Early and chronic captopril or Losartan therapy reduces infarct size and avoids congestive heart failure after myocardial infarction in rats

Martínez, Luisa; Villalobos‐Molina, Rafael

doi:10.1016/s0188-4409(03)00076-6

Cited by 15 publications

(10 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Losartan blood concentrations were not monitored in the two studies cited above, or in our study. However, the dose and method of administration of losartan that we used in our study was reported to prevent injury progression after myocardial infarction in rats 30 . In addition, because the contractile response of bladder strips to 0.1 µM AngII disappeared in the losartan group, it is believed that the signaling from the AT1s that were expressed in the bladder was sufficiently blocked.…”

Section: Effects Of Arb On a Boo Modelmentioning

confidence: 85%

See 1 more Smart Citation

Effect of the Renin‐Angiotensin System on the Obstructed Bladder

Ishibashi¹,

Sakai²,

Takahashi³

et al. 2012

LUTS

View full text Add to dashboard Cite

Bladder hypertrophy and dysfunction are well-known bladder responses to outlet obstruction (i.e. urodynamic overload). Cardiac hypertrophy and heart failure are also caused by hemodynamic overload, and many basic and clinical studies suggest that the local renin-angiotensin system (RAS) has a crucial role in load-induced cardiac pathogenesis. The similarity of the response of the heart and the bladder to overload suggests that angiotensin II (AngII) may have a similar regulatory role in pathological remodeling, such as muscle growth and collagen production of the obstructed bladder. Previous in vitro studies show that angiotensin I is converted to AngII by angiotensin converting enzyme (ACE) or chymase, which exists in the human bladder. In addition, many studies using contractile responses to AngII, autoradiography, radioreceptor assay and mRNA expression demonstrate the presence of AngII receptor in the bladder from various animals and the human. Recent evidence indicates that AngII is released from bladder smooth muscle cells (SMCs) in response to a repetitive stretch stimulus, and subsequently activates AT1 in an autocrine fashion. This AT1 activation has been shown to mediate heparin-binding epidermal growth factor-like growth factor gene expression and to increase the DNA synthesis rate of bladder SMCs. Consistent with this in vitro study, previous studies and our preliminary data suggest the usefulness of AT1 antagonists or ACE inhibitor in bladder outlet obstruction of the rabbit and rat. Taken together, the local RAS contributes to structural and functional alterations in the bladder after obstruction.Key words angiotensin converting enzyme inhibitor, angiotensin II type 1 receptor antagonist, bladder hypertrophy, bladder outlet obstruction, renin angiotensin system

show abstract

Section: Effects Of Arb On a Boo Modelmentioning

confidence: 85%

“…The dose chosen was based on published data. It is believed that this dose does not affect blood pressure in rat 30 . Six weeks after surgery, continuous cystometry was performed in eight rats of each group, and the bladder was removed from the remaining rats.…”

Section: Effects Of Arb On a Boo Modelmentioning

confidence: 99%

Effect of the Renin‐Angiotensin System on the Obstructed Bladder

Ishibashi¹,

Sakai²,

Takahashi³

et al. 2012

LUTS

View full text Add to dashboard Cite

show abstract

“…It is well recognized that the pathogenic actions of Ang II, signalling via AT 1 receptors, are involved in diseases such as hypertension. In support of this contention, therapy with angiotensin converting enzyme (ACE) inhibitors and AT 1 receptor antagonists have proven to be successful in patients and rats with diabetic nephropathy, heart failure, hypertension and left ventricular hypertrophy (Martínez & Villalobos‐Molina, 2003; Ferrario et al. , 2004).…”

Section: Discussionmentioning

confidence: 99%

Vascular α_1D‐adrenoceptors are overexpressed in aorta of the aryl hydrocarbon receptor null mouse: role of increased angiotensin II

Villalobos‐Molina

Vázquez‐Cuevas

López-Guerrero

et al. 2008

Auton Autocoid Pharmacol

View full text Add to dashboard Cite

Summary 1.The hypothesis that α 1D -adrenoceptors may mediate the pro-hypertensive actions of angiotensin II (Ang II) was tested in isolated aorta (α 1D -adrenoceptor bearing tissue) of the aryl hydrocarbon receptor null mouse (AhR −/− ), which shows increased levels of Ang II, cardiac hypertrophy and hypertension.2. The effect of captopril (an angiotensin converting enzyme inhibitor) on both blood pressure and aortic α 1D -adrenoceptor expression and function in mice were determined.3. Basal blood pressure was higher in AhR −/− mice, while captopril therapy decreased it to wild-type (WT) values. 4.Aortas of adult WT and AhR −/− mice were stimulated by phenylephrine or noradrenaline to induce contraction; the maximal effect was higher in AhR −/− mice, without a significant change in pEC 50 . 5. 7.Captopril therapy decreased α 1D -adrenoceptor-induced contraction and protein in AhR −/− mice to WT levels.8. These data support the hypothesis that under conditions where Ang II is elevated, vascular α 1D -adrenoceptors are increased, and further suggest that both Ang II and vascular α 1D -adrenoceptors could be related in the onset of hypertension.

show abstract

“…1 Ramipril is a weak but long acting angiotensin converting enzyme (ACE) inhibitor prodrug and is converted in the liver into the more active metabolite ramiprilat. Most experiments with this ACE inhibitor (ACEi) [2][3][4][5][6][7][8][9] and with angiotensin type 1 (AT 1 ) receptor blocker (ARB) losartan [10][11][12][13][14][15][16] have shown that these agents are able to protect the myocardium against ischemia reperfusion injury by reduction of infarct size and ventricular arrhythmias.…”

Section: Introductionmentioning

confidence: 99%

Influence of ramiprilat and losartan on ischemia reperfusion injury in rat hearts

Safari

Hajizadeh

Shekarforoush

et al. 2011

J Renin Angiotensin Aldosterone Syst

View full text Add to dashboard Cite

show abstract

Early and chronic captopril or Losartan therapy reduces infarct size and avoids congestive heart failure after myocardial infarction in rats

Cited by 15 publications

References 20 publications

Effect of the Renin‐Angiotensin System on the Obstructed Bladder

Effect of the Renin‐Angiotensin System on the Obstructed Bladder

Vascular α_1D‐adrenoceptors are overexpressed in aorta of the aryl hydrocarbon receptor null mouse: role of increased angiotensin II

Influence of ramiprilat and losartan on ischemia reperfusion injury in rat hearts

Contact Info

Product

Resources

About

Early and chronic captopril or Losartan therapy reduces infarct size and avoids congestive heart failure after myocardial infarction in rats

Cited by 15 publications

References 20 publications

Effect of the Renin‐Angiotensin System on the Obstructed Bladder

Effect of the Renin‐Angiotensin System on the Obstructed Bladder

Vascular α1D‐adrenoceptors are overexpressed in aorta of the aryl hydrocarbon receptor null mouse: role of increased angiotensin II

Influence of ramiprilat and losartan on ischemia reperfusion injury in rat hearts

Contact Info

Product

Resources

About

Vascular α_1D‐adrenoceptors are overexpressed in aorta of the aryl hydrocarbon receptor null mouse: role of increased angiotensin II