Different distribution of two types of angiotensin II-generating enzymes in the aortic wall

Okunishi, Hideki; Miyazaki, Mizuo; Okamura, Tomio; Toda, Noboru

doi:10.1016/0006-291x(87)90533-x

Cited by 145 publications

(74 citation statements)

References 20 publications

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“…In other words, if the failure of captopril to block the pressor response to SUB indicates that Ang I-convertase can produce pressor amounts of Ang II from SUB, we would expect the convertase to produce some Ang II from Ang I in the presence of captopril. It may be that exogenously administered Ang I has easier access to ACE than to convertase, an hypothesis compatible with the findings of Okunishi et al 6 suggesting a primarily adventitial location for convertase versus an endothelial location for ACE; on the other hand, the present study suggests that captopril remains highly effective in endothelium-denuded vessels, indicating that ACE is not confined to the endothelium. This question may be resolved by measurements of both plasma and tissue Ang II after administration of intravenous SUB as well as by the advent of an effective in vivo chymase inhibitor.…”

Section: Discussionsupporting

confidence: 91%

Vasoconstrictor action of angiotensin I-convertase and the synthetic substrate (Pro11,D-Ala12)-angiotensin I.

et al. 1994

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A chymase (also referred to as angiotensin I-convertase) specific for the conversion of angiotensin (Ang) I to Ang II has been identified in human heart. This serine protease is also present in dog and marmoset vasculature. We examined the vasoconstrictor effects of Ang II putatively generated from an angiotensin-converting enzyme (ACE)-resistant convertase synthetic substrate (SUB) in vivo and in vitro. In marmosets, SUB (7 to 700 /ig/kg IV) or Ang I (0.1 to 30 /ig/kg) caused similar dose-dependent increases in mean arterial pressure (10 to 100 mm Hg) and decreases in heart rate. Pressor effects of SUB were slightly attenuated at low (but not high) doses by captopril (CAP, 1 mg/kg IV) and blocked by losartan (5 mg/kg IV); in contrast Ang I pressor effects were substantially blocked by both. In isolated canine superior mesenteric artery, Ang I-induced contraction was

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Section: Discussionsupporting

confidence: 91%

Vasoconstrictor action of angiotensin I-convertase and the synthetic substrate (Pro11,D-Ala12)-angiotensin I.

et al. 1994

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“…We have found that in vascular tissues in rats and rabbits, Ang I is converted to Ang II by ACE alone, while in humans, monkeys, dogs, and hamsters, Ang I is possibly converted by both ACE and chymase. [14][15][16] These species-dependent pathways of vascular Ang II production strongly suggest the involvement of Ang II produced by chymase, and may be the cause of the apparent discrepant action of ACE inhibitors in the rat and human studies. Ang II-producing ability in human blood vessels is approximately 70% dependent on chymase, and only 30% dependent on ACE.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1999

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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

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“…formation in many tissues suggests the presence of noninhibitable converting enzyme activity (Okunishi et al, 1987) or other forms of angiotensin I convertase such as chymase (Urata et al, 1990). …”

Section: Resultsmentioning

confidence: 99%

Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

1995

Clinical Endocrinology

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Although the biosynthesis of aldosterone in the zona glomerulosa of the adrenal cortex is known to be regulated by a whole array of other agents (ACTH, serotonin, dopamine, atrial natriuretic peptide, acetylcholine) (Miiller, 1988) in this short review we will concentrate on the interplay between the two major regulators, angiotensin I1 and potassium ion ( K ' ) . For many years, specific diseases as well as pathophysiological clinical situations have taught us much about the relation between the renin-angiotensin system and potassium, which has been further explored by animal experimentation. More recently, considerable progress has been achieved in our understanding of the mode of action of both angiotensin I1 and K+ at the cellular level, putting their interplay into a new light. Clinical obsewatlonsThere are many diseases and clinical settings which are caused by abnormalities of secretion of one or other member of the renin-angiotensin system and of the mineralocorticoid family of compounds, mainly aldosterone, or in which these hormones react to or adapt to disturbances of potassium economy. The latter is easily disturbed, which is not surprising given that the total potassium available in the extracellular fluid is 65 mmol, compared with some 5 mol of intracellular potassium. This is distributed mainly in muscle (approximately 2650 mmol), with the erythrocytes, liver and bones each accounting for approximately 250-300 mmol. The turnover of body potassium reflects a daily intake of approximately 100 mmol in the diet, and equivalent excretion mainly by the kidney and to a smaller extent in the stool.In circumstances under which the renin-angiotensin system is primarily stimulated, secondary hyperaldosteronCorrespondence: Professor M.

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Different distribution of two types of angiotensin II-generating enzymes in the aortic wall

Cited by 145 publications

References 20 publications

Vasoconstrictor action of angiotensin I-convertase and the synthetic substrate (Pro11,D-Ala12)-angiotensin I.

Vasoconstrictor action of angiotensin I-convertase and the synthetic substrate (Pro11,D-Ala12)-angiotensin I.

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

Potassium‐angiotensin interplay in the regulation of aldosterone biosynthesis

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