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BMC Physiol. 2009 Jun 29;9:13. doi: 10.1186/1472-6793-9-13.

Acute heat stress brings down milk secretion in dairy cows by up-regulating the activity of the milk-borne negative feedback regulatory system.

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Biology of Lactation Laboratory, Inst, of Animal Sciences, Agricultural Research Organization, Bet Dagan 50250, Israel.



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.


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.


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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