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  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Hypothalamus. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (249 pages)
    Edition: 1st ed.
    ISBN: 9781483193038
    Language: English
    Note: Front Cover -- Hypothalamic Control of Lactation -- Copyright Page -- Table of Contents -- Preface -- Abbreviations -- Part I: Physiological Regulation of Lactation -- Chapter 1. Mechanism of Lactation -- Chapter 2. Hypothalamus-Pituitary Axis -- a) Hypothalamic Control of Prolactin Secretion -- b) Prolactin-Inhibiting Factor (PIF) -- c) Prolactin-Releasîng Factor (PRF) -- d) Hypothalamic Feedback of Prolactin -- e) Effects of Steroids -- f) Interrelation between Pituitary Tropins -- g) Suckling -- h) Conclusions -- Chapter 3. Prolactin -- a) Introduction -- b) Storage and Release -- c) Properties -- d) Prolactin in Body Fluids -- e) Prolactin in Pituitary Tumors -- f) Effect of Prolactin on Mammary Growth -- g) Levels of Pituitary Prolactin in Various Stage of Lactation -- h) Theories on the Mechanism of Onset of Lactation -- i) Conclusion -- Chapter 4. Growth Hormone -- Chapter 5. Gonadotropins and Sex Steroids -- Chapter 6. Adrenocorticotropin and Corticosteroids -- Chapter 7. Thyrotropin and Thyroid Hormones -- Chapter 8. Oxytocin and Vasopressin -- Chapter 9. Parathormone and Calcitonin -- Chapter 10. Insulin and Glucagon -- Chapter 11. Pineal Gland -- Chapter 12. Placental and Amniotic Fluid -- Part II: Pharmacological Regulation of Lactation -- Chapter 13. Hypothalamic Lactation Produced by Psychopharmaca -- a) History -- b) Dissociation of Mammotropic and Sedative Effects -- c) Biological Dissociation through Combined Treatment with Tranquilizers and Psychostimulants -- d) Chemical Dissociation by Molecular Changes of Tranquilizers -- e) Studies in Hypophysectomized Rats -- f) Conclusions -- Chapter 14. Mammotropic Effect of Phenothiazine Derivatives -- a) History -- b) Mammotropic Index (MTI) -- c) Body Temperature Drop (BTD) -- d) Screening of Phenothiazine Derivatives -- e) Screening of Phenothiazine Sulfoxides and Sulfodioxides. , f) Stimulation of Synthesis and Release of Prolactin by Perphenazine -- g) Intracerebral Implantation of Phenothiazine Derivatives -- h) Mammotropic Effect of Fluphenazine Enanthate in the Rat -- i) Comparative Study of Phenothiazine Effect on Hypothalamic Prolactin-Inhibiting Factor and MSH-Releasing Factor -- j) Conclusions -- Chapter 15. Mammotropic Effect of Phenothiazine-like Compounds -- Chapter 16. Mammotropic Effect of Reserpine Derivatives -- Chapter 17. Mammotropic Effect of Butyrophenones -- Chapter 18. Mammotropic Effect of Miscellaneous Psychotropics Drugs -- Chapter 19. Structure-Activity Relationship of Mammotropic Drugs and Receptor Theory -- Chapter 20. Pituitary-Ovary Axis in Hypothalamic Lactation -- Chapter 21. Pituitary-Adrenal Axis in Hypothalamic Lactation -- Chapter 22. Pituitary-Thyroid Axis in Hypothalamic Lactation -- a) Role of Thyroid in vivo and in vitro -- b) Thyroid and Hypothalamic Mammary Growth -- c) Thyroid and post-partum Galactopoiesis -- d) Conclusion -- Chapter 23. Prolactin Release by Hypothalamus of Nursing Rat Mothers -- Chapter 24. Prolactin as Luteotropic Hormone -- Part III: Prolactin Assay -- Chapter 25. In vitro Methods -- a) Effect of Hypothalamus -- b) Effect of Pituitary -- c) Effect of Steroids -- d) Effect of Neurohormones -- e) Effect of Phenothiazines -- f) Effect of Reserpine -- g) Effect of Thyroid -- h) Effect of Oxytocin -- i) Conclusion -- Chapter 26. In vivo Methods -- a) Rabbit Tests -- b) Rat Tests -- c) Pigeon Tests -- d) Concentration Methods -- Chapter 27. Radioimmunoassay -- Part IV. Problems of Lactation -- Chapter 28. Lactation in Humans -- a) Lactation and post-partum Amenorrhea -- b) Inhibition of Lactation and Breast Engorgement -- c) Persistence of Lactation and Menstrual Cycle -- d) Sterility during Lactation -- e) Galactorrhea as a General Syndrome. , f) Forbes-Albright-Castillo Syndrome -- g) Chiari-Frommel Syndrome -- h) Sheehan's Syndrome -- i) Hypothalamic Lactation -- j) Promotion of post-partum Lactation -- k) Gynecomastia -- l) Conclusion -- Chapter 29. Conclusions -- Chapter 30. Research Problems -- References -- Subject Index -- Monographs on Endocrinology.
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  • 2
    Keywords: Proteins-Metabolism. ; Electronic books.
    Description / Table of Contents: Sponsored by Ciba.
    Type of Medium: Online Resource
    Pages: 1 online resource (544 pages)
    Edition: 1st ed.
    ISBN: 9783642531477
    Language: English
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 56 (1934), S. 1116-1118 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial and engineering chemistry 1 (1962), S. 41-45 
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Pharmacology 13 (1973), S. 57-90 
    ISSN: 0362-1642
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    The @journal of organic chemistry 22 (1957), S. 1264-1265 
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 3 (1976), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Isolated rat kidneys were perfused at a constant pressure of 90 mmHg in a single-pass system with either a cell-free medium or a suspension of washed bovine red blood cells, free of the components of the renin-angiotensin system. In red blood cell perfused kidneys renal haemodynamics and sodium reabsorption corresponded closer to values observed in the intact rat than in cell-free perfused kidneys.2. In red blood cell-perfused kidneys in the absence of plasma renin substrate autoregulation of renal blood flow was almost complete at pressures above 90 mmHg, provided that perfusion pressure was changed rapidly.3. Renin release varied inversely with perfusion pressure within a pressure range from 50 to 150 mmHg; the greatest changes of renin release occurred, when perfusion pressure was reduced from 90 to 70 mmHg; maximal stimulation of renin release was observed at 50 mmHg. After reduction of perfusion pressure, renin release immediately started to rise and reached a new level within 5 min. Local reduction of perfusion pressure in small arteries and arterioles by the injection of microspheres induced a short-lasting decrease in renal plasma flow and a transient stimulation of renin release.4. High concentrations of furosemide stimulated renin release by a direct intrarenal mechanism.5. Isoproterenol stimulated renin release in low concentrations without a concomitant vasodilation, whereas high concentrations induced an increase in both renal plasma flow and renin release. The effects of isoproterenol were completely blocked by propranolol.6. Sodium nitroprusside induced similar increases in renal plasma flow, as did high concentrations of isoproterenol, but only a small and slow increase in renin release was observed.7. Angiotensin II (AII) suppressed renin release in concentrations corresponding to plasma levels measured in the intact rat independently of its vasoconstrictor effects, whereas vasopressin in antidiuretic concentrations did not affect renin release.8. AII, AI, synthetic tetradecapeptide renin substrate (TDP), crude and purified rat plasma renin substrate induced a dose-dependent reduction in renal plasma flow. SQ 20 881, a competitive inhibitor of converting enzyme, and low doses of l-Sar-8-Ala-AH (saralasin), a competitive antagonist of AH, did not change renal plasma flow, whereas high concentrations of saralasin had a vasoconstrictor effect on their own.9. Saralasin inhibited the vasoconstrictor effects of All and TDP to a similar degree. SQ 20 881 inhibited the vasoconstrictor effects of AI and purified renin substrate, but did not influence the actions of TDP and the crude renin substrate preparation.10. From these data it is concluded, that AI is converted into AH within the kidney at a rate of 1–2%. The vasoconstriction induced by the crude renin sub-strate probably does not involve the All receptors. TDP may act by itself on the AII receptors or via the direct intrarenal formation of AII. The vasoconstriction induced by purified renin substrate is probably due to the intrarenal formation of AI and its subsequent conversion to AII.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 7 (1980), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In Sprague-Dawley rats, two-kidney, one-clip renal hypertension was induced, and the drinking behaviour as well as total fluid and sodium intake were studied before and for 16 days after the operation.2. When water alone was offered as drinking fluid, the blood pressure reached values that were by about 20 mmHg higher than those in the rats which had free choice of drinking water or 2% saline.3. In those rats which had water and 2% saline to drink, the total sodium and fluid intake rose transiently for three days, as compared with that of the sham-operated controls, and increased steeply starting from the 7th and 10th day, respectively. When a tighter stenosis of the renal artery was induced, the pressure rose more rapidly, and the total fluid and sodium intake increased continuously after the operation until the end of the experiment.4. A positive correlation was demonstrable between the height of blood pressure and the total daily intake of fluid and sodium, respectively.5. The relation between the total daily fluid and the total daily sodium intake followed a straight regression line.6. The hypertensive rats which had a high total sodium intake responded to the withdrawal of the 2% saline solution, within 2 days, with increased water intake, decreased food intake, and loss of body weight, whereas the blood pressure remained high.7. In the two-kidney, one-clip hypertension, no ‘critical level of blood pressure’ can be defined, beyond which the contralateral kidney starts to lose sodium.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 2 (1975), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The acute malignant phase of hypertension in rats with an untouched contralateral kidney is characterized by salt and fluid loss, increased fluid intake, decrease in body-weight gain, and reduced food consumption. Plasma concentrations of sodium and potassium were reduced, and plasma angiotensin II rose to about four times normal.2. To investigate the significance of an untouched contralateral kidney for the development of the acute malignant phase in renal hypertensive rats, comparative studies were undertaken in unilaterally nephrectomized rats with stenosis of the remaining renal artery and in rats with bilateral renal artery stenosis. In addition, the effect of declamping one renal artery in rats with bilateral stenosis was studied.3. In unilaterally nephrectomized rats, no signs of sodium and fluid loss were demonstrable, despite marked increase in blood pressure. Similarly, rats with bilateral renal artery stenosis had no acute malignant phase of hypertension.4. In hypertensive rats with bilateral stenosis, removal of the clip from one renal artery was followed by an immediate fall in blood pressure and a subsequent gradual increase. Eleven of sixteen rats lost salt and fluid and developed an acute malignant phase. Plasma angiotensin II was high and serum urea elevated.5. Consumption of 2% saline in addition to water as drinking fluid had a beneficial effect, since only five of fourteen rats showed signs of the acute malignant phase, which were milder than in rats on water only.6. It is concluded that the untouched contralateral kidney is responsible for the negative salt and water balance and its consequences, which are characteristic of the acute malignant phase of experimental renal hypertension.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Inst. and Methods in Physics Research, B 24-25 (1987), S. 432-436 
    ISSN: 0168-583X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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