ABSTRACT
Exposure to heat stress (HS) induced a rapid and acute (within 24 hr) reduction in the milk yield (MY) in proportion to the heat load. This decrease was moderated by cooler night-time ambient temperature. The reduction in MY was associated with corresponding responses in plasminogen activator/plasminogen-plasmin activities, and with increased activity (concentration) of the (1-28) N-terminal fragment peptide that is released by plasmin from β-casein (β-CN (1-28)). These metabolites constitute the regulatory negative feedback system. Previously, it has been shown that β-CN (1-28) down-regulated milk secretion by blocking potassium channels on the apical aspects of the mammary epithelial cells. So we can calculate that the potassium channels in mammary tissue became more susceptible to β-CN (1-28) activity under HS. Thus, the present study highlighted two previously unreported features of this regulatory system: (i) That it modulates rapidly in response to stressor impact variations; and (ii) That the regulations of the mammary epithelial potassium channel sensitivity to the inhibitory effect of β-CN (1-28) is a part of the regulatory system.
