Angiotensin II stimulates collagen synthesis in cultured vascular smooth muscle cells

Katô, Hiroshi; Suzuki, Hiromichi; Tajima, S.; Ogata, Yasuhide; Tominaga, Takehiko; Sato, Akira; Saruta, Takao

doi:10.1097/00004872-199109010-00003

Cited by 244 publications

(109 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…There is much evidence to suggest that angiotensin II is involved in the production of myocardial (Pfeffer et al, 1982;Hall & Karlberg, 1986;Clozel et al, 1989;Childs et al, 1990;Schunkert et al, 1990;Brilla et al, 1991;Lindpaintner & Ganten, 1991) and vascular wall hypertrophy (Kato et al, 1991). ACE inhibition increases the levels of bradykinin which appears to give protection against the development of cardiovascular hypertrophy (Wiemer et al, 1991).…”

Section: Plasma Electrolytes and Renin Activitymentioning

confidence: 99%

Replacement of salt by a novel potassium‐ and magnesium‐enriched salt alternative improves the cardiovascular effects of ramipril

Mervaala

Paakkari

Laakso³

et al. 1994

British J Pharmacology

View full text Add to dashboard Cite

1The influence of salt (sodium chloride; NaCl) (an additional 6% in the diet) and that of a novel sodium-reduced, potassium-, magnesium-, and L-lysine-enriched salt alternative on the cardiovascular effects of ramipril was studied in stroke-prone spontaneously hypertensive rats in a 6-week study. The intake of sodium chloride was adjusted to the same level by adding the salt alternative at a 1.75 times higher amount than regular salt. 2 Salt produced a marked rise in blood pressure and induced cardiac hypertrophy and significant mortality, while the salt alternative neither increased blood pressure nor caused any mortality and produced less cardiac hypertrophy than salt. 3 Ramipril treatment at a daily dose of 3 mg kg' normalized blood pressure and prevented the development of cardiac hypertrophy of rats on control diet. These effects of ramipril were blocked by the addition of salt but were only slightly attenuated by the addition of the salt alternative. The mortality in -the salt group was prevented by ramipril. 4 Responses of mesenteric arterial rings in vitro were examined at the end of the study. Salt, but not the salt alternative, increased vascular contractile responses to noradrenaline. Ramipril treatment improved the arterial relaxation responses to acetylcholine and to sodium nitroprusside. The vascular relaxation enhancing effect of ramipril was blocked by salt but only slightly attenuated by the salt alternative. 5 Ramipril treatment did not significantly increase plasma renin activity in the presence or in the absence of salt supplementation. The salt alternative did not cause hyperkalaemia, either alone or in combination with ramipril treatment. 6 Both salt supplementations, irrespective of ramipril treatment, induced a six to eight fold increase in the urinary excretion of calcium. There was an expected 90 to 140% rise in the urinary excretion of magnesium and 200% rise in the urinary excretion of potassium in the salt alternative group. Salt also produced an approximately 50% increase in magnesuria. 7 Our findings suggest that replacement of salt by the potassium-, magnesium-and L-lysine-enriched salt alternative improves the cardiovascular effects of ramipril. In the present study the beneficial effect was related to the increased intakes of potassium and/or magnesium and L-lysine from the salt alternative because the amount of sodium chloride was the same.

show abstract

Section: Plasma Electrolytes and Renin Activitymentioning

confidence: 99%

Replacement of salt by a novel potassium‐ and magnesium‐enriched salt alternative improves the cardiovascular effects of ramipril

Mervaala

Paakkari

Laakso³

et al. 1994

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Studies have shown that: (1) vascular hypertrophy is reduced by angiotensinconverting enzyme (ACE) inhibitors or Ang II receptor antagonists; [1][2][3][4] (2) components of the reninangiotensin system, such as ACE, 5,6 and angiotensinogen mRNA 7 are activated or increased in the area of vascular hypertrophy; and (3) Ang II promotes migration, proliferation, and hypertrophy of vascular smooth muscle cells, and generation of extracellular matrix, as seen in in vitro and in vivo models. [8][9][10][11] Because intima hyperplasia after balloon injury could be reduced by treatment of ACE inhibitors in rats, 3 ACE inhibitors were expected to be effective in clinical use. However, ACE inhibitors failed to reduce the restenosis seen after clinical PTCA.…”

Section: Introductionmentioning

confidence: 99%

Effect of an angiotensin II receptor antagonist, candesartan cilexetil, on canine intima hyperplasia after balloon injury

et al. 1999

View full text Add to dashboard Cite

The roles of angiotensin (Ang) II as produced by two different enzymes, angiotensin-converting enzyme (ACE) and chymase, were investigated in a canine experimental model where intima hyperplasia was induced by balloon catheterization in the common carotid and femoral arteries. The animals received oral candesartan cilexetil (3 mg/kg) or enalapril (10 mg/kg) twice a day for 5 weeks. After 1 week of active drug therapy, the common carotid and femoral arteries were unilaterally injured by balloon catheterization. In the common carotid arteries, both ACE and chymase activities were increased by the injury, with the increase in chymase activities being greater than that in ACE activities. In the femoral arteries, ACE, but not chymase, activities were significantly increased by the injury. Both candesartan cilexetil and enalapril reduced blood

show abstract

“…Kato et al (1991) showed that Ang II stimulated collagen synthesis in cultured SMCs. ACE inhibition effectively prevents left ventricular hypertrophy, even without a reduction in afterload (Linz et al 1992;Nakamura et al 1993;Simko, 1996), and coronary artery hypertrophy (Takemoto et al 1997).…”

mentioning

confidence: 99%

Effect of Captopril in L-Name-Induced Hypertension on the Rat Myocardium, Aorta, Brain and Kidney

1999

View full text Add to dashboard Cite

summary Long-term administration of N G -nitro-¬_arginine methyl ester (¬_NAME) induces development of hypertension and hypertrophy of the left ventricle in rats. The aim of the present study was to demonstrate the effect of chronic ¬_NAME treatment on DNA and RNA concentration, and protein synthesis in the rat heart, aorta, brain and kidney and to determine the effect of angiotensin converting enzyme (ACE) inhibitor captopril on these potential alterations. Four groups of rats were investigated: control, ¬_NAME (40 mg kg¢ day¢), captopril (100 mg kg¢ day¢), and ¬_NAME (40 mg kg¢ day¢) + captopril (100 mg kg¢ day¢). NO synthase activity in the heart, aorta, brain and kidney was found to be decreased in the ¬_NAME group. In the group of rats treated with ¬_NAME + captopril, captopril did not affect NO synthase inhibition. Captopril, however, completely prevented development of hypertension and left ventricular hypertrophy in this group. In the ¬_NAME group, DNA and RNA concentrations, as well as [14 C]leucine incorporation, were significantly increased in all the tissues investigated. In the ¬_NAME + captopril group, captopril completely prevented the enhancement of DNA and RNA concentrations and [ 14 C]leucine incorporation in all tissues compared to the ¬_NAME group. Moreover, a significant decrease in RNA concentration and [ 14 C]leucine incorporation below control values was found in the captopril group as well as the ¬_NAME + captopril group in all the tissues investigated. We conclude that captopril prevented the development of hypertension and increase in nucleic acid concentration and protein synthesis in the heart, aorta, brain and kidney in rats treated with ¬_NAME + captopril. However, this protective effect of captopril was not associated with increased NO synthase activity in this model of hypertension.

show abstract

Angiotensin II stimulates collagen synthesis in cultured vascular smooth muscle cells

Cited by 244 publications

References 0 publications

Replacement of salt by a novel potassium‐ and magnesium‐enriched salt alternative improves the cardiovascular effects of ramipril

Replacement of salt by a novel potassium‐ and magnesium‐enriched salt alternative improves the cardiovascular effects of ramipril

Effect of an angiotensin II receptor antagonist, candesartan cilexetil, on canine intima hyperplasia after balloon injury

Effect of Captopril in L-Name-Induced Hypertension on the Rat Myocardium, Aorta, Brain and Kidney

Contact Info

Product

Resources

About