ELEVATED PLASMA-CORTISOL REDUCES PERMEABILITY OF MAMMARY TIGHT JUNCTIONS IN THE LACTATING BOVINE MAMMARY EPITHELIUM

Induction of tight junction permeability in the mammary epithelium dec reases milk secretion, and in cows tight junctions become leaky after 17 h of milk accumulation. In vitro studies demonstrate the importance of glucocorticoids for the formation and maintenance of tight tight j unctions. In this study we examined whether cortisol can prevent mamma ry tight junction permeability in the lactating gland in vivo, and inh ibit the associated milk loss, using our milk-accumulation model to ch allenge tight junction patency. Following a 4-day control period Jerse y cows were subjected to a 24-h period in which they were milked twice at 0700 and 1500 h (TM; n=6), once at 0700 h (OM; n=7), or once and t reated with ACTH (40 IU per 2 h, starting after 14 h of milk accumulat ion) to increase endogenous cortisol levels (OM+ACTH; n=7). Frequent b lood samples for cortisol, lactose and glucose analyses were taken via indwelling jugular catheters. ACTH treatment resulted in a sustained elevation of systemic cortisol concentrations. Plasma lactose, an indi cator of tight junction leakiness, was not changed in TM cows, but beg an to increase rapidly at 17 h oi milk accumulation in OM cows. Treatm ent with ACTH prevented the increase in plasma lactose, although level s were slightly, but not significantly, higher than in TM cows, indica ting that elevated plasma cortisol reduced mammary tight junction leak iness. Milk yield was reduced by 12% in both once-milked groups, despi te cortisol preventing tight junction leakiness. However, the milk los s in the latter group may not be related to leaky tight junctions, but be due to a reduction in milk precursor uptake by the mammary gland. Consistent with this notion was a 34% increase in plasma glucose level s in OM+ACTH cows only.