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  • 1
    Electronic Resource
    Electronic Resource
    Structural characterization of AlAs/AIP superlattices (2000)
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 76 (2000), S. 3885-3886 
    Details
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: (AlAs)n/(AlP)n (n=1–3) short-period superlattices were grown by gas-source migration-enhanced epitaxy at a low growth temperature. Dynamical-theory simulations of x-ray diffraction patterns were conducted and showed good agreement with experimentally obtained patterns. In addition, cross-sectional transmission electron microscopy analysis was performed, which confirmed that high-quality short-period superlattices of AlAs/AlP were grown. © 2000 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.126809
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  • 2
    Electronic Resource
    Electronic Resource
    THE ANGIOTENSIN-CONVERTING ENZYME INHIBITOR, PERINDOPRIL, PREVENTS CARDIAC HYPERTROPHY IN LOW-RENIN HYPERTENSIVE RATS (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. To examine whether an angiotensin-converting enzyme (ACE) inhibitor prevents left ventricular (LV) hypertrophy even in low-renin hypertension, we studied the effect of the administration of perindopril on cardiac hypertrophy induced by partial renal ablation in hypertensive rats.2. Rats that had undergone partial nephrectomy were randomly divided into four groups that received the following as drinking water: Group A, tap water; Group B, 1% sodium chloride (NaCl); Group C, NaCl + perindopril 3 mg/ kg per day; and Group D, NaCl + perindopril 1 mg/ kg per day. Plasma renin activity (PRA), angiotensin-II (AII) concentration and cardiac tissue AII were measured.3. Supplementation of NaCl following nephrectomy increased the blood pressure and cardiac weight compared with rats that had undergone nephrectomy alone (P〈0.05). Treatment with perindopril (3 mg/kg per day) did not affect the blood pressure and plasma AII but inhibited the increase of cardiac weight (P〈0.05). Left ventricular AII was decreased in cases of reduced renal mass hypertension, but was not changed by treatment with perindopril.4. These results demonstrate that perindopril may be able to prevent LV hypertrophy even in low-renin hypertension, which was not mediated by a reduction of blood pressure or suppression of the circulating and cardiac renin-angiotensin systems. Other mechanisms of ACE inhibitors may contribute to the cardioprotective effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01660.x
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  • 3
    Electronic Resource
    Electronic Resource
    EFFECT OF LONG-TERM TREATMENT WITH AN ANGIOTENSIN-CONVERTING ENZYME INHIBITOR ON THE RENIN-ANGIOTENSIN SYSTEM IN SPONTANEOUSLY HYPERTENSIVE RATS (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. To obtain information on regulation of the brain renin–angiotensin system, the effect of long-term administration of angiotensin-converting enzyme (ACE) inhibitor on brain renin and angiotensinogen mRNA was studied.2. Spirapril (3 mg/kg) was orally administered daily for 8 weeks to spontaneously hypertensive rats (SHR) from 12 weeks after birth. Renin and angiotensinogen mRNA in the brain and kidney were then quantitated by Northern blot analyses with [32P]-labelled rat renin and angiotensinogen cDNA as hybridization probes. Plasma renin activity (PRA), angiotensin II (AII) concentration, plasma ACE activity and brain tissue ACE activity were also measured.3. Compared with the control group, the Spirapril-treated group had significantly lower blood pressure (P〈0.01), significantly higher PRA (P〈0.01), a not significantly different plasma AII concentration, and lower plasma and brain ACE activities (P〈0.01). Interestingly, the brain renin and angiotensinogen mRNA levels of the two groups were similar, but the renal renin mRNA level was significantly higher in the Spirapril-treated group (P〈0.01).4. These results indicate that the mRNA levels of brain renin and angiotensinogen were not affected by chronic ACE inhibition in the circulation and suggest that AII in the brain might not be affected by systemic ACE inhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01381.x
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  • 4
    Electronic Resource
    Electronic Resource
    DISCREPANCY BETWEEN RENIN mRNA AND PLASMA RENIN LEVEL IN ANGIOTENSIN-CONVERTING ENZYME INHIBITOR-TREATED RATS (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. To investigate the role of transcriptional and post-transcriptional factors in increasing renin synthesis secondary to angiotensin-converting enzyme (ACE) inhibitors, we studied the changes in levels of renal renin mRNA, plasma renin and other hormonal factors.2. Spontaneously hypertensive rats were orally administered 10 mg/kg spirapril or vehicle daily for 3, 14 or 28 days.3. Plasma renin activity in the spirapril-treated group was significantly elevated compared with that in the vehicle group at any time (P〈0.01). However, there was no significant change in plasma angiotensin II concentration between the two groups. The ratio of renal renin mRNA to β-actin mRNA in the spirapril-treated group was higher than that in the control group (P〈0.01).4. At 28 days, plasma renin activity in the spirapril-treated group was significantly elevated compared with that at 14 days (P〈0.05). However, there was no change in renin mRNA between 14 and 28 days after ACE inhibitor administration.5. Plasma ACE activity in the treatment group was less than that in the control group at any time (P〈0.01).6. Our study demonstrated a non-proportional change in plasma renin and renal renin mRNA levels. It is suggested that the main determinant of the rate of renin synthesis after administration of an ACE inhibitor may be post-transcriptional factors, and that unknown mechanisms may be involved in the increase in plasma renin level after long-term administration of ACE inhibitor in addition to the short feedback mechanism brought about by the decrease in angiotensin II.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01497.x
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  • 5
    Electronic Resource
    Electronic Resource
    Increase in the blood pressure and decrease in the norepinephrine release in the ventrolateral medulla during intraventricular administration of hypertonic NaCl (1989)
    Springer
    Pflügers Archiv 414 (1989), S. 719-725 
    Details
    ISSN: 1432-2013
    Keywords: Blood pressure ; Ventrolateral medulla ; Intraventricular NaCl infusion ; Norepinephrine ; Microdialysis method
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Norepinephrine (NE) release in the ventrolateral medulla (VLM) was serially measured in anesthetized male Wistar rats during the rise in the blood pressure (BP) produced by acute intraventricular (ICV) administration of hypertonic (1.5 M) NaCl. Catecholamine release was determined by a brain microdialysis method using high performance liquid chromatography and electrochemical detector. The release of NE in the VLM was significantly decreased after ICV 1.5 M NaCl. In another set of rats, the pressor response to acute ICV 1.5 M NaCl was attenuated by selective administration of NE to the VLM using the microdialysis method. Chronic and continuous ICV infusion of 1.5 M NaCl to conscious rats caused an increase in BP on day 10 which was associated with a decrease in NE release in the VLM; concomitant ICV infusion of NE or of a synthetic NE precursor,l-threo-3,4-dihydroxyphenylserine (l-DOPS) prevented the rise in BP as well as the reduction in NE release. These results suggest that a decrease in the NE release of the VLM may contribute to the change in BP induced by ICV infusion of hypertonic saline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582141
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