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Kidney Renin-angiotensin system

PEPTIDE HORMONES OF THE KIDNEY (RENIN-ANGIOTENSIN SYSTEM)... [Pg.371]

Regardless of the etiology, fall in blood pressure (BP) is compensated by an increase in sympathetic outflow, activation of the renin-angiotensin system, and other humoral factors that stimulate peripheral vasoconstriction. Compensatory vasoconstriction redistributes blood away from the skin, skeletal muscles, kidneys, and GI tract toward vital organs (e.g., heart, brain) in an attempt to maintain oxygenation, nutrition, and organ function. [Pg.156]

The development of ascites is related to systemic arterial vasodilation that leads to the activation of the baroreceptors in the kidney and an activation of the renin-angiotensin system, with sodium and water retention and vasoconstrictor production. [Pg.252]

The activity of the renin-angiotensin system is reduced with age (Muhlberg and Platt 1999). The ability of the kidney to concentrate urine maximally after water deprivation decreases with age, as does the ability to excrete a water and salt load, particularly during the night. Nocturnal polyuria is common in the elderly (Lubran 1995). Diuretics are commonly used in the elderly. There is an increased risk for hypokalemia and hyponatremia from diuretics in the elderly (Passare et al. 2004). Electrolyte disturbances may also be caused by several types of drugs in the elderly and it is important to monitor serum electrolyte levels in the elderly. Treatment with... [Pg.15]

In addition, there is now good evidence indicating that methyldopa effectively suppresses the release of renin by the kidney(23,24). This effect may contribute to the antihypertensive efficacy of the drug in some hypertensive states in which the renin-angiotensin system plays a pathophysiologic role. Thus, it may be concluded that a) methyldopa lowers the blood pressure... [Pg.86]

Structure and physiology of the kidney glomerular filtration tubular activity selective reabsorption and secretion, often using specific carrier mechanisms carbonic anhydrase and acid-base balance. The kidney also produces, and is sensitive to, hormones actions of the hormones ADH, aldosterone and PTH the kidney as a secretory organ erythropoietin, the renin-angiotensin system vitamin D3. [Pg.261]

Angiotensin II, the primary end product of the renin-angiotensin system, acts on the juxtaglomerular cells to inhibit the release of renin this process is therefore a negative feedback mechanism. The half-life of renin in the circulation is 10 to 30 minutes, with inactivation occurring primarily in the liver. Small amounts of renin are eliminated by the kidneys. Pure human renin... [Pg.207]

Natriuretic peptides are naturally occurring substances in the body that oppose the activity of the renin-angiotensin system. The natriuretic peptide family consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). All three natriuretic peptides are synthesized from cleavage of a larger precursor polypeptide. In the ventricles and brain, the synthesis of BNP predominates ANP is synthesized by cardiac myocytes predominately in the atria and CNP is synthesized in the brain, blood vessels, and kidney. [Pg.215]

Ang II exerts important actions at vascular smooth muscle, adrenal cortex, kidney, heart, and brain. Through these actions, the renin-angiotensin system plays a key role in the regulation of fluid and electrolyte balance and arterial blood pressure. Excessive activity of the renin-angiotensin system can result in hypertension and disorders of fluid and electrolyte homeostasis. [Pg.376]

Peripheral vasculature and certain organs with a functional renin-angiotensin system (heart, kidneys]... [Pg.291]

The renin-angiotensin system involves several endogenous components that help regulate vascular tone in various organs and tissues.25,84,109 In systemic circulation, the renin-angiotensin system acts by a sequence of events summarized in Figure 21-2. Renin is an enzyme produced primarily in the kidneys. When blood pressure falls, renin is released from the kidneys into the systemic circulation. Angiotensinogen is a peptide that is produced by the liver and circulates... [Pg.297]

The rate at which renin is secreted by the kidney is the primary determinant of activity of the renin-angiotensin system. Renin secretion is controlled by a variety of factors, including a renal vascular receptor, the macula densa, the sympathetic nervous system, and angiotensin II. [Pg.412]

Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats. Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats.
Perlstein TS, Gumieniak O, Hopkins PN, Murphey LJ, Brown NJ, Williams GH, Hollenberg NK, Fisher ND (2004) Uric acid and the state of the intrarenal renin-angiotensin system in humans. Kidney Int 66 1465-1470... [Pg.99]


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