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  • 1
    ISSN: 1432-0568
    Keywords: Atrial natriuretic peptide ; Pekin duck ; Salt gland ; Immunocytochemistry ; High performance liquid chromatography ; Radioimmunoassay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A novel peptide hormone, atrial natriuretic factor/cardiodilatin (ANP/CDD), was recently isolated and characterized from mammalian heart. Its presence has been demonstrated in several organs that contribute to water and sodium homeostasis, such as salivary glands. This study demonstrates the presence of ANP/CDD immunoreactivity in the salt gland of Pekin ducks by high performance liquid chromatography, radioimmunoassay and immunocytochemistry, using a specific antibody against atriopeptide I. A small number of distinct, ovoid or cuboid shaped ANP/CDD-immunoreactive cells were localized in the connective tissue surrounding and separating the central secretory tubules, whereas no immunostaining was observed in the peripheral tubules. Salt glands of ducks that were adapted to salt water revealed a significant hypertrophy of their secretory lobules. However, no differences were found between the number or localization of immunoreactive cells in the salt gland of salt water-acclimatized ducks and non-stimulated glands of ducks that were housed with ad libitum access to fresh water. Our results indicate that ANP/CDD may play a role in the regulation of sodium secretion in the salt gland of aquatic birds.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Atrial natriuretic peptide ; Cyclic GMP ; Volume loading
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the effects of fluid expansion on endogenous atrial natriuretic peptide (ANP) and cyclic 3′,5′-guanosine monophosphate (cGMP), four male volunteers were studied before, during and after intravasal volume loading. Volume expansion was performed by intravenous infusion of 2,000 ml isotonic saline solution within 30 min. Mean plasma ANP levels increased 2.5-fold from 31.2 pg/ml to 81.7 pg/ml 40 min after the start of infusion. Plasma cGMP levels paralleled the rise in ANP, shwoing a mean cGMP increment from 2.7 pmol/ml to a maximum of 8.2 pmol/ml. Both ANP and cGMP levels were back to basal levels 120 min after termination of the infusion. Stimulation of endogenous ANP release by volume loading suggests that ANP is involved in the regulation of fluid homeostasis in man. The parallel rise in plasma cGMP levels supports the idea that cGMP is a mediator for the effects of ANP.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1106
    Keywords: Hypothalamus in vitro ; CRH ; Neurotransmitters ; Norepinephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of neurotransmitters on in vitro release of CRH from rat hypothalamic tissue were investigated. Three whole hypothalami or three mediobasal hypothalami from male rats, adrenalectomized 7 days before, were incubated for 10 min in a medium similar to cerebrospinal fluid at 37 ° C under 95% O2, 5% CO2. CRH activity was assayed by radioimmunological measurement of ACTH released by isolated pituitary cells from adrenalectomized rats. Norepinephrine (NE) at a concentration of 0.02×10−6 M to 2×10−6 M stimulated dose-related CRH release. At larger concentrations the response decreased again (bell-shaped dose-response relationship). The action of norepinephrine was completely blocked by coincubation with phentolamine. Similar results were obtained whether whole hypothalami or mediobasal hypothalami were incubated with norepinephrine. This suggests that the site of action of NE was within the mediobasal hypothalamus. The possibility that the observed effects were due to the CRH-like activity of vasopressin released from the hypothalamic tissue was excluded by simultaneous measurements of CRH activity and arginine-vasopressin concentrations in the medium. Dopamine at very large concentrations (17.6×10−6 M) also stimulated CRH release. Acetylcholine, serotonin, histamine and GABA did not influence the basal CRH release at any of the concentrations tested. These results suggest that in the rat, norepinephrine may have a physiological role as stimulator of CRH-release at the level of the mediobasal hypothalamus. However, in view of the conflicting results obtained with similar and other methods, no definite conclusions should yet be drawn.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 314 (1985), S. 264-266 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The rat synthetic peptides used here were the 21-amino acid atriopeptin I (AP I), the 23-amino acid atriopeptin II (APII) and the 24-amino acid atriopeptin III (APIII)8. To obtain antibodies, New Zealand White rabbits were injected with AP II coupled to bovine thyroglobulin. AP III, which ...
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 184 (1984), S. 171-178 
    ISSN: 1433-8580
    Keywords: Endogenous opioid peptides ; β-Endorphin ; Enkephalins ; Naloxone ; Hemorrhagic hypotension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sixteen anesthetized foxhounds were instrumented for hemodynamic measurements. The adrenolumbar vein was cannulated, and hemorrhagic hypotension (MAP=40 mmHg for 3 h) was induced by bleeding. The plasma levels ofβ-endorphin (β-END), methionine-enkephalin (M-ENK), and leucine-enkephalin (L-ENK) were determined in systemic and adrenal venous blood by specific RIA. Five dogs received an i.v. bolus of naloxone (2 mg/kg) and a subsequent naloxone infusion of 2 mg/kg per hour 1 h after onset of hypovolemia. Eleven dogs served as controls and received equivalent volumes (1 ml/kg per hour) of saline. Hemorrhage resulted in a sharp increase in plasma concentrations of all measured opioid peptides, particularly of M-ENK (26-fold) and L-ENK (24-fold) in the adrenal effluent. Systemicβ-END levels remained 3-fold increased, whereas the ENK release decreased spontaneously. Naloxone treatment inhibited the spontaneous fall of adrenal ENK release during the hypotensive phase; the ENK values remained elevated 20- to 35-fold. Reinfusion of the autologous blood resulted in a normalization of the concentrations of all peptides in both groups. These data demonstrate that hemorrhagic hypotension will cause stimulation of release of endogenous opioid peptides. The high levels of ENK in the adrenal effluent indicate that the adrenal gland is the main source of these peptides in the circulation. In addition toβ-END, the ENK have therefore to be considered as possible factors perpetuating circulatory shock.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1435-1803
    Keywords: atrial natriuretic peptide ; heart failure ; regionalblood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To characterize the systemic and regional vascular effects of atrial natriuretic peptide (ANP) in chronic heart failure, central hemodynamics, regional blood flow and plasma ANP levels were determined in a rat model of myocardial infarction and failure and in sham-operated animals. Measurements were made in the conscious state before and after intravenous rANP [99-126] (8 μg bolus followed by continuous infusion of 1.0 μg/kg/min). With this protocol, ANP significantly decreased cardiac output, right atrial, left ventricular enddiastolic and arterial pressures and there were increases in heart rate, systemic and intestinal vascular resistances in sham animals. Renal blood flow per gram of tissue was unchanged with ANP, but when expressed as a percentage of cardiac output, increased significantly, indicating a preferential renal vasodilatory effect of ANP. In rats with infarction and failure, this dose did not alter cardiac output or arterial pressure, but decreased right atrial and left ventricular blood flow. Although significantly reduced as compared to the control group, renal blood flow was not improved with ANP in the heart failure group. ANP plasma levels of the heart failure group were elevated at baseline (p〈0.01), and increased 5–10 times after infusion of rANP. Thus, in rats with chronic heart failure, the renal vascular effects of ANP are blunted, which may, in part, explain the failure of ANP to restore the altered volume homeostasis in heart failure despite elevated ANP plasma levels. However, the effects on venous return were preserved which, in turn, improved cardiac performance via a reduction of preload.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1439-6327
    Keywords: Almitrine ; Altitude ; Atrial natriuretic peptide ; Arginine vasopressin ; Diuresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diuresis at altitude was thought to be the result of chemoreceptor stimulation leading to a reduction of cardiac volume overload. This hypothesis was tested in ten young, healthy subjects by infusion of almitrine (0.5 mg · kg−1 body mass within 30 min) assuming analogous sites of action, i.e. arterial chemoreceptors and pulmonary vessels, for almitrine as for hypoxic hypoxia. The results show that almitrine increases ventilation, heart rate, systolic blood pressure, central venous pressure and natriuresis, but fails to increase significantly atrial natriuretic peptide plasma concentration and diuresis. It is concluded: (1) that almitrine has similar sites of action as hypoxic hypoxia at about 5000 m, (2) that natriuresis during arterial chemoreceptor stimulation might reduce cardiac volume overload, (3) that the volume excretion hypothesis, in particular the pathways from the cardiac volume overload to the water diuresis, need, for an understanding of the hypoxia-induced diuresis, further direct investigations at altitude.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0878
    Keywords: Vasopressin ; Oxytocin ; Neurohypophysis (Median eminence, Neural lobe) ; Adrenalectomy ; Salt loading ; Salt deprivation ; Plasma volume ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary In adrenalectomized rats the influence of salt loading or salt deprivation on the vasopressin and oxytocin content of the median eminence (ME) and the neural lobe (NL) was studied by means of various methods: (1) morphometric and microphotometric analysis of aldehyde fuchsin-stained sections of ME and NL; (2) immunohistochemical demonstration of neurophysin, oxytocin, and vasopressin in the ME and in the NL; (3) radioimmunological measurement of oxytocin and vasopressin in the ME and in the NL. Adrenalectomy in salt-substituted rats raised the vasopressin content of the outer layer of the ME (OLME) but had no influence on the amount of vasopressin in the inner layer of the ME and in the NL. Osmotic stimulation of adrenalectomized rats by hypertonic saline markedly diminished vasopressin and oxytocin in the inner layer of the ME and in the NL but did not, or only slightly reduced vasopressin in the OLME. Withdrawal of salt supplementation in adrenalectomized rats resulted in a decrease of plasma sodium and plasma volume. It did not change the vasopressin or oxytocin content of the inner layer of the ME and of the NL, but it was correlated with a decrease of vasopressin in the OLME. The present findings may suggest that vasopressin in the OLME is involved in salt and/or volume regulation by influencing the hypophysial-adrenal axis.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0878
    Keywords: Vasopressin ; Oxytocin ; Neurophysin ; Neurohypophysis ; Adrenalectomy ; Osmotic stress ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The influence of adrenalectomy and administration of hypertonic saline on the amount of vasopressin, oxytocin, and neurophysin contained in the median eminence and the neural lobe of rats was studied by means of the following methods: (i) morphometric and microphotometric analyses of aldehyde fuchsin-stained histological sections of the neurohypophysis; (ii) immunohistochemical demonstration of vasopressin, oxytocin, and neurophysin in the neurohypophysis, and (iii) radioimmunological measurement of vasopressin and oxytocin in extracts of the median eminence and the neural lobe. Adrenalectomy increases the amount of vasopressin and neurophysin in the external layer of the median eminence but does not change the content of oxytocin. It has no influence on the amount of vasopressin, oxytocin, and neurophysin demonstrable in the inner layer of the median eminence and in the neural lobe two weeks after the operation. Hypertonic saline markedly diminishes the vasopressin, oxytocin, and neurophysin content of the inner layer of the median eminence and the neural lobe but reduces only slightly, if at all, the amount of vasopressin and neurophysin in the outer layer of the median eminence. The findings support the concept that osmotic stress reduces only the vasopressin and oxytocin content of the hypothalamus-neural lobe system and has no or only little influence on the vasopressin content of the outer layer of the median eminence.
    Type of Medium: Electronic Resource
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