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In this article we will discuss about Role of Hormones in Osmoregulation, Excretion and Thermo Regulation.
Endocrine Control on Osmoregulation and Excretion:
In mammals, kidney is the main excretory organ. Kidney not only eliminates nitrogenous waste metabolites but also helps in osmoregulation.
1. Regulation of Water Retention:
Hormone vasopressin is secreted from neurohypophysis. The chief action of this hormone is to increase the reabsorption of water in the uriniferous tubule. It acts directly on distal convoluted tubule and the collecting duct. This is called antidiuretic effect and the hormone is also called as ADH (antidiuretic hormone).
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During fasting condition, water concentration of the body fluid is maintained by maximum reabsorption of water from the renal tubule. Loss of water in the body fluid stimulates osmotically sensitive neurons with cell bodies located in the hypothalamus. The hypothalamic neurosecretory cells send impulses to the neurohypophysis. Neurohypophysis then secretes ADH into the blood stream.
Increased level of ADH directly increases the permeability of distal convoluted tubules and collecting duct and water is maximally reabsorbed. This results in the excretion of more concentrated urine. The reabsorbed water then maintains the water balance of the body fluid. Dilution of body fluid inhibits the ADH secretion.
In human, the ingestion of ethyl alcohol inhibits the release of ADH and as a result leads to copious urination. Some degree of dehydration results and this contributes to the uncomfortable feeling of a “hangover”. In desert mammals, due to scarcity of water, ADH is continuously secreted for maximum reabsorption of water; hence urine is highly concentrated in nature. For instance in kangaroo rat, the neural lobe is relatively larger than laboratory rat and contains more ADH per microgram of tissue.
Administration of ADH (vasopressin) in laboratory rat quickly reduces the urine flow, because of reabsorption of water maximally from the glomerular filtrate (Fig. 11.1).
2. Aldosterone-Renin-Angiotensin System:
This system stimulates Na+ reabsorption. The juxtaglomerular apparatus secretes a hormone Renin, into the blood in response to fall of NaCI in extracellular fluid (ECF) blood. Renin then acts on a glycoprotein molecule that is manufactured in the liver and is present in the plasma as angiotensinogen (α-2-globulin).
Renin cleaves a leucin-leucin bond in globulin molecule, releasing a decapeptide, angiotensin I. Angiotensin converting enzyme (ACE) then removes two additional amino acids to form octapeptide angiotensin II. Angiotensin II primarily stimulates adrenal cortex for secretion of aldosterone which has a powerful stimulating effect on the Na+-K+ ATPase carriers into the basolateral membranes of the distal and collecting tubular cells.
The net result is a greater passive influx of Na+ into the tubular cells from the lumen and increased active pumping of Na+ out of the cells into the plasma i.e. an increase in Na+ reabsorption, with CI– following passively and H2O following by osmosis.
The renin angiotensin aldosterone system thus promotes salt retention resulting in H2O retention and elevation of arterial blood pressure. The opposite situation exists when Na+ load, ECF and plasma volume and arterial blood pressure are above normal. Under these circumstances, renin secretion is inhibited (Fig. 11.2).
Endocrine Control on Thermoregulation:
In mammals, endocrine system is intimately related with the thermoregulation. The endocrine glands like hypothalamus, pituitary, thyroid, and adrenal gland release specific hormones that generally, increase the cellular metabolism thereby increasing metabolic heat gain ultimately elevating body temperature (Fig. 11.3).
At cellular level the endocrine principles exert following actions:
(1) Increased oxygen consumption thereby accelerating oxidative metabolic routes employed in synthesis and thermogenesis.
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(2) Increased synthesis of different enzymes involved in the oxidative metabolism.
(3) Direct actions on muscles which undergo spontaneous contractions generating heat.
Thus, hormonal principles from different endocrine sources influence the process of thermogenesis ultimately aiding in adaptations to lowered environmental temperatures.
1. Role of Hypothalamus:
It has been found that anterior region of the hypothalamus contains the neurons responsible for reactions to warmth whereas the posterior region of it contains the neurons that respond to cold. Thus hypothalamus is the site of set point of temperature.
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Regarding thermogenesis, hypothalamus stimulates the pituitary, which in-turn stimulates adrenal, thyroid and pancreas for oxidative metabolism. For thermolysis, in mammals sweating and panting take place by the activation of hypothalamus. Sweating is under the control of hypothalamic thermostats responding to the changes in the core temperature. The thermostat may detect the temperature changes as conveyed to it by receptors on the skin.
The secretory activities of sweat glands with subsequent dilations on constriction are controlled by parasympathetic system u’ rough cholinergic nerves which are ultimately controlled by hypothalamic thermostats. Like sweating, panting mechanism regulates heat loss by the influence of hypothalamus (Fig. 11.4).
2. Role of Thyroid:
Thyroxine takes part in regulation of normal body temperature. Less thyroxine secretion increases susceptibility to moderate cold. The calorigenic effect of thyroxine is due to its direct effect on the cells. Thyroxine may cause catabolism of depot fat. The oxidative catabolism may lead to the formation of glucose by the process of gluconeogenesis and also there will be more production of heat. Hence thyroid hormones known as thermo genic hormone.
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Experimentally in thyroid ectomised rats, the temperature drops down. After artificial administration of thyroxine to this rat, body temperature becomes elevated and increases the BMR. Rhythmic control of body temperature takes place by negative feedback mechanism of thyroid hormone.
Cold climatic condition stimulates hypothalamus through CNS for secretion of TSH-RH which in turn stimulates adenohypophysis for secretion of TSH. TSH stimulates thyroid gland for secretion T3 and T4. Thyroid hormones regulate the number of active Na+-K+-ATPase pump to generate body heat (Fig. 11.5).
3. Role of Adrenal Medulla:
Epinephrine is calorigenic and heat production is immediate but comes to normal level quickly. It increases oxygen consumption and basal metabolic rate when given in moderate amounts; large doses may produce the opposite effect. Cold adapted rats have an increased ability to produce heat by means other than muscular contraction.
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Epinephrine stimulates liver glycogenolysis and may cause elevation of body temperature. Thermogenesis is also affected by gluconeogenesis. Both epinephrine and norepinephrine activate lipase in adipose tissue and increase the formation FFA (Free fatty acids) in the blood after breakdown of triglycerides. This oxidative metabolism of fat is calorigenic.