Thyroid hormone is one the few hormones that are derived from a single amino acid, in this case tyrosine. Amino acids (and subsequently their derivatives) are mostly hydrophilic, and are unable to pass through the cell membrane. They must bind to surface receptors in order to initiate their effects on the cell.

Understanding the difference between peptide hormones and glucocorticoids is important in answering this question. Peptide hormones function through cell surface receptors, and usually subsequent G-protein regulated signal amplification. Glucocorticoid hormones generally function by modifying gene expression directly in the nucleus. Generally, peptide hormones end with the suffix -in, while glucocorticoids end with -one or -en. Using this information we see that renin would be a peptide hormone and would therefore function through cell surface receptors.

Peptide hormones rely on a secondary messager system, such as cyclic AMP, to perform their functions on target cells/organs. Of the available answer choices, insulin, calcitonin, and parathyroid hormone (PTH) are peptide hormones, and are therefore incorrect.

Steroid hormones have intracellular receptors and can enter cells directly to cause changes in transcription rates, which result in their effects. Estrogen is a steroid hormone, and thus does NOT use a secondary messanger system.

Somatotropin, or human growth hormone, is responsible for both bone and cartilage growth. It is the main factor in human growth, up until puberty.

Calcitonin decreases blood calcium level. All other answer choices correctly pair a hormone with its function.

Acute high blood pressure is generally due to systemic vasoconstriction. Of the answer choices, only activating the alpha-1 receptor will elicit peripheral vasoconstriction.  

As mentioned from the passage, steroid hormones must pass through the lipid bilayer in order to reach the nucleus. Phosphoinositol bisphosphate and calmodulin are both secondary messengers as part of the G protein-coupled receptor pathway.  

Positive feedback describes an event in which a pathway generates a response that further triggers the pathway, increasing the pathway effects. In contrast, negative feedback occurs when a pathway generates a response to inhibit the pathway origin, diminishing the pathway effects. Negative feedback is a common control mechanisms in the body to maintain homeostasis, while positive feedback is inherently designed to disrupt homeostasis.

Fever during illness is enhanced via a positive feedback system that only ends once the illness begins to alleviate. Similarly, contractions during labor will intensify via positive feedback oxytocin stimulation until the child is born. Osteoporosis is caused by an imbalance in the negative feedback system that controls blood calcium. This imbalance simply means that bone is lost more than it is gained, and is still an example of negative feedback.

Triiodothyronine (T3) employs a negative feedback mechanism, meaning that when blood serum concentrations of T3 become too high, receptors on the thyroid gland inhibit the release of additional T3.

In contrast, a positive feedback mechanism would encourage additional release of a hormone when levels are high, resulting in an exponential increase in the hormone effects. An example of a positive feedback mechanism is the release of oxytocin during childbirth to help the uterus contract.

Oxytocin employs a positive feedback mechanism, meaning that existing levels of oxytocin encourage additional release of oxytocin. This results in an exponential increase in the hormone's effects.

In contrast, a negative feedback mechanism would prevent additional release of a hormone when levels of the existing hormone were too elevated. This results in stable homeostasis around a constant hormone concentration in the blood.