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  • 21
    Electronic Resource
    Electronic Resource
    Variable-temperature and -pressure multinuclear magnetic resonance study of solvent exchange at the tris(ethylenediamine)nickel(II) ion in ethylenediamine (1992)
    s.l. : American Chemical Society
    Inorganic chemistry 31 (1992), S. 536-538 
    Details
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ic00030a003
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  • 22
    Electronic Resource
    Electronic Resource
    Photoinduced alkylation of five-membered heteroaromatic compounds via electron-transfer reaction: heterodimer cation radical intermediacy (1981)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 103 (1981), S. 5570-5572 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00408a050
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  • 23
    Electronic Resource
    Electronic Resource
    IN VIVO AND IN VITRO EFFECTS OF ATRIAL NATRIURETIC PEPTIDE ON RENIN RELEASE (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study investigated the effect of atrial natriuretic peptide on renin release from the kidney. The in vitro direct effect was examined in the animal experiment using renal cortical slices of rat, and the in vivo effect was observed in the human infusion study.2. In the in vitro experiments, α-human atrial natriuretic peptide (α-hANP) ranging 10−9 to 10−6 mol/L did not change the basal renin release rate from the renal cortical slices (∼9% at 10−6 mol/L, NS). Isoproterenol (10−6 mol/L) increased renin release by 40% (P 〈 0.001), whereas angiotensin II (10−6 mol/L) suppressed it by 48% (P 〈 0.001). However, α-hANP did not affect the stimulative effect of isoproterenol or the inhibitory effect of angiotensin II.3. Also in the human study, infusion of 25 ng/kg per min α -hANP failed to change the plasma renin activity in normotensive subjects (–4%) or patients with essential hypertension (+5%), or even in patients with raised renin levels such as renovascular hypertension (+ 10%) or congestive heart failure (-13%).4. These results put forth negative views on the direct involvement of atrial natriuretic peptide in renin release from the juxtaglomerular apparatus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00408.x
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  • 24
    Electronic Resource
    Electronic Resource
    ATRIAL NATRIURETIC PEPTIDE INHIBITS THE ALDOSTERONE RESPONSE TO METOCLOPRAMIDE IN PATIENTS WITH GLOMERULAR DISEASE AND ESSENTIAL HYPERTENSION (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We examined the effects of metoclopramide (MCP: 10 mg i.v.) on plasma atrial natriuretic peptide (ANP) and aldosterone concentrations (PAC) and the effect of ANP on MCP-induced PAC in four patients with primary glomerular diseases and seven patients with essential hypertension.2. MCP injection caused no significant changes in plasma ANP. MCP produced a marked increase in PAC without a significant change in plasma renin activity.3. The increase in PAC induced by MCP injection was markedly attenuated when preceded by the infusion of ANP (25 ng/kg per min).4. These results suggest that the dopaminergic D2 mechanism is not involved in the regulation of ANP secretion and that ANP modulates the dopaminergic regulation of aldosterone secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01491.x
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  • 25
    Electronic Resource
    Electronic Resource
    ANGIOTENSIN II BLUNTS, WHILE AN ANGIOTENSIN-CONVERTING ENZYME INHIBITOR AUGMENTS, REFLEX SYMPATHETIC INHIBITION IN HUMANS* (1999)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 26 (1999), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The role of angiotensin (Ang)II in and the effects of angiotensin-converting enzyme (ACE) inhibitors on the regulation of sympathetic neural activity were examined in humans.2. We measured baseline values of muscle sympathetic nerve activity (MSNA) and its reflex inhibition in 28 patients with essential hypertension with elevated plasma renin activity (PRA; 〉1.0 ng/mL per h = 0.28 ng/L per s) before and after either acute or chronic oral administration of an ACE inhibitor or placebo and in 20 normotensive subjects before and after infusion of either AngII (5 ng/kg per min = 4.8 pmol/kg per min) or vehicle (5% dextrose). Muscle sympathetic nerve activity was recorded from the tibial nerve and its reflex inhibition was evaluated during pressor responses to bolus injection of phenylephrine (2 μg/kg, i.v.).3. Blood pressure was significantly decreased (P 〈 0.01) after the acute oral administration of captopril (25 mg), accompanied by a slight increase in MSNA in patients with essential hypertension compared with control patients who received placebo administration. Reflex changes in MSNA were significantly augmented after oral administration of captopril (–4.1±0.5 vs–6.2±0.6%/mmHg, respectively; P 〈 0.01), with a significant reduction of plasma AngII, while they were not affected by placebo administration.4. In contrast, acute AngII infusion was accompanied by decreases in both PRA and MSNA in normotensive subjects. Reflex changes in MSNA were significantly reduced after AngII infusion (–11.0±0.8 vs–7.4±1.0%/mmHg, respectively; P 〈 0.01) but not after vehicle alone.5. Chronic ACE inhibition by 12 week oral imidapril administration (5–10 mg/day) significantly (P 〈 0.05) decreased baseline values of MSNA, which were accompanied by a significant (P 〈 0.05) increase in the reflex inhibition of MSNA, while plasma concentrations of noradrenaline were unaffected.6. These results indicate that AngII blunts reflex inhibition of sympathetic neural activity and that inhibition of the renin–angiotensin system by an ACE inhibitor augments reflex regulation of sympathetic neural activity and reduces baseline values in patients with essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.1999.03122.x
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  • 26
    Electronic Resource
    Electronic Resource
    TIME-DEPENDENT CYCLOSPORINE A-INDUCED NEPHROTOXICITY IN RATS (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. We investigated the toxicity of cyclosporine A (CsA) with reference to the timing of its administration in rats.2. To elucidate the time-dependent effects of CsA on renal function and survival rate, CsA (75 mg/kg per day) or vehicle was orally administered once daily at four different times (3,9, 15 and 21 h after lights on; HALO) over a period of 21 days to male Wistar rats (n= 56) kept in rooms with a 12 h light-dark cycle.3. On the 7th day after treatment, creatinine clearances (Ccr) of groups dosed at 3 and 9 HALO (inactive period) were not reduced in comparison with clearances of time-matched control rats, whereas Ccr significantly decreased in rats dosed at 15 and 21 HALO (active period). Cyclosporine A markedly increased urinary N-acetyl-β-D-glucosaminidase (NAG) excretion in all dosed groups at the 7th day after treatment, except for rats dosed at 3 HALO. In rats dosed at 3 HALO, Ccr decreased progressively; however, it did not decrease progressively in rats dosed at 9 HALO. In surviving rats treated during the inactive period, urine NAG subsequently returned to control levels. Survival rates were greater in animals dosed during inactive periods than those in groups dosed during active periods.4. Significant differences in CsA-induced toxicity were obvious as a result of the timing of its administration. A different time course between Ccr and urine NAG excretion was observed during repeated CsA administration. Degenerative changes in proximal tubules were demonstrated after chronic administration of CsA, suggesting that severe and persistent tubular damage cannot be assessed by urinary NAG excretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02228.x
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  • 27
    Electronic Resource
    Electronic Resource
    ANGIOTENSIN II RECEPTORS IN CARDIAC LEFT VENTRICLES OF DAHL RATS (1998)
    Melbourne, Australia : Blackwell Science Asia Pty. 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. Dahl Iwai salt-sensitive (DS) rats have been reported as becoming hypertensive with left ventricular hypertrophy (LVH) and heart failure when on a high-salt diet. Their circulating renin–angiotensin system (RAS) has been reported to be suppressed. To evaluate the role of angiotensin II (AngII) type 1 and type 2 receptors (AT1 and AT2, respectively) in LVH, we compared cardiac AT1 and AT2 receptors in 10-week-old DS rats and Dahl Iwai salt-resistant (DR) rats.2. Seven pairs of 6-week-old male DS and DR rats were fed either a low- or high-salt diet (0.3 or 8% NaCl, respectively) for 4 weeks. Left ventricular AngII receptors were measured by radioligand binding assays using [125I]-[Sar1,Ile8]-AngII in plasma membrane fractions from these four groups. The AT1 and AT2 receptors were distinguished using their specific antagonists CV 11974 and PD 123319, respectively.3. The high-salt diet increased blood pressure and the left ventricle:bodyweight ratio in DS rats. However, neither Bmax for AT1 and AT2 receptors nor Kd for [125I]-[Sar1,Ile8]-AngII differed between the groups. These results are different from those of other reports of pressure-overload LVH, such as spontaneously hypertensive rats or renovascular hypertension rats, in which AT1 and AT2 receptors were reported to be up-regulated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.t01-16-.x
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  • 28
    Electronic Resource
    Electronic Resource
    AT1 RECEPTOR ANTAGONIST, TCV 116, DOES NOT PREVENT CARDIAC HYPERTROPHY IN SALT-LOADED DAHL SALT-SENSITIVE RATS (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We investigated the effects of direct blockade of angiotensin II (AngII) by a potent, non-peptide angiotensin II type 1 (AT1) receptor antagonist, TCV 116, on the development of cardiac hypertrophy in salt-loaded Dahl salt-sensitive rats.2. Six week old male Dahl salt-sensitive rats (n= 44) were fed a 4% salt diet and were simultaneously given various doses of TCV 116 orally for 7 weeks. Each control group received vehicle alone.3. Dietary high salt intake elevated blood pressure continuously and caused left ventricular hypertrophy in rats treated with vehicle. TCV 116 had a minor effect on the rise in blood pressure. Left ventricular mass (left ventricular weight/body-weight) decreased slightly but not significantly, in rats treated with 3mg/kg per day of TCV 116 (n= 8). Higher doses of TCV 116 (6 and 10 mg/kg per day; n= 8 each) did not show a decrease in left ventricular mass compared with the vehicle control.4. These results suggest that AngII blockade has only minor effects on hypertension and on cardiac hypertrophy in salt-loaded Dahl salt-sensitive rats and that the renin-angiotensin system may not contribute to the development of cardiac hypertrophy in Dahl salt-sensitive rats on a moderately high-salt diet.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02824.x
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  • 29
    Electronic Resource
    Electronic Resource
    CHARACTERISTIC LOCALIZATION OF α1- and α2-ADRENOCEPTORS IN THE HUMAN KIDNEY (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The localization of α-adrenoceptors in the plasma membranes of human kidney were investigated by radioligand binding, using an α1-antagonist, [3H]-bunazosin, and an α2-antagonist, [3H]-rauwolscine.2. Both the maximum binding (Bmax) and dissociation constant (Kd) of [3H]-bunazosin were greater in the cortex than in the medulla. The Bmax of [3H]-rauwolscine in the medulla was greater than in the cortex.3. Thus, α1-adrenoceptors appeared to be localized predominantly in the cortex, while the α2-adrenoceptors were mainly present in the medulla of the human kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01735.x
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  • 30
    Electronic Resource
    Electronic Resource
    The extrarenal effects of aldosterone on the distribution of extracellular fluid in conscious adrenalectomized-nephrectomized rats (1985)
    Springer
    Pflügers Archiv 404 (1985), S. 273-277 
    Details
    ISSN: 1432-2013
    Keywords: Arterial pressure ; Plasma volume ; ECFV ; Interstitial fluid ; 131I-RISA ; 35S-Na2SO4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to examine the extrarenal roles of aldosterone in cardiovascular homeostasis, the present study compared blood pressure, extracellular fluid volume (ECFV) and plasma volume (PV) in the three following groups: 10 nephrectomized (NX) rats, 10 nephrectomized-adrenalectomized (NX-AX) rats, and 10 NX-AX and aldosterone-treated (NX-AX-A) rats. Two-hundred and fifty micrograms of aldosterone, mixed with sesame oil, was given subcutaneously in the NX-AX-A rats. Mean arterial pressure (MAP) was recorded through previously implanted carotid catheters. ECFV and PV were measured using35S-Na2SO4 and131I-RISA, respectively, 24 h after the operation. These measurements were performed in an unanesthetized and unrestricted condition. MAP gradually increased in the NX group, while a gradual decrease was observed in the other groups. However, MAP was significantly higher in the NX-AX-A group than in the NX-AX group 6 h after the operation and thereafter. Changes in body weight were comparable in the three groups 24 h after the operation. ECFV and PV were both reduced in the NX-AX and NX-AX-A groups as compared to the NX group (P〈0.001 NX-AX vs NX, andP〈0.05 andP〈0.025 NX-AX-A vs NX, respectively). Although ECFV was comparable in the NX-AX and the NX-AX-A groups, PV was significantly greater in the NX-AX-A group than in the NX-AX group (P〈0.05). There was a significant positive correlation between MAP and PV in the rats as a whole (r=0.68,P〈0.001). The area under the curve for plasma aldosterone concentration (PAC), which was estimated in a separate group, was similar in the NX and the NX-AX-A groups, but definitely decreased in the NX-AX group. Thus, it is suggested that aldosterone redistributed ECFV so as to maintain intravascular volume, contributing to attenuation of the fall in blood pressure occuring after adrenalectomy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581250
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