Which promotes na and water retention

Follicle cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries, as illustrated in Figure Estradiol and progesterone are steroid hormones that prepare the body for pregnancy.

Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle. The posterior pituitary releases the hormone oxytocin , which stimulates uterine contractions during childbirth.

The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth.

Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete. Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary.

Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels.

Additional regulation is mediated by the thyroid hormones. Cells of the body require nutrients in order to function, and these nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake and utilizing reserves when necessary, the body uses hormones to moderate energy stores. Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise for example, after a meal is consumed.

Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production. It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use. Insulin also increases glucose transport into certain cells, such as muscle cells and the liver.

This results from an insulin-mediated increase in the number of glucose transporter proteins in cell membranes, which remove glucose from circulation by facilitated diffusion. As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane.

This allows glucose to enter the cell, where it can be used as an energy source. However, this does not occur in all cells: some cells, including those in the kidneys and brain, can access glucose without the use of insulin.

Insulin also stimulates the conversion of glucose to fat in adipocytes and the synthesis of proteins. This animation describe the role of insulin and the pancreas in diabetes. Impaired insulin function can lead to a condition called diabetes mellitus , the main symptoms of which are illustrated in Figure This can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin.

This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia high sugar. High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced; this may result in dehydration.

Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia , low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness, and can sometimes cause unconsciousness or death if left untreated.

When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis.

Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells.

Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis. Glucagon also stimulates adipose cells to release fatty acids into the blood. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels.

Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statement about these two conditions is true? The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine , also known as tetraiodothyronine or T 4 , and triiodothyronine , also known as T 3.

These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria resulting in increased ATP production.

In the nucleus, T 3 and T 4 activate genes involved in energy production and glucose oxidation. T 3 and T 4 release from the thyroid gland is stimulated by thyroid-stimulating hormone TSH , which is produced by the anterior pituitary.

TSH binding at the receptors of the follicle of the thyroid triggers the production of T 3 and T 4 from a glycoprotein called thyroglobulin. Thyroglobulin is present in the follicles of the thyroid, and is converted into thyroid hormones with the addition of iodine.

Iodine is formed from iodide ions that are actively transported into the thyroid follicle from the bloodstream. A peroxidase enzyme then attaches the iodine to the tyrosine amino acid found in thyroglobulin. T 3 has three iodine ions attached, while T 4 has four iodine ions attached.

T 3 and T 4 are then released into the bloodstream, with T 4 being released in much greater amounts than T 3. As T 3 is more active than T 4 and is responsible for most of the effects of thyroid hormones, tissues of the body convert T 4 to T 3 by the removal of an iodine ion.

Most of the released T 3 and T 4 becomes attached to transport proteins in the bloodstream and is unable to cross the plasma membrane of cells. These protein-bound molecules are only released when blood levels of the unattached hormone begin to decline. The follicular cells of the thyroid require iodides anions of iodine in order to synthesize T 3 and T 4. Iodides obtained from the diet are actively transported into follicle cells resulting in a concentration that is approximately 30 times higher than in blood.

The typical diet in North America provides more iodine than required due to the addition of iodide to table salt. Inadequate iodine intake, which occurs in many developing countries, results in an inability to synthesize T 3 and T 4 hormones. The thyroid gland enlarges in a condition called goiter , which is caused by overproduction of TSH without the formation of thyroid hormone. Thyroglobulin is contained in a fluid called colloid, and TSH stimulation results in higher levels of colloid accumulation in the thyroid.

In the absence of iodine, this is not converted to thyroid hormone, and colloid begins to accumulate more and more in the thyroid gland, leading to goiter. Disorders can arise from both the underproduction and overproduction of thyroid hormones. Hypothyroidism , underproduction of the thyroid hormones, can cause a low metabolic rate leading to weight gain, sensitivity to cold, and reduced mental activity, among other symptoms.

In children, hypothyroidism can cause cretinism, which can lead to mental retardation and growth defects. Hyperthyroidism , the overproduction of thyroid hormones, can lead to an increased metabolic rate and its effects: weight loss, excess heat production, sweating, and an increased heart rate.

Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive.

If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms can result. Blood calcium levels are regulated by parathyroid hormone PTH , which is produced by the parathyroid glands, as illustrated in Figure PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium.

PTH release is inhibited by rising blood calcium levels. Hyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany severe sustained muscle contraction.

The hormone calcitonin , which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity.

The intrarenal actions of ANGII include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles which increases tubular reabsorption by altering peritubular capillary physical forces. The constrictor action of ANGII on efferent arterioles also plays an important role in stabilizing GFR and therefore in preventing fluctuations in excretion of metabolic waste products that depend upon a high GFR for excretion.

ANGII is known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-known to stimulate proximal reabsorption, but the effects on more distal tubular segments have not been completely elucidated. The primary extra-renal effect of ANGII which influences sodium excretion is stimulation of aldosterone secretion.

In the absense of antidiuretic hormone, the collecting ducts are virtually impermiable to water, and it flows out as urine. The principal action of ADH is to regulate the amount of water excreted by the kidneys.

As ADH which is also known as vasopressin causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine.

ADH then acts primarily in the kidneys to increase water reabsorption, thus returning the osmolarity to baseline. The posterior lobe produces two hormones, vasopressin and oxytocin. These hormones are released when the hypothalamus sends messages to the pituitary gland through nerve cells. Vasopressin is also known as antidiuretic hormone ADH.

Antidiuretic hormone is a substance that regulates water balance in the body by controlling water loss in the urine. The adrenal medulla, the inner part of an adrenal gland, controls hormones that initiate the flight or fight response. The main hormones secreted by the adrenal medulla include epinephrine adrenaline and norepinephrine noradrenaline , which have similar functions.

The hormone that is responsible for facultative water reabsorption is the antidiuretic hormone ADH.