the respective growth charts for boys aged 2-20 years (Center for Disease Control and Prevention), and the statistical significance of differences determined using the chi-square test. RESULTSThe height and weight distributions of patients with varicocele indicated a significant deviation from normal in the 25-95th percentiles for stature and in the 25-75th for weight ( P < 0.05). Deviations in BMI were insignificantly different from normal at each percentile. CONCLUSIONThese results indicate that patients with varicocele are significantly taller and heavier than age-matched controls. Future studies to address the key areas identified in this study will help to further assess the distribution of the incidence of varicocele in closely defined subsets of adolescent growth and development, which may provide some insight into the cause of varicoceles. KEYWORDS varicocele, body mass index, height, weight, cause OBJECTIVETo determine if there is an association with habitus in young males with varicocele, as adolescent boys with varicoceles appear to be mostly taller and leaner than age-matched controls. PATIENTS AND METHODSRetrospectively reviewing our records we obtained the height and weight of 43 consecutive males (mean age 14.3 years, range 11-19) under long-term follow-up for varicocele. The body mass index (BMI), heights and weights were compared with values from

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The calcineurin pathway has a significant role in bladder wall hypertrophy following partial outlet obstruction. Bladder hypertrophy could not be fully prevented by cyclosporin A, suggesting that multiple signaling pathways are involved in this pathophysiology. The expression of myosin heavy chain AB isoforms is regulated in part by the calcineurin pathway.

Partial bladder outlet obstruction (PBOO) alters the function of the whole bladder and produces specific alterations in the contractility of the bladder smooth muscle cell. The goal of this study was to test the hypothesis that PBOO affects smooth muscle contraction at the level of the receptor- and G protein-dependent increase in myofilament Ca2+ sensitivity. To address this question, we used alpha-toxin-permeabilized strips of bladder smooth muscle from control animals and animals subjected to 2 wk of PBOO. Increasing free [Ca2+] increased force in permeabilized strips from control animals; the addition of 10 microM carbachol and 10 microM GTP increased both the Ca2+ sensitivity of the contractions and the maximal levels of force attained. In contrast, although increases in [Ca2+] increased force in permeabilized strips from PBOO animals, the addition of carbachol and GTP had no additional effects. Myosin light chain phosphorylation levels increased with [Ca2+], and although they tended to be higher in strips from PBOO animals, they did not reach statistical significance. Assessment of G protein activity from both animal models suggests this is not a site responsible for the loss of carbachol and GTP enhancement of myofilament Ca2+ sensitivity. The addition of phorbol dibutyrate increased the Ca2+ sensitivity of force development in strips from both animal models, suggesting that an alteration in PKC signaling is not involved. Our results are consistent with the hypothesis that PBOO decreases receptor-mediated myofilament calcium sensitization and that the site of action is downstream from either the G proteins or PKC.

We propose that partial bladder outlet obstruction does not alter protein kinase C activation, but rather abolishes or uncouples the pathway(s) downstream of protein kinase C, leading to contraction. Loss of this pathway may contribute to the loss of normal voiding behavior and the resultant decompensated state.