Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role of muscarinic cholinergic mechanisms in mediating the pancreatic and pituitary hormonal responses to hypoglycaemia, six normal subjects were studied during acute insulin-induced hypoglycaemia under control conditions, and during blockade with intravenous atropine. During atropine blockade the response of pancreatic polypeptide was suppressed while the maximum response of plasma glucagon was significantly higher. The increment in plasma vasopressin was also increased significantly during cholinergic blockade. During blockade with atropine the responses of plasma prolactin was reduced, with a slight but significant reduction in the growth hormone response, and although a similar maximum response of plasma ACTH was achieved, this rise was delayed. These results implicate involvement of a cholinergic muscarinic inhibitory and stimulatory mechanisms in regulating the responses of pancreatic and pituitary hormones to hypoglycaemia.
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PMID:Pancreatic and pituitary hormonal responses to insulin-induced hypoglycaemia during muscarinic cholinergic blockade in man. 133 62

Endocrine abnormalities in patients with chronic renal failure are well documented. The present study aimed to assess the influence of long-term erythropoietin (EPO) therapy on endocrine abnormalities in haemodialyzed patients. Two groups of haemodialyzed patients, each of which comprised 17 subjects, were examined. The first one treated by EPO (EPO group) while the second one did not receive this hormone (NO-EPO group). A complete biochemical and hormonal check-up was performed before and at the 3, 6, 9 and 12 months of the study period. Normal values for the estimated parameters were obtained in appropriately selected sex and age-matched healthy subjects. After EPO therapy an increase of the haematocrit value from 21.8 +/- 0.9% to 32.6 +/- 0.9% was observed which was accompanied by a significant decline of plasma ferritin and saturation of transferrin. In patients of the NO-EPO group a significant although less marked rise of the haematocrit value (21.4 +/- 0.4% to 24.2 +/- 0.6%) was also noticed. EPO therapy did not change electrolytes (Na, K, Ca, inorganic phosphate), osteocalcin, creatinine, glucose and alkaline phosphatase plasma levels as well as plasma concentrations of calcium related hormones (PTH, calcitonin, 1.25(OH)2D3) and vasopressin (AVP). EPO treatment induced a significant decline of somatotropin (HGH), prolactin (PRO), follitropin (FSH), lutropin (LH), ACTH, cortisol, plasma renin activity, aldosterone, insulin (IRI), glucagon (IR-G), pancreatic polypeptide (PP) and gastrin plasma levels and an increase of plasma estradiol, testosterone and atrial natriuretic peptide (ANP). These EPO induced endocrine alterations were restricted mostly to the first 6 months of EPO administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of long-term erythropoietin therapy on endocrine abnormalities in haemodialyzed patients. 145 6

Pathophysiologic mechanisms of bradycardia during epidural anaesthesia (L3-L4 with 1% lidocaine, 38 ml) were evaluated by studying changes in selected cardiovascular and hormonal parameters. Six of eight subjects (analgesia to T8-T10) remained circulatory stable with no significant changes in heart rate (HR), mean arterial pressure (MAP) and thoracic impedance (TI). In one of two subjects MAP decreased after 25 min from 85 to 50 mmHg (11.3 to 6.7 kPa), HR from 80 to 45 beats.min-1 while thoracic impedance increased from 25.5 to 26.5 ohm. End-systolic diameter (ESD) and end-diastolic diameter (EDD) of the left ventricle determined with echocardiography were reduced from 3.8 to 3.2 cm (17%) and 5.6 to 5.0 cm (11%), respectively. In the other subject MAP decreased after 25 min from 75 to 50 mmHg (10.0 to 6.7 kPa) and HR from 82 to 60 beats.min-1 while thoracic impedance increased from 28.8 to 29.6 ohm. ESD was reduced from 3.8 to 3.3 cm (13%), and EDD from 5.6 to 5.0 cm (11%). Both subjects recovered after infusion of saline and being placed in the head-down position. There were no consistent changes in plasma catecholamines, whereas pancreatic polypeptide increased from 5 and 3 to 152 and 69 pmol.l-1, vasopressin from 3 and 2 to 152 and 46 pmol.l-1, and aldosterone from 282 and 229 to 383 and 485 pmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia. 146 23

Animal experiments have shown that severe haemorrhage often is characterized by an initial general increase in sympathetic activity leading to an increase in heart rate and a subsequent vagally mediated, reversible decrease in heart rate. It is likely that the decrease in heart rate is triggered by mechanoreceptors situated in the left ventricle. The receptors are supposed to be activated by a reduction in end-systolic volume occurring as a result of a decrease in venous return concomitant with the initial increase in heart rate. SA vago-vagal reflex elicited from and returning to the heart is thereby activated, resulting in a slowing of the heart. It has been hypothesized that the left ventricular receptors are activated when the ventricle contracts around an almost bloodless chamber. The decrease in heart rate may allow for an increased filling of the heart and an improved coronary perfusion. However, these experimental observations are in clear contradiction to the general description of the regulatory mechanisms operating during haemorrhagic shock in man as presented by authoritative medical, surgical and anesthesiological textbooks. Until now the (over-simplified) notion has been, that progressive haemorrhage results in an increased activation of the sympathetic nervous system leading to an increase in heart rate and that the occurrence of bradycardia was a sign of irreversible shock. The present systematic measurements in patients in haemorrhagic shock showed that the heart rate during severe haemorrhage often was normal (mean value 73 beats/min, range 46-98 beats/min). Simultaneous measurements of plasma concentrations of pancreatic polypeptide (an index of vagal activity) indicated that organs other than the heart also were exposed to increased vagal activity. A marked increase in the plasma concentration of vasopressin was not a constant finding as it was during the experimental-induced hypotensive central hypovolemia. This difference may be due to a decline in the release of vasopressin during prolonged haemorrhage. In order to elucidate essential regulatory mechanisms behind the clinical observations, central hypovolemia was induced experimentally by "head-up tilt", "lower-body negative pressure", "venous tourniquets of the thighs plus haemorrhage", and by epidural anesthesia. The initial stage of central hypovolemia was characterized by an increase in sympathetic nervous activity resulting in an increase in heart rate. Activation of the renin-angiotensin-aldosterone system occurred prior to marked increases in plasma concentrations of vasopressin. During progression of the central hypovolemia a qualitative shift in the regulatory mechanisms was evident.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Heart and endocrine changes during central hypovolemia in man. 180 34

Heart rate (HR), mean arterial pressure (MAP), indices of sympathetic and parasympathetic activity (plasma concentrations of adrenaline, noradrenaline and pancreatic polypeptide, PP), vasopressin (VP) and aldosterone (ALDO) were measured in six pigs during continuous bleeding resulting in hypovolaemic shock, from which five survived. Three stages of haemorrhage could be defined. Stage I. Resting MAP was 85 +/- 6 mmHg and increased to 96 +/- 5 mmHg with a blood loss of 275 (range 250-300) (10 (9-12)% of the estimated blood volume) concomitant with an increase in HR from 105 +/- 5 to 113 +/- 6 beats min-1 (P less than 0.05). Stage II. After a blood loss of 375 (300-500) ml (15 (13-16)%) MAP fell to 62 +/- 9 mmHg and HR to 95 +/- 5 beats min-1 (P less than 0.05). Stage III. A blood loss of 1113 (825-1450) ml (44 (30-52)%) resulted in a MAP of 50 +/- 4 mmHg and an increase in HR to 206 +/- 3 beats min-1 (P less than 0.05). Adrenaline increased from 0.3 +/- 0.1 to 0.8 +/- 0.3 (stage II) and 3.6 +/- 1.1 nmol l-1 (stage III) (P less than 0.05); noradrenaline from 0.4 +/- 0.1 to 1.5 +/- 0.4 (stage II) and 5.9 +/- 1.7 nmol l-1 (stage III) (P less than 0.05); PP from 6.2 +/- 1.6 to 13.3 +/- 2.3 (stage II) and 20.9 +/- 7.8 pmol l-1 (stage III) (P less than 0.05). VP changed only marginally, but ALDO increased from 496 +/- 54 to 623 +/- 76 pmol l-1 (stage III) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular and endocrine responses to haemorrhage in the pig. 231 78

A whole mount immunofluorescence method was used for the localization of immunoreactivity (IR) to four regulatory peptides and the bioamine serotonin in the nervous system of Stenostomum leucops (Turbellaria, Platyhelminthes). The flatworm S. leucops belongs to the taxon Catenulida which, according to the new phylogenetic system by Ax [2], forms a key group between the coelenterates and more advanced flatworm species. Positive IR was obtained using antisera against FMRF-amide, beta-endorphin, growth hormone releasing factor (GRF), substance P, and serotonin. The distribution patterns of these neuropeptide-like immunoreactivities differ significantly from each other. Antisera against Leu-enkephalin, bovine pancreatic polypeptide (BPP), bombesin, cholecystokinin (CCK-8), neurotensin, somatostatin, growth hormone (GH), secretin, and neurophysin II gave negative results. This primitive flatworm shows similarities with hydra in the lack of IR to anti-somatostatin, anti-Leu-enkephalin, and anti-BPP. These antisera give positive IR in more advanced flatworm species, indicating a later convergent evolution of vertebrate-like peptides within the phylum Platyhelminthes.
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PMID:Neuropeptides in a microturbellarian--whole mount immunocytochemistry. 242 Dec 67

Based on studies in animals and humans, it has been suggested that nausea activates the hypothalamo-neurohypophyseal system with resultant increases in circulating concentrations of oxytocin or vasopressin. The purpose of these studies was to determine in humans whether nausea is associated with increases in circulating concentrations of neurohypophyseal hormones or various enteropancreatic peptides (vasoactive intestinal polypeptide, substance P, or pancreatic polypeptide). Nausea, induced by intravenous infusion of apomorphine, was associated with fivefold to 75-fold increases in plasma vasopressin concentrations in 7 subjects (mean increase, 41-fold), with no change in plasma oxytocin levels. Furthermore, nausea was associated with sevenfold to 16-fold increases in plasma pancreatic polypeptide concentrations (mean increase, ninefold), with no change in plasma levels of vasoactive intestinal polypeptide or substance P. In 1 subject refractory to nausea, there was no increase in plasma vasopressin or pancreatic polypeptide concentrations with apomorphine. These studies indicate that nausea in humans is associated with vasopressin and pancreatic polypeptide release.
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PMID:Apomorphine-induced nausea in humans: release of vasopressin and pancreatic polypeptide. 245 45

Insertion into the mouse genome of the hybrid oncogene made up of bovine vasopressin gene derived 5' upstream sequences and the coding sequences of SV40 large T-antigen promoted tumours in anterior pituitary and endocrine pancreas of mice bearing this transgene. In order to investigate the morphology of the steps in the neoplastic process, we used light and electron microscopy to study these organs in 42 animals belonging to the 3rd, 4th and 5th generations, subdivided into 4 age groups from 20 days to 100 days of life. Antibodies to large T-antigen were used to identify sites of expression of the hybrid oncogene, thus monitoring the steps in neoplastic transformation. Large T-antigen immunoreactivity was identified in dysplastic lesions of younger animals and in both dysplastic lesions and tumours of older mice. Insulin (100% of cases) and pancreatic polypeptide (25% of cases) immunoreactivities were revealed in pancreatic lesions but no hormonal immunoreactivity was detected in the pituitary lesions. The ultrastructural study confirmed that the majority cell population of the pancreatic neoplasms was B-type and that the anterior pituitary tumours were poorly granulated. The subcellular localization of large T-antigen immunoreactivity was investigated by the immunogold method and was confined to the heterochromatin of tumour cell nuclei. These findings provide evidence for the dysplasia-neoplasia sequence in the genesis of endocrine tumours of pituitary and pancreas of transgenic mice. The vasopressin-SV40 large T-antigen transgenic mice may therefore be an useful model for the study of endocrine cell oncogenesis.
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PMID:A morphological analysis endocrine tumour genesis in pancreas and anterior pituitary of AVP/SV40 transgenic mice. 282 18

Circulatory variables and hormone concentrations in arterial plasma were measured in six normal subjects during angiotensin II (ANG II) step-up infusion of 0.25 and 1.00 ng kg-1 X min. During the 1.00 ng kg-1 X min infusion ANG II plasma concentrations increased from 11 +/- 2 to 48 +/- 6 pg ml-1; i.e., similar to those obtained during acute hypotensive hypovolaemia in man. Mean arterial pressure increased (P less than 0.05) from a resting value of 89 +/- 3 to 97 +/- 5 mmHg. Heart rate and catecholamine concentrations did not change. Plasma aldosterone increased (P less than 0.05) from 36 +/- 4 to 77 +/- 10 pg ml-1 during the infusion. Plasma concentrations of vasopressin, adrenalin and pancreatic polypeptide did not change during the investigation. During the 0.25 and 1.00 ng kg-1 X min infusion subcutaneous blood flow decreased (P = 0.06) to 67 +/- 20 and 66 +/- 26%, respectively, of control. It is concluded that: (1) ANG II in physiological doses in man may augment the sympathetic activity on the circulatory system since compensatory decreases in heart rate or in plasma catecholamines were not observed during the increased arterial pressure; (2) ANG II does not induce a general decrease in vagal tone as plasma pancreatic polypeptide concentrations were unchanged; (3) the obtained plasma concentrations of ANG II do not stimulate the release of vasopressin to plasma; and (4) the threshold for reducing the subcutaneous blood flow is reached within relatively small increments in plasma ANG II.
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PMID:Angiotensin II attenuates reflex decrease in heart rate and sympathetic activity in man. 334 55

Circulatory changes and arterial plasma hormone concentrations were measured in seven healthy young adults during 30 and 60 degrees passive head-up tilt with the subjects supported by a saddle. The 30 degrees tilt induced a decrease in pulse pressure (Pp) from 45 +/- 2 to 35 +/- 4 (mean +/- SE) mmHg concomitant with an increase in heart rate (HR) from 58 +/- 4 to 78 +/- 8 beats/min and a marginal increase in mean arterial pressure (MAP). Norepinephrine increased from 180 +/- 20 to 310 +/- 40 pg/ml, aldosterone increased fivefold, and angiotensin II increased from 8 +/- 2 to 22 +/- 7 pg/ml. The 60 degrees tilt initially produced changes, which were qualitatively similar to the 30 degrees tilt. However, after 19 +/- 3 min sudden decreases were seen in MAP (94 +/- 3 to 50 +/- 8 mmHg), in Pp (38 +/- 5 to 18 +/- 4 mmHg), and in HR (90 +/- 7 to 57 +/- 6 beats/min). Concomitantly, epinephrine doubled while norepinephrine remained unchanged; the vagally controlled hormone pancreatic polypeptide increased from 29 +/- 3 to 51 +/- 8 pmol/l, vasopressin from 4 +/- 1 to 126 +/- 58 pg/ml, and angiotensin II from 23 +/- 9 to 35 +/- 12 pg/ml. The hypotensive bradycardiac episode was immediately reversible on termination of the head-up tilt.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypotension induced by passive head-up tilt: endocrine and circulatory mechanisms. 376 74


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