Effects of Angiotensin II on DNA, RNA and Protein Synthesis

Khairallah, Philip A.; Robertson, Abel L.; Davila, D.

doi:10.1007/978-3-642-65343-8_28

Cited by 61 publications

(32 citation statements)

References 7 publications

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“…Angiotensin II contracts efferent arterioles more markedly than afferent arterioles and increases blood pres sure (18). Sustained stimulation by angiotensin II pro motes the proliferation of vascular smooth muscle cells and injures blood vessels (19,20). Imidapril inhibits the conversion of angiotensin I to angiotensin II in blood and vascular walls and prevents injuries of renal afferent and efferent arterioles.…”

Section: Discussioncontrasting

confidence: 41%

Histopathological Investigation on Salt-Loaded Stroke-Prone Spontaneously Hypertensive Rats, Whose Biochemical Parameters of Renal Dysfunction Were Ameliorated by Administration of Imidapril

Fujiwara¹,

Yuasa²,

Ogiku

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-Ourprevious studies showed that imidapril prevented the occurrence of cerebral stroke and ameliorated biochemical parameter changes of renal dysfunction at a dose that did not inhibit the progres sion of hypertension in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). To confirm these findings, a histopathological investigation was conducted on the kidney of salt-loaded (from 11 to 16 weeks of age) SHRSP, which was the subject of the preceding study. Their brains and hearts were also ex amined. Histopathologically, renal lesions such as fibrinoid necrosis and proliferative arteritis of small calibration arteries, necrotizing glomerulitis and tubular degeneration, and cerebral hemorrhage and slight cardial hypertrophy were observed in salt-loaded control SHRSP. The occurrence of these lesions were prevented in a dose-dependent manner by the administration of imidapril (1 and 2 mg/kg/day). Especially, the preventive effects on the renal lesions were apparently noted. Enalapril also prevented these renal lesions, but its preventive effects were weaker than those of imidapril at the same dose (2 mg/kg/day). It became evident from the results of the present and previous studies that imidapril reduced renal biochemical and histopathological injuries.

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Section: Discussioncontrasting

confidence: 41%

Histopathological Investigation on Salt-Loaded Stroke-Prone Spontaneously Hypertensive Rats, Whose Biochemical Parameters of Renal Dysfunction Were Ameliorated by Administration of Imidapril

Fujiwara¹,

Yuasa²,

Ogiku

et al. 1994

Japanese Journal of Pharmacology

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“…Cardiac ACE activity as well as the rate of angiotensin-II production is enhanced in hypertrophied rat hearts (12) and associated with altered diastolic properties possibly contributing to the vulnerability of diastolic function in hypertrophy during hypoperfusion ( 19). Other potential actions of the cardiac renin angiotensin system include a trophic effect, as suggested by identifying angiotensin-il as a growth-promoting factor in cardiac muscle cells (20)(21)(22). This hypothesis is supported by recent data demonstrating that ACE inhibitors given in very low doses not affecting blood pressure prevented the development of cardiac hypertrophy in pressure-overloaded rats (23, 24).…”

Section: Introductioncontrasting

confidence: 37%

Increased angiotensin-I converting enzyme gene expression in the failing human heart. Quantification by competitive RNA polymerase chain reaction.

Studer¹,

Reinecke²,

Müller³

et al. 1994

J. Clin. Invest.

187

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Local activation of the components of the renin angiotensin system in the heart is regarded as an important modulator of cardiac phenotype and function; however, little is known about their presence, regulation, and potential activation in the human heart. To investigate the gene expression of major angiotensin-II-forming enzymes in left ventricles of normal (n = 9) and failing human hearts (n = 20), we established a competitive RNA-polymerase chain reaction (PCR) for mRNA quantification of angiotensin-I converting enzyme (ACE) and human heart chymase. For each gene, competitor RNA targets with small internal deletions were used as internal standards to quantify the original number of transcripts and to control reverse transcription and PCR. In PCR, each target and the corresponding competitor were amplified by competing for the same primer oligonucleotides. The variability of ACE RNA-PCR was 11% indicating a high reproducibility of this method. In addition, ACE mRNA levels obtained by competitive RNA-PCR correlated favorably with traditional slot blot hybridization (r = 0.69, n = 10; P < 0.05). Compared with nonfailing hearts, the number of ACE transcripts referred to 100 ng of total RNA was increased threefold in patients with chronic heart failure (4.2±2.5 vs. 12.8±6 x 105; P < 0.0005). In contrast, no significant difference was found in chymase gene expression between normal and failing hearts. Thus, the expression of the cardiac ACE but not of human heart chymase is upregulated in failing human heart indicating an activation of the cardiac renin-angiotensin system in patients with advanced heart failure. (J. Clin. Invest. 1994. 94:301-310.)

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“…All also increases DNA turnover, RNA content turnover, and protein synthesis in isolated atrial and ventricular myocytes (38)(39)(40). In addition, All induces expression of transforming growth factor i, platelet derived growth factor and epidermal growth factor as well as protooncogenes c-fos, cmyc and c-j un in cardiac and vascular cells (41)(42)(43).…”

Section: Discussionsupporting

confidence: 38%

Effects of Early Treatment of Spontaneously Hypertensive Rats with an Angiotensin Converting Enzyme Inhibitor on Blood Pressure, Baroreflex Function and Cardiac Hypertrophy.

Edwards

Zhang

et al. 1994

Hypertens Res

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The purpose of the current study was to define the critical phase in the development of genetic hypertension during which time application of an angiotensin converting enzyme inhibitor, captopril, would produce long-term antihypertensive effects. In addition, we evaluated two potential mechanisms underlying the long-term antihypertensive effect of early treatment with captopril: alterations in baroreflex sensitivity and cardiovascular remodeling. Separate groups of SHR were placed on captopril in utero, or at 1, 7 or 30 days post birth. The length of therapy was 1-2 months. We also removed captopril from SHR treated in utero at 1, 7 and 30 days post birth. Mean arterial pressures and heart weights were monitored in all rats between 3-4 months of age. Tests of baroreflex function (control of heart rate) were performed in 4-and 9-month old rats using intravenous infusion of phenylephrine and nitroprusside to raise and lower blood pressure, respectively. Mean arterial pressures of SHR placed on captopril at 1 (145 ± 9), 7(141 ± 4) and 30 days (129 ± 4) for 1 month were significantly lower than control SHR (176 ± 7, mmHg), but higher than SHR treated in utero with captopril and maintained on therapy for two months (114 ± 4 mmHg). Similarly, SHR treated with captopril in utero with treatment discontinued at 1, 7 or 30 days post birth showed significantly lower mean arterial pressures than untreated SHR. None of these groups showed blood pressures as low as SHR treated in utero until 2 months of age. These rats continued to show normotensive mean arterial pressures even at 9 months of age. In 4-and 9-month-old captopril treated SHR the sensitivities of baroreflex control of heart rate (slope of the relationship between changes in mean arterial pressure and change in pulse interval) were significantly greater than in untreated SHR. Additionally, the heart weight to body weight ratios of these rats were significantly lower than control rats. These results indicate that early treatment with captopril enhances baroreflex control of heart rate in SHR. This enhancement of baroreflex function may be permanent since it persisted even after captopril had been stopped for 7 months; moreover, the effect of captopril on baroreflex sensitivity may be due to mechanisms other than lowering arterial blood pressure. Our data suggest that captopril treatment applied in short-term intervals from in utero to 2 months of age is effective in lowering the magnitude of hypertension in SHR. Augmentation of baroreflex function and prevention of remodeling of the cardiovascular system may contribute to the permanent prevention of the evelopment of hypertension in SHR treated with captopril. (Hypertens Res 1994; 17: 243-251) Key Words: angiotensin converting enzyme inhibitor, spontaneously hypertensive rats The brain has been found to possess a tissue reninangiotensin system (RAS) independent of the plasma RAS (1-4). Anatomical and functional studies have suggested that enhanced RAS activity in the central nervous system may be involved in t...

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Effects of Angiotensin II on DNA, RNA and Protein Synthesis

Cited by 61 publications

References 7 publications

Histopathological Investigation on Salt-Loaded Stroke-Prone Spontaneously Hypertensive Rats, Whose Biochemical Parameters of Renal Dysfunction Were Ameliorated by Administration of Imidapril

Histopathological Investigation on Salt-Loaded Stroke-Prone Spontaneously Hypertensive Rats, Whose Biochemical Parameters of Renal Dysfunction Were Ameliorated by Administration of Imidapril

Increased angiotensin-I converting enzyme gene expression in the failing human heart. Quantification by competitive RNA polymerase chain reaction.

Effects of Early Treatment of Spontaneously Hypertensive Rats with an Angiotensin Converting Enzyme Inhibitor on Blood Pressure, Baroreflex Function and Cardiac Hypertrophy.

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