Calcitonin decreases blood calcium levels, while parathyroid hormone increases blood calcium levels.

FSH, LH, estrogen, and progesterone all increase around ovulation to make an environment in the uterus that will be healthy if fertilization occurs. Prolactin promotes milk production at the end of pregnancy and while a mother is breast feeding a child.

Release of ADH would not be associated with release of atrial naturitic hormone. ADH increases blood pressure, while atrial naturitic hormone decreases blood pressure.

Parathyroid hormone (PTH) does not enhance absorption of vitamin D through the skin.

It does, however, act independently on the bones, kidneys, and gut, to increase blood calcium. Interestingly, cancer cells in various types of cancers (breast and lung) can secrete parathyroid hormone-related protein (PTHrP), which acts similarly to PTH and can cause hypercalcemia (high serum calcium) in cancer patients.

Insulin functions to decrease blood glucose levels, causing cells to take up glucose from the blood. If someone takes too much insulin it would result in hypoglycemia, or decreased blood glucose levels. Insulin has no effect on calcium levels. Glucose is rarely found in the urine and can be a sign of extremely high blood glucose levels, or hyperglycemia.

This question requires knowledge of the negative feedback loop between the anterior pituitary hormones (FSH and LH) and the sex hormones (estrogen and progesterone). Prior to menopause, FSH and LH production is inhibited by estrogen production in the ovaries. When ovarian estrogen production decreases, during menopause, FSH and LH levels increase uninhibited.

Aldosterone functions to make the collecting duct and distal convoluted tubule in the kidneys to make them more permeable to Na+, Cl–, K+, and H+. When Na+ and Cl– are reabsorbed, water follows them into the blood, thus increasing total blood volume and raising blood pressure.

An increase in aldosterone will cause an increase in sodium reabsoption, an increase in blood osmolarity, an increase in antidiuretic hormone (ADH) release, an increase in water reabsoption, and an increase in blood volume.

Addison's disease is a disorder in which the adrenal cortex is unable to be stimulated by adrenocorticotropic hormone (ACTH). The adrenal cortex is responsible for the secretion of aldosterone and cortisol. Aldosterone is responsible for the increased reabsorption of sodium and increased excretion of potassium, leading to water retention. This process helps raise the blood pressure. Since aldosterone is not being adequately produced in a patient with Addison's disease, the patient's blood pressure will be lower than normal.

Estrogen is a very versatile hormone that regulates several biological processes, including structural roles (such as increasing fat stores and developing female reproductive organs) and reproductive roles (such as promoting ovulation and preparing the uterine lining to support a fertilized egg). In order for estrogen to have such diverse effects, it enters the cell and binds to the estrogen receptor. The estrogen-receptor complex translocates to the nucleus and binds to hormone response elements (also call estrogen response elements) to activate target gene expression. Finally, although estrogen plays a role in the differentiation and formation of the milk duct system, following birth estrogen levels are dramatically reduced because high levels of estrogen inhibit lactation.