BACKGROUND: The objective of this study was to determine if acute heat stress (HS) decreases milk secretion by activating the milk-borne negative feedback system, as an emergency physiological response to prevent a life-threatening situation. To induce HS, summer acclimatized dairy cows were exposed to full sun under mid-summer Mediterranean conditions, with and without conventional cooling procedures. RESULTS: Exposure to HS induced a rapid and acute (within 24 h) reduction in milk yield in proportion to the heat load. This decrease was moderated by cooler night-time ambient temperature. The reduction in milk yield 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 beta-casein (beta-CN (1-28)). These metabolites constitute the regulatory negative feedback system. Previously, it has been shown that beta-CN (1-28) down-regulated milk secretion by blocking potassium channels on the apical aspects of the mammary epithelial cells. CONCLUSION: Here we demonstrate that the potassium channels in mammary tissue became more susceptible to beta-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 beta-CN (1-28) is part of the regulatory system.
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Silanikove et al. (2009) studied this question.