Angiotensin Ii Modulates Detrusor Contraction by Up-regulating Caveolin Proteins

Hypothesis / aims of study Angiotensin II (AngII), the effector molecule of the renin-angiotensin system, is known to participate in smooth muscle remodelling during hypertrophy in several tissues including the bladder. Although autocrine AngII can be released from bladder smooth muscle (BSM) cells in response to mechanical stimulation [1], little is known about the mechanisms by which AngIImediated signals are regulated in the bladder. Previous studies showed that contractile responses induced by AngII depend on the integrity of BSM caveolae [2], specific membrane invaginations involved in the regulation of signal transduction. Moreover, alterations in caveolar elements have been described in hypertrophic detrusor tissue from obstructed rat bladders [3], an animal model in which AngII upregulation has also been implicated. In this study, we investigated the molecular effects of AngII stimulation on the expression of caveolins (Cav, the structural proteins of caveolae), and whether changes in caveolins induced by AngII may be associated with functional alterations responsible for the development of bladder dysfunction.