Lung stretch receptors.

Mechanoreceptors are present in the smooth muscle of the

airways. When stimulated by distention of the lungs and airways, mechanoreceptors
initiate a reflex decrease in breathing rate called the Hering-Breuer reflex. The reflex
decreases breathing rate by prolonging expiratory time.
Joint and muscle receptors. Mechanoreceptors located in the joints and muscles
detect the movement of limbs and instruct the inspiratory center to increase the
breathing rate. Information from the joints and muscles is important in the early
(anticipatory)ventilatory response to exercise.
Irritant receptors. Irritant receptors for noxious chemicals and particles are located
between epithelial cells lining the airways. Information from these receptors travels to
the medulla via CN X and causes a reflex constriction of bronchial smooth muscle and
an increase in breathing rate.
J receptors. Juxtacapillary (J) receptors are located in the alveolar walls and,
therefore, are near the capillaries. Engorgement of pulmonary capillaries with blood and
increases in interstitial fluid volume may activate these receptors and produce an
increase in the breathing rate. For example, in left-sided heart failure, blood backs
up in the pulmonary circulation and J receptors mediate a change in breathing pattern,
including rapid shallow breathing and dyspnea (difficulty in breathing).











Satiety
The centers that control appetite and feeding behavior are located in the hypothalamus.
A satiety center, which inhibits appetite even in the presence of food, is located in the
ventromedial nucleus (VPN) of the hypothalamus and a feeding center is located in the
lateral hypothalamic area (LHA). Information feeds into these centers from the arcuate
nucleus of the hypothalamus. The arcuate nucleus has various neurons that project
onto the satiety feeding centers. Anorexigenic neurons release pro-opiomelanocortin
(POMC) and cause decreased appetite; orexigenic neurons release neuropeptide Y
and cause increased appetite. The following substances influence the anorexigenic and
orexigenic neurons of the arcuate nucleus and, accordingly, decrease or increase
appetite and feeding behavior.
Leptin. Leptin is secreted by fat cells in proportion to the amount of fat stored in
adipose tissue. Thus, leptin senses body fat levels, is secreted into the circulation,
crosses the blood-brain barrier, and acts on neurons of the arcuate nucleus of the
hypothalamus. It stimulates anorexigenic neurons and inhibits orexigenic neurons,
thereby decreasing appetite and increasing energy expenditure. Because leptin
detects stored body fat, it has chronic (longterm) effects to decrease appetite.
Insulin. Insulin has similar actions to leptin, in that it stimulates anorexigenic neurons
and inhibits orexigenic neurons, thus decreasing appetite. In contrast to leptin, insulin
levels fluctuate during the day, thus it has acute (short-term) effects to decrease
appetite.
GLP-1. As discussed earlier, GLP-1 is synthesized and secreted by intestinal L cells.
Among its actions (like leptin and insulin), it decreases appetite.
Ghrelin. Ghrelin is secreted by gastric cells just before ingestion of a meal. It acts
oppositely toleptin and insulin to stimulate orexigenic neurons and inhibit anorexigenic
neurons, thus increasing appetite and food intake. Periods of starvation and
weight loss strongly stimulate ghrelin secretion.
Peptide YY (PYY). PYY is secreted by intestinal L cells following a meal. It acts to
decrease appetite, both through a direct effect on the hypothalamus and by inhibiting
ghrelin secretion.