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Blood samples were collected from unstressed cattle and from cattle undergoing handling stress, transport stress and slaughter. The blood was analysed for ACTH, cortisol, thyroxine stimulating hormone, tri-iodothyronine (T3) and catecholamine concentrations, and for haematocrit, total plasma protein, plasma lipid, lactate and glucose concentrations. Compared to control values handling significantly increased T3, cortisol, lipid and lactate concentrations. Compared to handling, transport stress was associated with increased catecholamines and lactate concentrations, a decreased cortisol concentration and similar concentrations of T3, lipid and glucose. Compared to transport, slaughter resulted in high catecholamines, lactate and glucose, and low T3, cortisol and lipid levels. It is concluded that the response to stress has two phases, a hypothalamic-adrenal cortex phase which is associated with perceived environmental stress such as noise, and a sympathetic-adrenal-medulla phase which is associated with neurogenic stress such as transport or specifically the massive sympathetic discharge caused by stunning. Combinations of stresses produce a mixed response.

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The fundamental mechanism that underlies essential hypertension is a high total peripheral resistance. We review here possible origins of high total peripheral resistance in physiologically hypertensive giraffes, spontaneously hypertensive rats and humans with essential hypertension. We propose that a common link could be reduced brainstem perfusion, as first suggested by Cushing in 1901. Any tendency towards reduction of cerebral blood flow to the cardiovascular control centres in rest and sleep will be prevented by activation of a response arising in the brainstem. The response will proportionately increase systemic blood pressure and return cerebral blood flow to a new homeostatic level. New evidence we review here supports this idea and leads us to suggest that central regulation of blood pressure has two components: the classic Cushing's response, which is a terminal event, and a Cushing's mechanism, which is a physiological mechanism for long-term control of mean arterial pressure. In giraffes, Cushing's mechanism is activated by increasing neck length during growth and subsequent gravitational hypotension that stimulates a rise in basal arterial blood pressure. In man and rats, the mechanism is activated by narrowing of the arteries supplying the brainstem. If we are correct, future successful treatment of essential hypertension in man will include methods of reducing cerebral arterial resistance.