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Blood pressure vasopressin

Logically, ADH receptor antagonists, and ADH synthesis and release inhibitors can be effective aquaretics. ADH, 8-arginine vasopressin [113-79-17, is synthesized in the hypothalamus of the brain, and is transported through the supraopticohypophyseal tract to the posterior pituitary where it is stored. Upon sensing an increase of plasma osmolaUty by brain osmoreceptors or a decrease of blood volume or blood pressure detected by the baroreceptors and volume receptors, ADH is released into the blood circulation it activates vasopressin receptors in blood vessels to raise blood pressure, and vasopressin V2 receptors of the nephrons of the kidney to retain water and electrolytes to expand the blood volume. [Pg.211]

Before administering die first dose of vasopressin for die management of diabetes insipidus, die nurse takes die patient s blood pressure, pulse, and respiratory rate. The nurse weighs the patient to obtain a baseline weight for future comparison. Serum electrolyte levels and odier laboratory tests may be ordered by die primary health care provider. [Pg.519]

Before administering vasopressin to relieve abdominal distention, the nurse takes the patient s blood pressure pulse, and respiratory rate. The nurse auscultates the abdomen and records the finding. The nurse measures and records the patient s abdominal girth. [Pg.519]

Vasopressin levels are increased during hypotension to maintain blood pressure by vasoconstriction. However, there is a vasopressin deficiency in septic shock. Low doses of vasopressin increase MAP, leading to the discontinuation of vasopressors. However, routine use of vasopressin is not recommended because of lack of evidence of efficacy. Vasopressin is a direct vasoconstrictor without inotropic or chronotropic effects and may result in decreased cardiac output and hepatosplanchnic flow. Vasopressin use may be considered in patients with refractory shock despite adequate fluid resuscitation and high-dose vasopressors.24,27-28... [Pg.1194]

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). [Pg.99]

Vasopressin (antidiuretic hormone) is a peptide synthesized in the hypothalamus and secreted from the neurohypophysis of the pituitary gland. This substance plays an important role in the long-term regulation of blood pressure through its action on the kidney to increase reabsorption of water. The major stimulus for release of vasopressin is an increase in plasma osmolarity. The resulting reabsorption of water dilutes the plasma toward its normal value of 290 mOsM. This activity is discussed in more detail in Chapter 10 (the endocrine system) and Chapter 19 (the renal system). [Pg.209]

Vasopressin also plays an important role in short-term regulation of blood pressure through its action on vascular smooth muscle. This hormone is the most potent known endogenous vasoconstrictor. Two types of vasopressin receptors have been identified V, receptors mediate vasoconstriction... [Pg.209]

Vasopressin is a potent vasoconstrictor that increases blood pressure and systemic vascular resistance. It may have several advantages over epinephrine. First, the metabolic acidosis that frequently accompanies cardiopulmonary arrest can blunt the vasoconstrictive effect of epinephrine this does not occur with vasopressin. Second, stimulation of P receptors by epinephrine can increase myocardial oxygen demand and complicate the postresuscitative phase of CPR. Vasopressin can also have a beneficial effect on renal blood flow in the kidney, causing vasodilation and increased water reabsorption. [Pg.92]

Vasopressin plays a major role in the control of blood pressure, which is probably essential for vasocongestion or erection. cOxytocin gene expression occurs in ovary and testes, but the exact functions remain unknown. dProgestins, such as cyproterone acetate, are used clinically as anti-androgens (Kravitz, et ah, 1995). [Pg.147]

Posterior pituitary Two hormones, vasopressin and oxytocin, are synthesised in the hypothalamus and then transported through nerve axons to the posterior pituitary, where they are stored until released. Vasopressin acts on the kidney to conserve water. Its secretion is stimulated by thirst and a decrease in blood pressure. Secretion of oxytocin initiates uterine contraction for parturition. It also stimulates milk ejection from the mammary glands. [Pg.254]

ADH, a nonapeptide, released from the posterior pituitary gland promotes re-absorption of water in the kidney. This response is mediated by vasopressin receptors of the V2 subtype. ADH enhances the permeability of collecting duct epithelium for water (but not for electrolytes). As a result, water is drawn from urine into the hyperosmolar inter-stitium of the medulla. Nicotine augments (p. 110) and ethanol decreases ADH release. At concentrations above those required for antidiuresis, ADH stimulates smooth musculature, including that of blood vessels ( vasopressin ). The latter response is mediated by receptors of the Vi subtype. Blood pressure rises coronary vasoconstriction can precipitate angina pectoris. Lypres-sin (8-L-lysine vasopressin) acts like ADH. Other derivatives may display only one of the two actions. [Pg.164]

Vasopressin occurs in two variations arginine-vasopressin (AVP) and lysine-vasopressin (LVP), in which Arg is replaced by Lys. The conformation of these hormones is almost identical to that of oxytocin, except that the terminal tail is con-formationally free and not held by the ring. The physiological role of the vasopressins is the regulation of water reabsorption in the renal tubules (i.e., an antidiuretic action). In high doses, they promote the contraction of arterioles and capillaries and an increase in blood pressure hence the name of these hormones. Because of their very similar structures, OT and VP overlap in a number of effects. [Pg.348]

ADH in larger dose increases the blood pressure by direct stimulation of vascular smooth muscle. It also stimulates the smooth muscle of gastrointestinal tract and increase the peristalsis. It is inactive orally because it is destroyed by trypsin. It can be administered by any parenteral route or by nasal spray. Vasopressin is indicated in diabetes insipidus and in treatment of postoperative abdominal varices. [Pg.210]

Unlike isoflurane, desflurane may stimulate the sympathetic nervous system at concentrations above 1 MAC. Sudden and unexpected increases in arterial blood pressure and heart rate have been reported in some patients, accompanied by increases in plasma catecholamine and vasopressin concentrations and increased plasma renin activity. These pressor effects may increase morbidity or mortality in susceptible patients. The mechanism of sympathetic activation is unclear but does not appear to be baroreceptor-mediated. Clonidine, esmolol, fentanyl and propofol partially block the response but lignocaine (lignocaine) is ineffective. [Pg.62]

In addition to its central effects on blood pressure, Ang II acts on the central nervous system to stimulate drinking (dipsogenic effect) and increase the secretion of vasopressin and adrenocorticotropic hormone (ACTH). The physiologic significance of the effects of Ang II on drinking and pituitary hormone secretion is not known. [Pg.377]

Vasopressin also plays an important role in the short-term regulation of arterial pressure by its vasoconstrictor action. It increases total peripheral resistance when infused in doses less than those required to produce maximum urine concentration. Such doses do not normally increase arterial pressure because the vasopressor activity of the peptide is buffered by a reflex decrease in cardiac output. When the influence of this reflex is removed, eg, in shock, pressor sensitivity to vasopressin is greatly increased. Pressor sensitivity to vasopressin is also enhanced in patients with idiopathic orthostatic hypotension. Higher doses of vasopressin increase blood pressure even when baroreceptor reflexes are intact. [Pg.382]

Administration of ANP produces prompt and marked increases in sodium excretion and urine flow. Glomerular filtration rate increases, with little or no change in renal blood flow, so that the filtration fraction increases. The ANP-induced natriuresis is due to both the increase in glomerular filtration rate and a decrease in proximal tubular sodium reabsorption. ANP also inhibits the secretion of renin, aldosterone, and vasopressin these changes may also increase sodium and water excretion. Finally, ANP causes vasodilation and decreases arterial blood pressure. Suppression of ANP production or blockade of its action impairs the natriuretic response to volume expansion, and increases blood pressure. [Pg.384]

Vasopressin and oxytocin are peptide hormones secreted from the posterior lobe of the pituitary gland. They function primarily to raise blood pressure (vasopressin), as antidiuretic (vasopressin), and to promote contraction of uterus and lactation muscies (oxytocin). The isolation, identification, and synthesis of these hormones was accomplished by Vincent du Vigneaud, for which he was awarded the Nobel Prize in chemistry in 1955. [Pg.1243]

Scheurer MA, Bradley SM, Atz AM. Vasopressin to attenuate pulmonary hypertension and improve systemic blood pressure after correction of obstructed total anomalous pulmonary venous return. J Thorac Cardiovasc Surg 2005 129 464-6. [Pg.523]

The vasopressor antagonists have been particularly useful in revealing the important role that vasopressin plays in blood pressure regulation in situations such as dehydration and hemorrhage. They have potential for the treatment of hypertension and heart failure. [Pg.422]

Vasopressin is a peptide hormone released by the posterior pituitary in response to rising plasma tonicity or falling blood pressure. Vasopressin possesses antidiuretic and vasopressor properties. A deficiency of this hormone results in diabetes insipidus (see Chapters 15 and 17). [Pg.876]


See other pages where Blood pressure vasopressin is mentioned: [Pg.547]    [Pg.547]    [Pg.418]    [Pg.187]    [Pg.528]    [Pg.132]    [Pg.149]    [Pg.274]    [Pg.1068]    [Pg.348]    [Pg.37]    [Pg.326]    [Pg.33]    [Pg.330]    [Pg.389]    [Pg.371]    [Pg.372]    [Pg.223]    [Pg.383]    [Pg.891]    [Pg.1261]    [Pg.288]    [Pg.416]    [Pg.371]    [Pg.228]    [Pg.424]    [Pg.219]   
See also in sourсe #XX -- [ Pg.670 ]




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