The parabrachial nucleus receives visceral sensory and pain inputs, and organizes patterns of cardiovascular response seen during arousal due to pain, respiratory distress, or gastrointestinal discomfort (increased blood pressure and heart rate). It does this by direct projections to sympathetic and parasympathetic cell bodies, as well as to medullary pattern generators.
In the medulla, there are distinct pattern generators in the ventromedial and ventrolateral areas. The ventromedial medulla receives inputs from hypothalamic cell groups involved in thermoregulation, and it organizes patterns of sympathetic response necessary for thermogenesis (increased heart rate and activation of brown adipose tissue, with shifting of blood flow from cutaneous to deep vascular bed). This also requires elevation of heart rate to deal with the increased cardiac demand of hyperthermia. The ventrolateral medulla, by contrast produces patterns of cardiovascular response necessary for maintaining blood pressure during erect posture, called baroreceptor reflexes.
Other descending hypothalamic axons go directly to the nucleus of the solitary tract, as well as the preganglionic neurons in the nucleus ambiguus in the medulla, which control heart rate through the vagus nerve and the intermediolateral column of the spinal cord, which controls vasoconstriction. These may produce patterns of autonomic activation that are organized at a hypothalamic level, such as stress or starvation responses.
The brainstem targets of this descending system coordinate cardiovascular reflexes. For example, the carotid sinus nerve (a branch of the glossopharyngeal nerve) and the aortic depressor nerve (a branch of the vagus nerve) bring information to the nucleus of the solitary tract about aortic and carotid stretch. When blood pressure is high, neurons in the nucleus of the solitary tract activate cardiovagal neurons in the nucleus ambiguus to slow the heart and inhibit neurons in the ventrolateral medulla that maintain tonic blood pressure by means of activating sympathetic preganglionic vasoconstrictor neurons. This baroreceptor reflex can be modified by descending hypothalamic input so that during times of stress, for example, there can be a simultaneous increase in blood pressure and heart rate without activating the baroreceptor reflex.
Projections from the hypothalamus to the intermediolateral column can directly activate sympathetic ganglion cells concerned with cardioacceleration and the strength of contraction, to increase cardiac output. Other descending hypothalamic axons can contact adrenal preganglionic neurons, resulting in increased circulating adrenalin, which also increases vasoconstriction and cardiac output.

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