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  • 1
    Electronic Resource
    Electronic Resource
    INVERTED RESPONSE OF ARGININE VASOPRESSIN TO POSTURAL CHANGE IN PATIENTS WITH ESSENTIAL HYPERTENSION (1982)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 9 (1982), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: This study was designed to compare the response of plasma arginine vasopressin (AVP) to head-up tilt in hypertensive patients and in normals.As expected, plasma AVP showed a consistent increase (P〈 0.005) in normal subjects after tilt while plasma volume decreased significantly (P〈0.02). On the contrary, in hypertensive patients, after tilt both plasma AVP (P〈 0.025) and plasma volume (P〈0.05) decreased.These findings, thus, indicate that essential hypertension is characterized by an inverted response of arginine vasopressin to postural change.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1982.tb00783.x
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  • 2
    Electronic Resource
    Electronic Resource
    Chromosomal mapping of quantitative trait loci contributing to stroke in a rat model of complex human disease (1996)
    [s.l.] : Nature Publishing Group
    Nature genetics 13 (1996), S. 429-434 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Stroke is a complex disorder with a poorly understood multifactorial and polygenic aetiology. We used the stroke–prone spontaneously hypertensive rat (SHRSP) as a model organism, mated it with the stroke–resistant spontaneously hypertensive rat (SHR) and performed a genome–wide ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng0896-429
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  • 3
    Electronic Resource
    Electronic Resource
    Role of angiotensin II AT1 and AT2 subtype receptors in the regulation of atrial natriuretic peptide expression in salt-restricted rats (2000)
    Springer
    Basic research in cardiology 95 (2000), S. 64-69 
    Details
    ISSN: 1435-1803
    Keywords: Key words ANP – angiotensin II receptors – heart – losartan – PD123319
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have suggested that angiotensin II modulates ANP secretion and this action appears to be largely independent from its hemodynamic effects. In order to explore the contribution of angiotensin II AT1 (AT1r) and AT2 (AT2r) receptor subtypes in the regulation of cardiac ANP, we studied the effects of selective antanonists of these receptors on ANP mRNA levels in the cardiac chambers of salt-restricted rats. Thirty-one Sprague-Dawley rats (12 weeks-old) weighing 250–350 g were studied during a low salt regimen and randomly assigned to the following treatment groups: AT1r-blockade (losartan) (10 mg7kg/day) (n = 18), AT2r-blockade (PD123319) (50 μg/kg/min) (n = 6), Control (salt-restriction) (n = 7). Treatments were maintained for 7 days; subsequently 12 rats from the AT1r-blockade group were subdivided in to two groups: AT1r-blockade (losartan+PD123319) (n = 6) and AT1r-blockade/vehicle (losartan-vehible) (n = 6), and treated for 7 additional days. Systolic blood pressure was significantly reduced by AT1r-blockade (p 〈 0.001), while it was not affected by AT2r-blockade. Concomitant treatment with both antagonists (AT1r/AT2r-blockade) restored blood pressure values to baseline (p 〈 0.001 vs. AT1r-blockade, p = n.s. vs Control). Atrial ANP mRNA was reduced by AT1r-blockade (-42%, p 〈 0.05) and did not change during AT2r-blockade alone. On the contrary, concomitant treatment with both antagonists resulted in a further significant inhibition of ANP expression (-65% and -36% vs Control and AT1r-blockade, respectively, both p 〈 0.05). ANP expression in ventricles was not affected by any of these treatments. Our results demonstrate that angiotensin II tonically modulates cardiac ANP expression in our experimental model. In particular, angiotensin II receptor subtypes AT1r and AT2r regulate atrial ANP mRNA levels through a synergic action and independently from blood pressure changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050009
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  • 4
    Electronic Resource
    Electronic Resource
    Defective suppression of the aldosterone biosynthesis during stroke permissive diet in the stroke-prone phenotype of the spontaneously hypertensive rat (2000)
    Springer
    Basic research in cardiology 95 (2000), S. 84-92 
    Details
    ISSN: 1435-1803
    Keywords: Key words Adrenal – aldosterone – hypertension – renin-angiotensin system – stroke
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have shown that short-term high salt intake unmasks blunted plasma aldosterone suppression in stroke-prone spontaneously hypertensive rats (SHRsp). The aim of this study was to evaluate the response of aldosterone biosynthesis and production to a sustained exposure to the stroke-permissive Japanese-style diet (JD) in young stroke-prone and stroke-resistant SHRs. For this purpose, 6-week old male rats from both strains were divided into 2 dietary groups and received regular diet (SHR = 37, SHRsp = 32) or the JD and 1% saline to drink (SHR = 34, SHRsp = 30) for 4 weeks. All measurements were carried out at the end of the dietary periods. After JD, plasma aldosterone levels were significantly decreased in SHR (from 357.8±57 to 163.3±31.5 pg/ml, p 〈 0.05) but markedly increased in SHRsp (from 442±56.5 to 739±125.7 pg/ml, p 〈 0.05). Consistently, the adrenal aldosterone synthase expression was reduced by JD in SHR (p 〈 0.05), whereas it was even slightly raised by JD in SHRsp so that, at the end of JD, aldosterone synthase mRNA was 5-fold higher in SHRsp than in SHR. Urinary sodium excretion (mEq/24h) achieved lower levels in SHRsp, so that fractional excretion of sodium was 80.2±9% in SHR and 40.3±8% in SHRsp (p 〈 0.05) in balance studies performed at the end of JD. These different responses of mineralocorticoid biosynthesis and urinary sodium excretion to JD were not accounted for by different adaptions of the renin-angiotensin and atrial natriuretic peptide systems, of serum potassium levels, or of adrenal 11β-hydroxylase expression in the two strains. Systolic blood pressure was comparable in both strains throughout the experiment. These results demonstrate enhanced aldosterone biosynthesis, associated with reduced urinary excretion of sodium in response to JD in SHRsp before the onset of stroke. This abnormality may play a role in the higher susceptibility of stroke of this model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050168
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of atrial natriuretic peptide on glomerular filtration rate in essential hypertension: a radionuclide study (1991)
    Springer
    European journal of nuclear medicine 18 (1991), S. 32-37 
    Details
    ISSN: 1619-7089
    Keywords: Radionuclide renography ; Atrial natriuretic peptide ; Glomerular filtration rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A number of studies show that atrial natriuretic peptide (ANP) raises renal sodium excretion with a concomitant increase in glomerular filtration rate (GFR) in both experimental animals and normal humans. Studies using indirect evaluation of GFR have provided less consistent results in hypertensive patients. We studied the effects of intravenously administered (iv) α-human ANP on GFR in patients with hypertension by a radionuclide technique using technetium 99m diethylenetriaminepenta-acetic acid. In six patients (ANP group), GFR was determined under control conditions, during iv ANP (initial bolus of 0.5 μg/kg followed by a 21-min maintenance infusion at 0.05 μg · kg−1 · min−1) and during a recovery phase. In six other patients (control group), GFR was determined under control conditions, during saline iv infusion and during recovery. The two groups did not differ with respect to age, sex, basal blood pressure, heart rate or GFR. In the ANP group, the infusion of the peptide induced a significant decrease of mean blood pressure (from 133 ± 5 to 120 ± 5 mmHg, P 〈 0.01), no change in heart rate and a significant increase in GFR (from 104 ± 4 to 125 ± 5 ml/min, P 〈 0.01). During recovery, blood pressure, heart rate and GFR were not different from the values recorded under control conditions. No changes in blood pressure, heart rate or GFR (from 106 ± 5 to 108 ± 5 ml/min, n.s.) were detected during saline infusion in the control group. Our results demonstrated that in patients with essential hypertension, ANP induces an augmentation in GFR in spite of a decrease in blood pressure; this suggests a unique role for atrial peptide-related drugs in the treatment of human hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00177682
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