Induction of angiotensin I-converting enzyme in rat lung with captopril (SQ 14225)

Fyhrquist, Frej; Forslund, Terje; Tikkanen, Ilkka; Grönhagen‐Riska, Carola

doi:10.1016/0014-2999(80)90189-2

Cited by 86 publications

(13 citation statements)

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“…Our results in fact indicate that CCX could also have ACE inhibitory properties. An elevation in plasma ACE concentration has been documented in humans and rats treated with ACE inhibitors (Boomsma, Debruyn, Derkx, & Schalekamp, 1981;Fyhrquist, Forslund, Tikkanen, & Grönhagen-Riska, 1980;Wu & Ding, 2001). In previous works, our research group also demonstrated increased ACE activity in the plasma from SHR that had been long-term treated with captopril (Miguel et al, 2007).…”

Section: Discussionsupporting

confidence: 49%

Mechanisms for antihypertensive effect of CocoanOX, a polyphenol-rich cocoa powder, in spontaneously hypertensive rats

Quiñones

Sánchez

Muguerza

et al. 2011

Food Research International

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Section: Discussionsupporting

confidence: 49%

Mechanisms for antihypertensive effect of CocoanOX, a polyphenol-rich cocoa powder, in spontaneously hypertensive rats

Quiñones

Sánchez

Muguerza

et al. 2011

Food Research International

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“…Previous investigations have also observed that the magnitude of serum ACE inhibition poorly predicts the hypotensive response in normotensive and hypertensive animal models.29-34 Chronic treatment with both enalapril and captopril has been shown to cause induction of total circulating ACE activity; therefore, this lack of correlation is not unexpected. [35][36][37] In our study, the long-term blood pressure response correlated best with renal ACE activity. The nature of this relation is not known.…”

Section: Blood Pressure Responsementioning

confidence: 75%

Differential effects of captopril and enalapril on tissue renin-angiotensin systems in experimental heart failure.

et al. 1992

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Backgrund. Angiotensin converting enzyme (ACE) inhibitor therapy elicits beneficial responses from patients with heart failure. We hypothesized that a major site of action of these drugs is tissue ACE and that ACE inhibitors might differ in their ability to inhibit tissue ACE. To test this hypothesis, we assessed the effects of captopril and enalapril on blood pressure and renal function and on serum and tissue ACE activities in sham-operated rats and rats with heart failure induced by coronary artery ligation.Methods and Results. During short-term (1-week) treatment, captopril (200 mg kg`-day-') and enalapril (25 mg * kg`* day-') elicited equipotent effects on blood pressure and inhibition of serum ACE activity (85%). The effects of long-term treatment (47 days) were then studied beginning 45±5 days after coronary ligation in four treatment groups: sham-operated, vehicle (n=14); heart failure, vehicle (n=10); heart failure, captopril (n=8); and heart failure, enalapril rats (n=7 Conclusions. These data suggest that chronic treatment with these two agents elicits differential effects on tissue ACE activities and renal angiotensinogen regulation. The differential renal effects of these agents may be important in the treatment of heart failure. (Circulation 1992;86:1566-1574 KEY WORDs * angiotensin converting enzymes angiotensin II A ngiotensin II is produced in vivo in the systemic circulation or at local tissue sites. In response to decreases in cardiac function, as in acute or decompensated heart failure, the endocrine renin-angiotensin system is activated. Increased circulating levels of angiotensin II may serve a vasoconstrictor role or promote renal sodium retention. Additionally, acute inhibition of circulating angiotensin converting enzyme

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“…22 Although it is tempting to claim that the signaling via ACE that is initiated by the binding of an ACE inhibitor is protective/ beneficial to vascular cell function and or the development of cardiovascular disease, this is currently speculation because the end point identified in the present study, ie, an increase in the expression of ACE itself, could also be expected to have deleterious effects by leading to the enhanced generation of angiotensin II. However, it should be noted that the latter phenomenon has been demonstrated in lung tissue and plasma from ACE inhibitor-treated rats 21,35 and in serum from patient populations which distinctly benefit from ACE inhibitor therapy. 36,37 Additional investigation is therefore required to identify additional components of the ACE signaling cascade that influence endothelial cell function.…”

Section: Discussionmentioning

confidence: 98%

Angiotensin-Converting Enzyme Is Involved in Outside-In Signaling in Endothelial Cells

Kohlstedt

Brandes

Müller‐Esterl

et al. 2004

Circulation Research

123

118

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Abstract-Not all of the cardiovascular effects of angiotensin-converting enzyme (ACE) inhibitors can be attributed to changes in angiotensin II and bradykinin levels. Because the cytoplasmic tail of ACE is phosphorylated, we determined whether ACE inhibitors affect the phosphorylation of ACE and whether ACE possesses the characteristics of a signal transduction molecule. The ACE inhibitors ramiprilat and perindoprilat, and the substrate bradykinin (but not angiotensin I), enhanced the activity of ACE-associated CK2 and the phosphorylation of ACE Ser 1270 in cultured endothelial cells. Mitogen-activated protein kinase kinase 7 and c-Jun N-terminal kinase (JNK) coprecipitated with ACE, and stimulation of endothelial cells with ACE inhibitors increased the activity of ACE-associated JNK and elicited the accumulation of phosphorylated c-Jun in the nucleus. Ramiprilat was however unable to activate JNK or to stimulate the nuclear accumulation of c-Jun in endothelial cells expressing a S1270A ACE mutant or in ACE-deficient cells. Because the ACE inhibitor-induced increase in ACE expression has been linked to the formation of c-Jun homodimers, we investigated whether ACE signaling via JNK contributes to this response in vitro and in vivo. Prolonged ramiprilat treatment increased ACE expression in primary cultures of human endothelial cells and in vivo (mouse lung), a response that was prevented by pretreatment with the JNK inhibitor SP600125. Thus, ACE is involved in outside-in signaling in endothelial cells and "ACE signaling" may be an important cellular mechanism contributing to the beneficial effects of ACE inhibitors. T he angiotensin-converting enzyme (ACE) is an ectoenzyme that catalyzes the conversion of angiotensin I to the vasoconstrictor angiotensin II as well as the degradation of the potent vasodilator bradykinin (see review 1 ). Two distinct forms of ACE are expressed in humans, a somatic form that is particularly abundant on the endothelial surface of the lungs, and a smaller isoenzyme that is found exclusively in testis. The activity of somatic ACE is thought to play a crucial role in blood pressure regulation and in processes involved in vascular remodeling, effects best highlighted by the fact that the in vivo gene transfer of ACE into the uninjured rat carotid artery results in the development of vascular hypertrophy independent of systemic factors and hemodynamic effects. The inhibition of ACE activity is reported to improve endothelial function 2 and to stimulate vascular remodeling, 3 as well as attenuate the progression of arteriosclerosis 4 and the occurrence of cardiovascular events in humans. 4 -6 The deleterious effects of ACE on the cardiovascular system were initially thought to be a consequence of the formation of angiotensin II, which initiates a cascade of events involving increased free radical production and vascular smooth muscle cell proliferation. However, as bradykinin is much more readily hydrolyzed by ACE than angiotensin I, 1,7 the hydrolysis of bradykinin may also contribute t...

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Induction of angiotensin I-converting enzyme in rat lung with captopril (SQ 14225)

Cited by 86 publications

References 4 publications

Mechanisms for antihypertensive effect of CocoanOX, a polyphenol-rich cocoa powder, in spontaneously hypertensive rats

Mechanisms for antihypertensive effect of CocoanOX, a polyphenol-rich cocoa powder, in spontaneously hypertensive rats

Differential effects of captopril and enalapril on tissue renin-angiotensin systems in experimental heart failure.

Angiotensin-Converting Enzyme Is Involved in Outside-In Signaling in Endothelial Cells

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