat produces irreversible abnormalities in renal function and morphology.
median umbilical ligament.
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.
Epithelial-mesenchymal inductive interactions appear to be necessary for proper bladder development.
By the 12th week the urachus involutes to become a fibrous cord, which becomes the median umbilical ligament.
Bladder compliance seems to be low during early gestation, and it gradually increases thereafter.
The paramesonephric duct derivatives are absent in patients with complete androgen insensitivity syndrome.
In male embryos the paramesonephric ducts degenerate under the influence of the müllerian-inhibiting substance (MIS) produced by the Leydig cells.
Both male and female embryos form paramesonephric (müllerian) ducts.
In male embryos the paramesonephric ducts become the appendix testis and the prostatic utricle.
In female embryos the paramesonephric ducts form the female reproductive tract, including fallopian tubes, uterus, and upper vagina.
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.
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.
Gartner duct cysts.
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