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  • 1
    Book
    Book
    Textbook of medical physiology / (2002)
    Philadelphia [u.a.] :Saunders,
    Details
    Title: Textbook of medical physiology /
    Author: Guyton, Arthur C.
    Contributer: Hall, John E.
    Edition: 10. ed., 4. print.
    Publisher: Philadelphia [u.a.] :Saunders,
    Year of publication: 2002
    Pages: XXXII, 1064 S. : zahlr. Ill. und graph. Darst.
    ISBN: 0-7216-8677-X , 0-8089-2187-8
    Type of Medium: Book
    Language: English
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of Proline and Glutamine on the Functional Properties of Wheat Dough in Winter Wheat Varieties (2005)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of food science 70 (2005), S. 0 
    Details
    ISSN: 1750-3841
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Notes: : Combinations of proline and glutamine significantly increased the functional properties of soft wheat that were unseen when added individually. To hard wheat, proline contributed more positively than glutamine on most dough and bread properties, which is different from the observations with soft wheat. Addition of glutamine to hard wheat increased the amount of gluten and glutenin after mixing, whereas proline hinders gluten formation despite the increase in glutenin. The ability of proline and glutamine to modify the functional properties of dough and bread appears to be interdependent. Addition of either proline or glutamine appears to have a protective effect on the retention of the other amino acid during breadmaking.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2621.2005.tb07183.x
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    CARDIOVASCULAR ACTIONS OF INSULIN: ARE THEY IMPORTANT IN LONG-TERM BLOOD PRESSURE REGULATION? (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In recent years, there has been considerable interest in the possibility that insulin may have important cardiovascular as well as metabolic actions. Perhaps the best documented cardiovascular effect of insulin is to cause peripheral vasodilation, especially in skeletal muscle. Hyperinsulinaemia also stimulates sympathetic activity and causes antinatriuresis, but these effects may be linked, at least in part, to the metabolic actions of insulin that elicit peripheral vasodilation and a tendency toward hypotension. Normal, fasting levels of insulin appear to have very little influence on peripheral vascular resistance, sympathetic activity or renal sodium excretion.2. Decreased sensitivity of the peripheral tissues to the metabolic effects of insulin and compensatory hyperinsulinaemia have been postulated to play key roles in the pathophysiology of diseases such as hypertension and atherosclerosis. Although impaired insulin action (insulin resistance) and hyperinsulinaemia often accompany essential hypertension, especially when associated with obesity, there is currently little direct evidence for a cause and effect relationship between insulin resistance, hyperinsulinaemia and increased arterial pressure. Chronic increases in plasma insulin levels in dogs and humans have not been shown to cause hypertension, although hyperinsulinaemia raises blood pressure in rats.3. Further research is needed to determine whether there are pathophysiological conditions or genetic factors that may predispose humans to a hypertensive effect of hyperinsulinaemia and/or insulin resistance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1995.tb01922.x
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  • 4
    Electronic Resource
    Electronic Resource
    A Symposium in Memory of A Clifford Barger (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02145.x
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    ABNORMAL KIDNEY FUNCTION AS A CAUSE AND A CONSEQUENCE OF OBESITY HYPERTENSION (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Obesity is the most common nutritional disorder in the US and is a major cause of human essential hypertension. Although the precise mechanisms by which obesity raises blood pressure (BP) are not fully understood, there is clear evidence that abnormal kidney function plays a key role in obesity hypertension.2. Obesity increases tubular reabsorption and this shifts pressure natriuresis towards higher BP. The increased tubular re-absorption is not directly related to hyperinsulinaemia, but is closely linked to activation of the sympathetic and renin-angiotensin systems, and possible changes in intrarenal physical forces caused by medullary compression due to accumulation of adipose tissue around the kidney and increased extracellular matrix within the kidney.3. Obesity is also associated with marked renal vasodilation and increased glomerular filtration rate, which are compensatory responses that help overcome the increased tubular re-absorption and maintain sodium balance. However, chronic renal vasodilation causes increased hydrostatic pressure and wall stress in the glomeruli which, along with increased lipids and glucose intolerance, may cause glomerulosclerosis and loss of nephron function in obese subjects. Because obesity is a primary cause of essential hypertension as well as type II diabetes, there is good reason to believe that obesity may also be the most frequent cause of end-stage renal disease.4. Future research is needed to determine the mechanisms by which excess weight gain activates the neurohumoral systems and alters renal structure and function. Because of the high prevalence of obesity in most industrialized countries, unravelling these mechanisms will likely provide a better understanding of the pathophysiology of human essential hypertension and chronic renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02146.x
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  • 6
    Electronic Resource
    Electronic Resource
    IS INSULIN RESISTANCE LINKED TO HYPERTENSION? (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The volume of work reporting insulin resistance in multiple forms of chronic hypertension has generated tremendous interest in whether this abnormality is an important factor in causing hypertension. Insulin resistance, however, is an imprecise term used interchangeably to describe widely disparate types of impairment in insulin action throughout the body and the type of insulin resistance has major ramifications regarding its potential for inducing long-term increases in blood pressure (BP).2. Hepatic insulin resistance (impaired insulin-mediated suppression of hepatic glucose output) is the primary cause of fasting hyperinsulinaemia and is a cardinal feature of obesity hypertension. Evidence from chronic insulin infusion studies in rats suggests hyperinsulinaemia can increase BP under some conditions; however, conflicting evidence in humans and dogs leaves in question whether hyperinsulinaemia is a factor in hypertension induced by obesity.3. Peripheral insulin resistance (impaired insulin-mediated glucose uptake, primarily of an acute glucose load in skeletal muscle) also present in obesity hypertension, but now reported in lean essential hypertension as well, is linked most notably to impaired insulin-mediated skeletal muscle vasodilation. This derangement has also been proposed as a mechanism through which insulin resistance can cause hypertension.4. The present review will discuss the lack of experimental or theoretical support for that hypothesis and will suggest that a direct link between insulin resistance and BP control may not be the best way to envision a role for insulin resistance in cardiovascular morbidity and mortality.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02148.x
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    The juxtaglomerular complex: its possible control of multiple nephron functions (1979)
    [s.l.] : Nature Publishing Group
    Nature 277 (1979), S. 601-602 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] THE discovery of a new secretory cell in the juxtaglomerular complex of the renal nephron is announced in this issue of Nature (page 655) by Ryan, Coghlan, and Scoggins. This cell, the granulated peripolar epithelial cell, contains large numbers of granules that are obviously secretory in nature, ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/277601a0
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    Paper (German National Licenses)
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  • 8
    Electronic Resource
    Electronic Resource
    Ask the expert (1990)
    Springer
    Pediatric nephrology 4 (1990), S. 87-87 
    Details
    ISSN: 1432-198X
    Keywords: Renin angiotensin system ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00858448
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    Paper (German National Licenses)
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