We tested the hypothesis that maternal protein deprivation during gestation results in changes in expression of the systemic renin-angiotensin system in fetal mice. Fetal weight was decreased significantly as a consequence of 50% maternal protein deprivation during second half of gestation. In fetal liver, angiotensinogen protein expression was reduced significantly despite a significant increase in messenger RNA (mRNA). In fetal kidneys, both mRNA and protein levels of renin were increased significantly. In the lungs, we observed a decrease in both angiotensin-converting enzyme I and II mRNA expression, whereas protein expression of both isoforms was increased significantly. The fetal heart showed significant increases in expression of angiotensin II type 1 (AT-1) and type 2 (AT-2) receptors mRNA. Protein expression of AT-1 receptors increased, while that of AT-2 receptors decreased. We conclude that maternal low-protein diet during gestation leads to significant changes in expression of the systemic renin-angiotensin system in fetal mice and may be important in the genesis of hypertension in the adult.

OBJECTIVES:Underactive bladder (UAB) and detrusor underactivity (DU) are receiving increasing clinical and research attention. Although lacking a formalized definition, UAB is described as a symptom complex, while DU is a standardized statement of urodynamic function. Both terms nominally suggest impaired detrusor contractility leading to disordered emptying. We sought to evaluate the relationship between UAB, DU and detrusor contractility. METHODS:A chart review of 256 urodynamic records from clinical practice was conducted. Data about symptoms and urodynamic performance were extracted and analyzed, comparing measures of sensory and motor function among groups based on symptoms and urodynamic observations. RESULTS:One hundred and ninety eight complete urodynamic studies met ad hoc defined criteria for inclusion. UAB is specific (0.90) for, but not sensitive (0.22) to, DU. Increased post-void residual volume is common to both UAB and DU, but neither is associated with impaired contractility as measured by Watts factor. Patients with UAB and DU demonstrate higher sensation volume thresholds than do those without these symptoms or observations. CONCLUSIONS:The symptom complex of UAB is not a reliable predictor of the urodynamic observation of DU, and neither condition is associated with a diminished Watts factor. Our results suggest that UAB and DU are typically disorders of volume hyposensitivity rather than of impaired contractility, and may differ in their relationship to bladder perceptions. Thus, these terms should not be used interchangeably.