Angiotensin II: Hemodynamic regulator or growth factor?

Katz, Arnold M.

doi:10.1016/0022-2828(90)90086-h

Cited by 89 publications

(34 citation statements)

References 35 publications

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“…The AT1 receptor mediates many biological effects of the RAS leading to the remodelling of cardiac tissue, including cell growth and the deposition of extracellular matrix proteins [20,21]. It also mediates the positive inotropic effects of angiotensin II in cardiac tissue.…”

Section: Discussionmentioning

confidence: 99%

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

et al. 2006

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Aims/hypothesis The angiotensin II (type 1) (AT1) receptor mediates many biological effects of the renin-angiotensin system (RAS), leading to remodelling of cardiac tissue. The present study was designed to analyse changes in the function and expression of the AT1 receptor as principal effector of the RAS in myocardium from type 2 diabetic patients compared with non-diabetic myocardium as control. In addition, we determined the effect of treatment with ACE inhibitors or AT1 receptor blockers on expression levels of the receptor in diabetic patients. Methods Gene expression of the AT1 receptor was analysed by quantitative RT-PCR and protein expression was determined by immunoblot analysis in human right atrial myocardium. We investigated functional coupling of the receptors by measuring contractility in isolated trabeculae stimulated with increasing concentrations of angiotensin II. Results Diabetic myocardium showed a significant increase in protein expression (170±16% of control) and median mRNA expression (186% of control) of the AT1 receptor.The additional receptors were functionally coupled, resulting in a stronger inotropic response upon stimulation with angiotensin II (89±5.5% vs 29±1.6% in controls), whereas receptor affinity was similar in both groups. However, myocardium from diabetic patients treated with ACE inhibitors or AT1 receptor blockers showed no increase in AT1 receptor expression. Conclusions/interpretation AT1 receptor expression in myocardium of type 2 diabetic patients is dynamic, depending on the level of glycaemic control and the activity of the RAS. These findings could at least in part explain the strong therapeutic benefit of RAS inhibition in diabetic patients.

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Section: Discussionmentioning

confidence: 99%

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

et al. 2006

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“…The c-fos protein can promote growth of myocardial or vascular smooth muscle cells and lead to myocardial hypertrophy. As a result, compensated myocardial function turns decompensated followed by heart failure (Katz 1990, Morgan & Baker 1991, Sernia et al 1993, Basset et al 2001. These findings were derived from biochemical research on the pathogenesis of hyperthyroid heart disease.…”

Section: Introductionmentioning

confidence: 99%

Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

Liu

Li²,

Shi³

et al. 2007

Journal of Endocrinology

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Thyroid dysfunction is classified into hyperthyroidism and congenital hypothyroidism (CH). Both hyperthyroidism and CH can cause heart lesions; however, the mechanisms involved remain unclear. The left ventricle was collected from eu-, hyper-, and hypothyroid rat. RNAwas extracted and reverse-transcripted to cDNA. Real-time fluorescence quantitation-PCR was used to quantify the differential expression of thyroid hormone receptor (TR) subtype mRNA among eu-, hyper-, and hypothyroid rat myocardium. Here, we show that compared with the normal myocardium, TRa1 mRNA expression was upregulated by 51% (P!0 . 01), TRa2 mRNA expression was downregulated by 58% (P!0 . 01), and TRb1 mRNA expression remained unchanged in hyperthyroid rat myocardium (PO0 . 05). TRa1, TRa2, and TRb1 were expressed in normal and hypothyroid rat myocardium throughout the developmental process. In hypothyroid rats, myocardial TRa1 mRNA expression was generally downregulated and the expression peak appeared late. Myocardial TRa2 mRNA expression was generally upregulated and the expression peak appeared late. Myocardial TRb1 mRNA expression was generally downregulated and changed similarly with the control group. In addition, the hypogenetic myocardium can be seen in the hypothyroid rat by pathology study. Taken together, the abnormal expression of TR subtype mRNA may have a close relationship with the pathogenesis of CH and hyperthyroidism heart disease.

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“…3 Angiotensin II (Ang II), the main effector peptide of the reninangiotensin system has long been known to play a major role in the regulation of BP and body fluid homeostasis. Moreover, Ang II has been reported to induce hyperplasia and/or hypertrophy in cultured aortic smooth muscle cells [4][5][6][7] in small resistance arteries 8 and in cardiomyocytes. 9 The tissue response to Ang II is mediated by specific receptors located on the cell surface.…”

Section: Introductionmentioning

confidence: 99%

The potential role of angiotensin II in the vasculature

Levy

1998

J Hum Hypertens

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Arterial hypertension is associated with marked changes in the structure of both resistance and large arteries. The renin-angiotensin system is largely involved in these alterations; chronic blockade of the renin-angiotensin system prevents and/or reverses most of the alterations of the vasculature in experimental and clinical hypertension. In this review we have analysed the differential role of AT 1 and AT 2 receptors in the response of the vessels to arterial hypertension. It emerges that the relative involvement of each receptor

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Angiotensin II: Hemodynamic regulator or growth factor?

Cited by 89 publications

References 35 publications

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

The increased angiotensin II (type 1) receptor density in myocardium of type 2 diabetic patients is prevented by blockade of the renin–angiotensin system

Effects of hyper- and hypothyroid on expression of thyroid hormone receptor mRNA in rat myocardium

The potential role of angiotensin II in the vasculature

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