UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diverse biological actions of endothelins (ET) appear to be mediated by specific cell-surface receptors. Autoradiography and membrane binding studies have shown abundant ET binding sites in the kidney. However, their expression in specific types of renal cells is unclear. We studied the binding of 125I-labelled endothelin-1 in freshly isolated cell suspensions from canine inner medullary collecting duct. Competition binding experiments revealed the presence of specific high-affinity binding sites: unlabelled ET-1 and ET-2 compared with the radioligand with an IC50 of 135 and 83 pM, respectively, while the IC50 of ET-3 and big ET-1 were 2 and 4 orders of magnitude higher, indicating the presence of ETA-type receptor. Angiotensin II, vasopressin, and atrial natriuretic peptide (ANP) did not compete for ET binding even at a concentration of 10(-6) M. Saturation binding experiments showed a single class of binding sites of high density (Bmax = 56.7 +/- 10.3 fmol/10(6) cells) and high affinity (Kd = 69.8 +/- 10 pM). In contrast, ANP receptors in the same cell preparations appeared as two classes of binding sites with widely different affinity and density. The high-affinity ANP site (Kd = 311 +/- 48 pM) was compatible with ANP-B (guanylate cyclase-coupled) receptor. ET-1 did not compete for this receptor. ET-1 (10(-7) M) did not alter ANP-induced cGMP generation in these cells (3.8-fold increase at 10(-7) M ANP), nor basal levels of cGMP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific endothelin binding sites in renal medullary collecting duct cells: lack of interaction with ANP binding and cGMP signalling. 128 83

The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. Although the patients received an adequate amount of fluid (more than 4080ml/day; daily average in seventeen cases) and sodium (more than 277 mEq/day; daily average in seventeen cases), eight out of the seventeen cases showed transient hyponatremia of a slight degree beginning on 8.8 days after SAH. ANP values were elevated markedly in fifteen out of the seventeen cases, remaining high during the first two weeks following SAH. ADH values were elevated remarkably in eight out of the seventeen cases. However, these values declined immediately to a normal range within two days following SAH. PRA were increased or came within the normal range, suggesting the lack of water retention. Overall sodium balance and water balance did not differ significantly between hyponatremia cases and normonatremia ones, whereas, sodium balance in acute phase was significantly negative, associated with marked natriuresis in patients with hyponatremia. These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.
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PMID:[Pathogenesis of hyponatremia observed in the treatment of acute subarachnoid hemorrhage]. 128 91

1. A symptomatic diuresis, polyuria, sometimes accompanies paroxysmal tachycardias in man. A study was undertaken in patients with inducible supraventricular tachycardia, irrespective of the symptom of polyuria, to measure simultaneous changes in urine output and plasma hormone levels during the arrhythmia. 2. During 14 episodes of induced tachycardia in 10 patients, there was a significant increase in mean urine flow, which was independent of the state of patient hydration. During a mean tachycardia duration of 30 +/- 3 min, the mean group urine flow increased from 3.2 +/- 2.3 ml/min to 7.6 +/- 3.7 ml/min (P less than 0.001). This was characterized by a consistent increase in free water excretion and a variable increase in sodium excretion. 3. The plasma atrial natriuretic peptide level (five patients) significantly increased from 7.6 +/- 4.6 pg/ml to 34.6 +/- 21.7 pg/ml (P less than 0.02) during the arrhythmia. There was no significant change in the plasma arginine-vasopressin level and a non-significant reduction in plasma renin activity. 4. This study has shown that induced supraventricular tachycardias in man are accompanied by a significant diuresis. The mechanisms responsible remain unknown, but do not appear to involve the plasma arginine-vasopressin level alone.
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PMID:Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man. 131 Sep 15

Plasma atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), plasma renin activity (PRA), and circulatory haemodynamics were studied in five patients with chronic congestive heart failure undergoing ultrafiltration on two consecutive days. The patients were in the New York Heart Association class IV, and were considered candidates for heart transplantation. A mean of 3.3 +/- 0.5 litres of fluid was removed during each ultrafiltration. Plasma ANP concentration remained unchanged during ultrafiltration: 369 +/- 151 pg/ml at start and 316 +/- 116 pg/ml at the end, while plasma ADH concentration and PRA increased from 5.1 +/- 2.1 to 7.5 +/- 3.4 pg/ml (P less than 0.02), and 5.9 +/- 3.0 to 7.7 +/- 3.2 ng/ml (P less than 0.03) respectively (n = 10). After treatment, plasma ADH and PRA declined to baseline values within 1 h. Pulmonary artery, pulmonary capillary wedge, and right atrial pressures decreased significantly, while blood pressure and heart rate remained constant during ultrafiltration. A volume of 3.3 +/- 0.5 litres of fluid was removed, and caused an increase in colloid osmotic pressure from 22.0 +/- 3.0 to 33.7 +/- 3.9 mmHg (P less than 0.02). It was unexpected that plasma ANP concentration did not decline. Due to long-standing severe heart failure the atrial wall may have lost some of its elastic properties, resulting in less ability to adapt to reduced filling pressures. Accordingly, atrial wall stretch remained unchanged, explaining the constant ANP levels. Ultrafiltration treatment caused an increased responsiveness to diuretic therapy, and four patients survived long enough to receive heart transplants.
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PMID:Hormonal changes in patients with severe chronic congestive heart failure treated by ultrafiltration. 131 20

1. The effect of atrial natriuretic peptide on osmotically stimulated thirst appreciation and consequent fluid intake was investigated in healthy man. 2. Six seated male subjects were studied on two occasions: synthetic alpha-human atrial natriuretic peptide (99-126) (2 pmol min-1 kg-1) or placebo (saline, 150 mmol/l NaCl) was infused intravenously for 105 min; 30 min after the start of atrial natriuretic peptide/placebo infusion, hypertonic saline (855 mmol/l NaCl) was infused (0.06 ml min-1 kg-1) for 60 min. Subjects were then allowed free access to water for the next 2 h; infusion of atrial natriuretic peptide/placebo continued for the first 15 min of the drinking period. 3. The plasma atrial natriuretic peptide concentration did not alter significantly during infusion of hypertonic saline and placebo; it rose to a steady state of 12.7 +/- 1.1 pmol/l (mean +/- SEM) during the infusion of atrial natriuretic peptide and hypertonic saline, and remained at this level during the first 15 min of the drinking period. During infusion of hypertonic saline and atrial natriuretic peptide or placebo, similar increases in plasma osmolality (P less than 0.001) and plasma vasopressin concentration (P less than 0.005) occurred. During infusion of hypertonic saline and atrial natriuretic peptide or placebo, thirst increased significantly over the time course of both studies (P less than 0.01), but the effect of atrial natriuretic peptide infusion compared with placebo infusion was to significantly decrease thirst at 60 min. 4. Drinking rapidly abolished thirst and vasopressin secretion before changes in plasma osmolality occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide inhibits fluid intake in hyperosmolar subjects. 132 19

Experimental and clinical studies seem to prove that both endogenous opioids and atrial natriuretic peptide (ANP) are involved in blood pressure regulation. This raised the question, whether these two factors are functionally interrelated to each other. We tried to answer this question by assessing plasma ANP levels in 15 patients with II degrees essential hypertension and in 15 healthy subjects under water immersion (WI) conditions. In all subjects two WI tests were performed--one without pretreatment with naloxone, and a second one after blockade of opioid receptors by this opioid receptor antagonist. Parallel to ANP, plasma renin activity (PRA), aldosterone (ALD) and vasopressin (AVP) were assessed. In hypertensive patients significantly higher basal plasma ANP levels were found than in control subjects. WI induced a significant increase of plasma ANP in both examined groups which became markedly reduced after blockade of opioid receptors by naloxone. Naloxone did not influence the WI induced decrease of PRA, ALD and AVP respectively. From results presented in this study we conclude, that a.) opioid receptors seem to influence regulation of ANP secretion both in healthy normotensive subjects and patients with essential hypertension, and b.) that WI induced alterations of ANP on the one side and of PRA, ALD and AVP on the other side are not interrelated.
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PMID:Do opioid receptors participate in the regulation of atrial natriuretic peptide (ANP) secretion in hypertensive patients? 133 Mar 91

1. The renal effects of angiotensin II were investigated (a) with and without acute blockade of the effects of aldosterone and (b) with and without concomitant infusion of vasopressin. Angiotensin II (2 ng min-1 kg-1) and/or vasopressin (5 pg min-1 kg-1) was infused intravenously into conscious water-diuretic dogs and the effects were quantified by measurements of renal excretion of water, Na+ and K+, as well as determination of plasma renin activity and plasma levels of atrial natriuretic peptide and catecholamines. 2. Angiotensin II alone increased blood pressure by 7% (P < 0.05), decreased effective renal blood flow markedly and reduced urine flow and osmolar and free water clearances. Na+ and K+ excretion did not change significantly. Aldosterone blockade with canrenoate increased Na+ excretion by a factor of 10; subsequent infusion of angiotensin II decreased Na+ excretion by about 50%, the other renal effects being qualitatively similar to those seen without blockade. As expected, vasopressin also decreased diuresis and free water clearance substantially; however, the effect of combined infusion of angiotensin II and vasopressin was not compatible with the notion of additive effects of the two peptides. 3. Angiotensin II alone or in combination with vasopressin did not change the plasma concentrations of atrial natriuretic peptide, adrenaline, noradrenaline, or dopamine. Vasopressin alone exerted its antidiuretic effect without affecting plasma renin activity, plasma aldosterone concentration or renal excretion of Na+ and K+.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin and angiotensin II in the conscious dog: synergistic effects on renal excretory parameters? 133 Apr 10

Our previous studies have shown that stimulation of the anteroventral third ventricle region increases atrial natriuretic peptide (ANP) release, whereas lesions of the anteroventral third ventricle or median eminence block the release of ANP from blood volume expansion, suggesting a critical central nervous system participation in this response. ANP is also produced within neurons that have cell bodies in the rostral hypothalamus and axons that extend to the median eminence and neural lobe. In addition to its natriuretic effect, the peptide can inhibit the release of corticotropin (ACTH) and prolactin, anterior pituitary hormones that are released during stress. To determine the physiologic significance of ANP in the control of basal and stress-induced release of anterior pituitary hormones, highly specific antiserum against the peptide (AB-ANP) was microinjected into the third cerebral ventricle of conscious freely moving male rats to immunoneutralize hypothalamic ANP. In the initial experiment, the antiserum or control normal rabbit serum (NRS) was injected into the third cerebral ventricle to determine the effect of the antiserum on basal release of pituitary hormones. The antiserum had no effect on the concentrations of plasma ACTH, prolactin, or thyroid-stimulating hormone for 3 hr after the injection; however, plasma growth hormone concentration, although unchanged for 2 hr, was markedly elevated at 3 hr. These results indicate that although ANP appears to have no effect on the basal release of the other hormones, it has a physiologically significant inhibitory effect on growth hormone release. The delay of the effect is probably related to the time required for the antiserum to diffuse to the site of action of the peptide, presumably at some distance from the ventricle. Since this effect was demonstrable only after 3 hr, in the stress experiment, the antiserum or NRS was microinjected into the third ventricle 3 hr prior to application of ether stress. The rapid elevation of plasma ACTH in NRS-injected rats was markedly augmented by AB-ANP. Ether also induced a rapid increase in plasma prolactin in the NRS-injected animals, as expected. Contrary to the ACTH response, the maximal increase in plasma prolactin after ether was attenuated in animals preinjected with AB-ANP. In the NRS-injected animals, there was a significant decline in plasma growth hormone after the application of ether that was significantly accentuated by AB-ANP, but this was probably the result of the higher initial levels of plasma growth hormone in the ANP-AB group followed by its disappearance with a half-time similar to that of the NRS-injected group. The decline in plasma thyroid-stimulating hormone after ether stress was unaltered in the animals injected with AB-ANP. The results of these immunoneutralization studies suggest that endogenous ANP does not play a role in thyroid-stimulating hormone release. On the other hand, the endogenous peptide appears to have a physiologically significant inhibitory role in suppressing ACTH release during stress, mediated at least partly by suppression of vasopressin release. Endogenous ANP has a pathophysiologic role in augmenting the prolactin release in stress either by inhibiting release of prolactin-inhibiting factors or, alternatively, by enhancing release of prolactin-releasing factors. Endogenous ANP appears to inhibit resting, without altering stress-induced inhibition of growth hormone release by stimulating somatostatin release and/or inhibiting growth hormone-releasing hormone release or by both actions.
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PMID:The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone. 133 8

The natriuretic peptide system consists of three endogenous ligands, i.e., atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), and at least three subtypes of receptors. All of the peptides and receptors exist in the central nervous system (CNS). ANPs in the brain are N-terminally truncated forms: ANP (4-28) and ANP (5-28). The primary structure of BNP varies considerably among species, whereas that of CNP is highly conserved. ANP, BNP, and CNP are distributed in discrete brain regions, although the distribution varies in different species. Few immunohistochemical studies have so far been performed on BNP and CNP. There are three subtypes of receptors: ANP-A and ANP-B, which are bioactive, and the C receptor, which does not seem to be directly related to bioactivity. In the rat, the major subtype of ANP receptor in the CNS is the ANP-B receptor, based on the results of Northern blotting. Since the ligand for ANP-B receptor is CNP, the CNP-ANP-B receptor system may be most important, at least in rat brain. It is still unknown whether or not a specific receptor for BNP exists in central or peripheral tissues. Further studies should clarify the exact localization of ANP, BNP, and CNP and the three receptor subtypes in the CNS. Although natriuretic peptides and their receptors are distributed widely in the CNS, the AV3V regions, basal medial hypothalamus, brainstem, and circumventricular organs are the most prominent sites. This suggests an important physiological role of the natriuretic peptide system in the central control of cardiovascular homeostasis. The natriuretic peptide system seems to be involved in the regulation of water and salt intake, blood pressure, and secretion of vasopressin in the direction of reducing body fluid and lowering blood pressure. Such actions of natriuretic peptides are antagonistic to the central actions of angiotensin II (AII). In fact, the distribution of ANP and AII and their receptors in the CNS overlaps considerably. It is highly likely, therefore, that the central natriuretic peptide system and the renin-angiotensin system play important roles in the central control of cardiovascular and body fluid homeostasis in opposite directions. The natriuretic peptide system may also be involved in neuroendocrine control and some other CNS functions, although the physiological significance of these actions is less clear at the present time. It is now clear that there is considerable plasticity in the regulation of natriuretic peptides and their receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The natriuretic peptide system in the brain: implications in the central control of cardiovascular and neuroendocrine functions. 133

The distribution of binding sites for atrial natriuretic peptide (ANP) has been examined in frozen sections of the guinea pig inner ear by means of autoradiography. The highest density was found in the stria vascularis of all cochlear turns. In membrane preparations of stria vascularis in vitro, the production of the second messenger cGMP was strongly stimulated by synthetic ANP in a dose dependent manner. Adenylate cyclase was neither stimulated nor inhibited by ANP, thus suggesting, that the binding sites coincide with an ANP receptor, which is coupled to guanylate cyclase but not negatively coupled to an adenylate cyclase molecule. The production of cyclic GMP could not be reduced by GDP-beta S, a strong inhibitor of the Gs protein. We conclude the existence of an ANP receptor-guanylate cyclase signal transfer system, similar to the beta 2 receptor-adenylate cyclase system in the inner ear, without coupling to a G protein. ANP might play a role in sodium and water regulation of the endolymph and might antagonize the action of vasopressin.
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PMID:Binding sites of atrial natriuretic peptide (ANP) in the mammalian cochlea and stimulation of cyclic GMP synthesis. 133 79

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