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Diuretics are drugs which block renal ionic transport, causing diuresis {an increase in urine . Pharmacological blockade of sodium and chloride co- transporter.
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In the years since Homer Smith did his pioneering work in renal physiology, interest in the kidney has grown steadily and robustly. That this wondrously designed machine-in addition to its filtering, secreting, and reabsorptive functions-can serve While we have attempted to provid Du kanske gillar. Lifespan David Sinclair Inbunden. Renal Pharmacology av Manuel Martinez-Maldonado.

Spara som favorit. Skickas inom vardagar. Laddas ned direkt. Frequently attempts to design experiments utilizing the methodology de- scribed in articles in trade journals can be frustrating. Description of procedures, because of space constraints, are not always complete. Blood flow through the kidney goes from the renal artery into smaller arteries until it reaches the afferent arteriole Figure The afferent arteriole becomes the glomerular capillaries where glomerular filtration occurs then the efferent arterioles.

The efferent arterioles carry blood into the peritubular capillaries, which surround the renal tubules and is where the majority of the glomerular filtrate water, electrolytes, glucose, etc. Formation of urine starts in the glomerulus, where a portion of plasma water is filtered through fenestrated glomerular capillary endothelial cells, a basement membrane, and, finally, filtration slit diaphragms formed by the visceral epithelial cells that cover the basement membrane on its urinary space side. Small solutes e. The primary constituent of the glomerular capillary colloid osmotic pressure is albumin in the plasma and there is little colloidal osmotic pressure in normal urine produced by healthy glomeruli.

The colloid osmotic pressure in the plasma is higher than the glomerular filtrate, resulting in an opposing force to filtration. The net filtration pressure Figure Changes in glomerular capillary hydrostatic pressure e. Animals with hyperglycemia e. In the nephron bicarbonate combines with a hydrogen ion to produce carbonic acid. Carbonic acid is converted to water and carbon dioxide by CA and carbon dioxide freely diffuses into the PCT cell.

Carbon dioxide in the PCT cell then combines with water to form carbonic acid, catalyzed by CA, and the carbonic acid dissociates into bicarbonate and a hydrogen ion effectively transporting bicarbonate from the nephron into the PCT cell. Bicarbonate is then cotransported with sodium to the interstitial fluid where it can diffuse into the peritubular capillaries.

Carbonic anhydrase inhibitors e. The Loop of Henle consists of a thick descending loop, thin descending loop, thin ascending loop, and thick ascending loop. Water pores aquaporins are present in the thin descending loop that allow water to osmotically move out of the nephron into the interstitial space, which is hyperosmolar up to four times osmolarity as the original nephron contents. The thick ascending loop is impermeable to water. The thick ascending limb of the loop of Henle is of particular importance since this is the site of action of the most effective diuretic drugs i.

The thick ascending loop connects with the distal convoluted tubule to make a critical contact with the afferent arteriole through a cluster of specialized epithelial cells, referred to as the macula densa, which monitors the sodium and tubular flow rates and is discussed in more detail in Section Renin—Angiotensin—Aldosterone System Figure Water, sodium, chloride, bicarbonate, and calcium are reabsorbed in the DCT.

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Spironolactone, an aldosterone antagonist, is a diuretic that exerts its effects in the DCT and the collecting duct. The collecting duct produces the final effects on urine volume based on plasma osmolarity.

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More water is reabsorbed if the plasma osmolarity is high e. Two main cell types are present in the collecting duct, the principal cells and intercalated cells. The principal cells possess channels for the recovery or loss of sodium and potassium and the intercalated cells secrete or absorb acid and bicarbonate.

Antihypertensives: Diuretics

Intercalated cells are important factors in regulating urine and plasma pH through absorption of bicarbonate and excretion of hydrogen ions. Antidiuretic hormone ADH, arginine vasopressin, or specifically in swine lysine vasopressin is released from the posterior pituitary gland when plasma osmolarity increases with an effect of increasing water reabsorption in the collecting duct through aquaporins water channels.

Antidiuretic hormone stimulates aquaporin channels to be inserted on the apical side tubular side of the principal cells, resulting in water movement from the nephron into the principal cells due to an osmotic gradient. Different aquaporin channels on the basolateral cell membrane allow water movement from the cell into the interstitial space by osmotic movement.

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The water than diffuses into the peritubular capillaries and reenters the circulation. Alcohol ethanol consumption decreases ADH resulting in a diuretic effect, which is observed in animals treated for ethylene glycol toxicity. Water passively follows sodium, resulting in a net increased reabsorption of sodium and water and net excretion of potassium. The macula densa is located at the junction of the thick ascending limb and distal convoluted tubule and sits between the afferent and efferent arterioles. Together with the juxtaglomerular cells, which produce renin, these components form the juxtaglomerular apparatus Figure Increased reabsorption of Na and Cl detected by the macular densa results in inhibition of renin release into the efferent arteriole by the juxtaglomerular cells through activation of adenosine A 1 receptors.

Conversely, decreased reabsorption of Na and Cl detected by the macular densa stimulates renin release into the efferent arterial through prostaglandins PGE 2 , PGI 2.


Renin release is also enhanced when low blood pressure is detected by intrarenal baroreceptors, triggering the release of prostaglandins PGE 2 , PGI 2. Renin release from the juxtaglomerular cells results in a cascade of events known as the renin—angiotensin—aldosterone system RAAS Figure Renin converts angiotensinogen, which is released from the liver, to angiotensin I ATI.

Angiotensin II is a vasoconstrictor, which binds to AT receptors in the vasculature resulting in increased vascular tone and increased blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, which enhances sodium and subsequently water reabsorption in the distal convoluted tubule and collecting ducts, increasing circulating blood volume and blood pressure.

ATII increases vascular tone by multiple mechanisms. Peripheral sympathetic neurotransmission is enhanced by ATII, resulting in increased release of norepinephrine from nerve terminals. Centrally mediated enhanced sympathetic outflow is also stimulated by ATII.

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ATII also stimulates catecholamine release from the adrenal medulla. ATII has affects on renal function. The vasoconstriction induced by ATII in most cases decreases GFR by affecting the afferent arteriole greater than the efferent arterial.

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However, during renal hypotension ATII affects the efferent arterial to a greater extent than the afferent, resulting in increased GFR. Administration of ACE inhibitors during renal hypotension increases the risk of acute renal failure. Increased cardiac afterload, due to increased vascular tone, and increased preload, due to aldosterone-mediated sodium and water retention, contribute to cardiac remodeling and hypertrophy. Direct effects of ATII on cardiac myocytes, vascular smooth muscle, and fibroblasts also result in cardiac hypertrophy and remodeling and vascular remodeling resulting in increased vascular wall thickness and decreased vascular compliance.

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Renin release is modulated by feedback inhibition. Angiotensin II stimulates AT receptors on the juxtaglomerular cells decreasing the release of renin and is known as the short negative feedback loop. Increases in afferent arterial pressures decrease renin release and is termed the long loop negative feedback. The RAAS is classically described as an endocrine system response as described above in this section, but locally active and alternative pathways for angiotensin synthesis are present. Addition tissues brain, vasculature, heart, adrenal glands, etc.

The kidneys are innervated by the sympathetic nervous system. Osmoreceptors are specialized cells in the hypothalamus that are sensitive to changes in blood osmolarity primarily influenced by sodium ion concentration. If blood osmolarity increases, typically due to sodium ingestion or water deprivation , ADH is released from the posterior pituitary with its primary effects on the collecting duct cells to increase water reabsorption from the tubular fluid by inserting aquaporins on the apical lumen side of the cells.

ADH release is controlled by a negative feedback loop in which low blood osmolarity detected by the osmoreceptors inhibits the release of ADH. Diabetes insipidus is a disease characterized by insufficient production of ADH, resulting in blood hyperosmolarity. Ethanol, which is used in the management of ethylene glycol toxicity, inhibits the release of ADH, which can cause diuresis.

ADH is also known as vasopressin as high concentrations result in vasoconstriction. Both COX isoforms are constitutively expressed in the kidneys, but COX2 expression can be induced to produce substantial local effects within the kidneys during periods of hypotension or decreased blood flow. Eicosanoids, products of COX, can exert prominent roles in renal physiology during certain conditions including hypotension cardiac disease, vasodilation , hypovolemia dehydration, hemorrhage , and hyponatremia. The eicosanoids can produce afferent arteriole vasodilation PGE 2 , PGI 2 locally antagonizing the effects of systemic vasoconstriction such as sympathetic stimulation, ATII, and vasopressin.

Prostaglandins PGE 2 , PGI2 also produce local vasodilation to maintain medullary blood flow during states of systemic vasoconstriction. Therefore it is not surprising that COX inhibitors can have profound renal effects, with renal adverse effects of nonsteroidal antiinflammatory drugs being the second most common organ system affected with adverse effects.