course hero: what is the action of urodilatin?

Full Answer

What is URO in natriuresis?

Chemical compound. Urodilatin (URO) is a hormone that causes natriuresis by increasing renal blood flow. It is secreted in response to increased mean arterial pressure and increased blood volume from the cells of the distal tubule and collecting duct.

Which organ produces its own natriuretic peptide?

The kidneys produce their own natriuretic 32-residue peptide. Urodilatin renal natriuretic peptide potency equals or exceeds that of Atriopeptin [ANP- (99-126)], the prototype of cardiodilatin. Atriopeptin is only of trivial importance in the regulation of sodium excretion during normal living conditions.

Does urodilatin cause diuresis?

When administered intravenously, urodilatin induces strong diuresis and natriuresis with tolerable hemodynamic side effects. Urodilatin is localized in the kidney, differentially processed (involved in the regulation of body fluid volume and water-electrolyte excretion, while circulating), and secreted into the urine.

Is urodilatin a natriuretic hormone?

Urodilatin (CDD/ ANP-95-126) is a homologue natriuretic peptide that differs from CDD/ANP-99-126, which is excreted into the circulation via exocytosis. The prototype of the natriuretic hormones is cardiodilatin / atrial natriuretic peptide (CDD/ANP).

Does urodilatin affect atriopeptin?

Urodilatin is little affected by renal enzymes that inactivate atriopeptin, as the kidney elutes with urodilatin rather than with ANP. The degradation rates of ( 125I )-urodilatin and [125I]-ANP by pure recombinant NEP (rNEP) were compared.

Which hormone stimulates renal hydroxylation?

Parathyroid hormone stimulates renal hydroxylation in the process of producing vitamin D. The first step occurs in the liver with hydroxylation at the 25th carbon (calcifediol); the second step in hydroxylation occurs at the first carbon position in the kidneys. (1334)

Which cells are responsible for controlling renal blood flow, glomerular filtration, and renin secretion?

Control of renal blood flow, glomerular filtration, and renin secretion occur at the JGA. Together, the juxtaglomerular cells and macula densa cells form the JGA. The control of renal blood flow, glomerular filtration, and renin secretion is not directed by any of the other options. (1322)

What hormones are produced when the heart dilates?

Natriuretic peptides inhibit renin and aldosterone during heart failure when the heart dilates. These make up a group of peptide hormones, including atrial natriuretic peptide (ANP), secreted from myocardial cells in the atria and brain natriuretic peptide (BNP) secreted from myocardial cells in the cardiac ventricles. When the heart dilates during volume expansion or heart failure, ANP and BNP inhibit sodium and water absorption by kidney tubules, inhibit the secretion of renin and aldosterone, vasodilate the afferent arterioles, and constrict the efferent arterioles. The result is increased urine formation, leading to decreased blood volume and blood pressure. (1327)

What hormone is required for water to be reabsorbed in the distal tubule and collecting duct?

Antidiuretic hormone is required for water to be reabsorbed in the distal tubule and collecting duct. The later, straight segment of the distal tubule and the collecting duct are permeable to water as controlled by antidiuretic hormone. The other options are not involved in this process. (1331)

What is the functional unit of the kidney?

The nephron is the functional unit of the kidney. Although the other options are also located in the kidney, they are not its functional units. (1320)

What causes arteriolar vasoconstriction?

The blood vessels of the kidney are innervated by the sympathetic noradrenergic fibers that cause arteriolar vasoconstriction and reduce renal blood flow. The other options are not involved in this process. (1326)

Which organ contains all the glomeruli and portions of the tubules of the kidneys?

The cortex contains all the glomeruli and portions of the tubules of the kidneys. Although the other options are also located in the kidney, they do not contain the glomeruli. (1320)

What is ularitide used for?

Ularitide is a synthetic form of urodilatin, a natriuretic peptide, which is produced in the distal renal tubules. Ularitide binds to natriuretic peptide receptors located on medullary collecting duct cells and vascular smooth muscle cells, which leads to increased diuresis, natriuresis, and arterial and venous vasodilation.18 Clinically, ularitide has been shown to induce natriuresis and, at the same time, decrease plasma concentrations of renin, aldosterone, and angiotensin II, contrary to findings with conventional diuretics. 19,20 In the Safety and Efficacy of an Intravenous Placebo-Controlled Randomised Infusion of Ularitide II (SIRIUS II) trial, 221 patients with ADHF were randomly assigned to receive one of three doses of ularitide or placebo, in addition to baseline loop and thiazide diuretics. Subjects treated with ularitide exhibited an improvement in dyspnea and hemodynamic parameters (decrease in pulmonary capillary wedge pressure, reduction in systemic vascular resistance, decrease in right atrial pressure, and increase in cardiac index without significant change in heart rate). No difference in urine output was noted between subjects treated with ularitide and those given placebo, which suggests that the predominant mechanism for the hemodynamic changes is vasodilation. A trend toward improved rates of 30-day mortality was noted in the ularitide recipients. The most common side effect of ularitide was hypotension, which was most prominent with the highest dose. No significant worsening of renal function was noted. 21 The Ularitide Global Evaluation in Acute Decompensated Heart Failure (URGENT) trial, a prospective, randomized, placebo-controlled trial, is in the planning phases and is directed toward evaluating the effect of ularitide in 3000 patients with ADHF on dyspnea, safety, and morbidity and mortality both during and after hospitalization.

Which peptides bind to NPR-A?

Natriuretic peptides activate guanylyl cyclase–coupled natriuretic peptide receptors (NPR) ( Endlich and Steinhausen, 1997). ANP, BNP, and urodilatin bind NPR-A with similar affinities greatly exceeding that of C-type natriuretic peptide (CNP). Conversely, CNP has far greater affinity for NPR-B than do the other ligands. NPR-C binds all four peptides with similar affinity (Endlich and Steinhausen, 1997 ). NPR-C, which lacks guanylyl cyclase, may mediate proximal tubular endocytosis of ANP and BNP to initiate their degradation.

What are the effects of natriuretic peptides?

The effects of an acute administration of these peptides include a reduction of arterial blood pressure and an increase in renal NaCl excretion. The effects of natriuretic peptides are mediated by at least two membrane-bound receptors (NPRA, NPRB) that are linked to guanylate cyclase, and a so-called clearance receptor (NPRC) without guanylate cyclase activity.

What is the ligand for NPR-A?

Both ANP and BNP (as well as DNP and URO) are ligands for the natriuretic peptide receptor-A (NPR-A) ( Figure 20.2 ), which is a member of the transmembrane guanylyl cyclase family and is widely distributed in the myocardium and other organ systems ( Garbers et al., 2006 ). Based on competition binding experiments, Singh et al. (2006) reported the following rank order of potency for NPR-A: DNP > BNP ∼ ANP ≫ CNP in a study that used a radioiodinated analog of DNP to evaluate the selectivity of DNP for NPR-A in the human myocardium. The ligand–receptor interactions result in activation of cyclic guanosine monophosphate (cGMP), which generates multiple important biological effects, including vasorelaxation, natriuresis, inhibition of renin and aldosterone, lusitropism, cytoprotection, anti-fibrosis, anti-hypertrophy, anti-apoptosis and anti-inflammation ( Figure 20.2) ( Furuya et al., 1991; Rautureau and Baxter, 2004; Chen et al., 2005; Lee and Burnett, 2007 ). In addition, the NPs have been demonstrated to be involved in the control of lipolysis in human adipose tissue ( Sengenes et al., 2000 ).

Does urodilatin have vasodilation?

Vasodilation#N#Urodilatin has vasodilatory effects similar to those of ANP.30 9,315 This would be expected, since the ANP prohormone post-translational processing in the kidney results in an additional four a.a. from kaliuretic peptide being added to the N-terminus of ANP (proANP 95–126, urodilatin) 205,240,315 ( Figure 37.2 ). The rest of the amino acids in urodilatin are identical, and in the same sequence as those in ANP ( Figure 37.2 ). Urodilatin and ANP have identical ring structures formed with cysteine-to-cysteine bonding ( Figure 37.2 ). The four a.a. added to form urodilatin are the same four a.a. present in the C-terminus of kaliuretic peptide in other tissues, but in the kidney the ANP prohormone is cleaved between a.a. 94 and 95 rather than between a.a. 98 and 99 to form urodilatin. 315 Urodilatin is not formed in the heart or in other tissues except the kidney. 205 Urodilatin at first was thought not to be a hormone, in that it was thought that it did not circulate, 315 but sensitive assays revealed that it circulates at very low concentrations (9–12 pg/ml). 392 Infusion of ANP increases the circulating concentration of urodilatin, suggesting that some ANP effects may be mediated by urodilatin. 392 Infusion of long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide, on the other hand, do not affect the circulating concentration of urodilatin in healthy humans. 392

Which hormone controls the final urine concentration?

Urea. Antidiuretic hormone controls final urine concentration. It is secreted from the posterior pituitary and increases water permeability in the last segment of the distal tubule. Renin stimulates the renin-angiotensin-aldosterone system, which can increase systemic arterial pressure and change renal blood flow.

Which hormone is converted to angiotensin II?

Renin forms angiotensin I that is converted to angiotensin II, which stimulates the secretion of aldosterone.

What is the process of reabsorption of fluids and solutes from the tubular lumen to the?

Tubular reabsorption is the movement of fluids and solute from the tubular lumen to the peritubular capillary plasma. Ultrafiltration is the process of filtration across the glomerular capillaries to form a filtrate of protein-free plasma.

When is renin released?

Primarily, renin is released when a person experiences hypotension, which starts a cascade of events that leads to the release of the angiotensins. The movement of fluids and solute from the tubular lumen to the peritubular capillary plasma is called: Ultrafiltration. Tubular reabsorption .

What is the specific gravity of urine?

The pH is generally 5 to 6.5, the urine is light yellow, the specific gravity is 1.016 to 1.022, and no white or red blood cells are present.

What is tubular secretion?

Tubular secretion refers to substances moving from the plasma of the capillary to the tubular lumen.

How much blood does the kidneys receive per minute?

The kidneys receive 1000 to 1200 ml of blood per minute.