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  • 1980-1984  (4)
  • 1984  (1)
  • 1982  (3)
Material
Years
  • 1980-1984  (4)
Year
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 9 (1982), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Angiotensin II (ANG II) may increase blood pressure by central nervous system mechanisms. The involvement of the sympathetic nervous system in the centrally-induced pressor effect of ANG II in the rat was investigated.2 Plasma noradrenaline concentrations, measured as an index of sympathetic nervous system activity, increased after intracerebroventricular (i.e.v.) injection of pressor doses of ANG II, both in normotensive and in spontaneously hypertensive rats.3 To assess the functional significance of this, the sympathetic nervous system was inhibited by phentolamine, reserpine, and guanethidine. In phentolamine-infused rats, low doses of i.c.v. ANG II elicited a blood pressure decrease, but at maximal pressor doses, no difference between phentolamine-treated and control rats was observed. In reserpinized rats, the central pressor effect of ANG II was greater than in controls. Guanethidine pretreatment did not affect the blood pressure response to i.c.v. injected ANG II.4 It is concluded that the central pressor effects o f ANG II are accompanied by a stimulation of the sympathetic nervous system. In the rat, this stimulation may be functionally important for the initial phase of the central pressor action. This could not be established for the maximal pressor responses.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Intracerebroventricular injections of angiotensin II in anesthetized rhesus monkeys increase systemic blood pressure and heart rate. These effects are accompanied by an increase in plasma ADH, cortisol, adrenaline and noradrenaline. Angiotensin II may participate in central mechanisms of blood pressure regulation by its stimulatory effect on the sympathetic nervous system, on ADH and on ACTH release in primates.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 15 (1984), S. 111-118 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In male spontaneously hypertensive rats (SHRSP) of the stroke prone strain (Okamoto) and in normotensive Wistar-Kyoto rats (WKY) urinary kallikrein excretion was investigated at different age and at drug-induced diuresis. In rats of both strains from 7th till 19th week of age urinary kallikrein excretion increased with age. In SHRSP of 7th till 11th week of age kallikrein excretion was higher than in WKY rats, while it was lower in the 48-week-old SHRSP. No correlation was found between urinary kallikrein excretion and systolic blood pressure. In SHRSP and WKY rats a similar daily rhythm of kallikrein excretion in urine was found being high in the early morning and low in the afternoon. Kallikrein excretion correlated significantly with urine volume. The loop diuretic bumetanide (4 and 40 mg/kg) induced diuresis and natriuresis in both strains, however more marked in the WKY rats than in the SHRSP. Urinary kallikrein excretion, however, showed in both strains the same biphasic course with a short lasting increase and a secondary decrease. Thus, in the average urinary kallikrein excretion was not effected by the drug. Prolonged treatment with furosemide over 5 days (125 mg/kg) resulted in an increase in kallikrein excretion in urine, more pronounced in the WKY rats than in the SHRSP. The observed results suggest that renal kallikrein-kinin system is not involved in the development of spontaneous hypertension as a pathogenetic factor, but rather is influenced by other factors like hormone interactions, i.e. mineralocorticoids and catecholamines, as well as renal function and acute changes in urine flow.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 395 (1982), S. 71-74 
    ISSN: 1432-2013
    Keywords: Noradrenaline ; Adrenaline ; Vascular reactivity ; Noradrenaline uptake ; Phosphate depletion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plasma catecholamines and vascular response to noradrenaline were studied in phosphate depleted rats. Phosphate depletion was induced in rats by dietary phosphorus deprivation for 6 weeks. Basal plasma concentrations of noradrenaline, adrenaline and dopamine were elevated in phosphate depleted rats compared to pairfed control rats. After exposure to cold (4° C, 45 min) the rise in plasma catecholamines was much more pronounced in phosphate depleted rats. In the isolated perfused rat heart, the uptake of tritiated noradrenaline was unchanged. In the isolated perfused hindlimb preparation the vascular response to noradrenaline, but not to potassium chloride and argininevasopressin was significantly diminished in phosphate depleted rats. It is concluded that in phosphate depletion sympathetic activity is elevated and vascular response to noradrenaline diminished.
    Type of Medium: Electronic Resource
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