Effect of long-term treatment with $beta;-blocker on cardiac hypertrophy in SHR

Ieki, Keiko; Yazaki, Yoshio; Yamaoki, Kazuhide; Tsuchimochi, Hidetsugu; Yoshizumi, Masao; Komuro, Issei; Sugiyama, Takeyoshi; Seko, Yoshinori; Takaku, Fumimaro

doi:10.1016/0022-2828(89)90777-3

Cited by 20 publications

(7 citation statements)

References 23 publications

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“…Judged by the normal hematocrits, water intake, BW, and urine output, it is unlikely that volume overload is the major factor. One surprising conclusion from the results of chronic antihypertensive treatment of Npr1 -/-mice is that absence of NPRA not only uncouples the tight correlation between cardiac growth and BP, but also that cardiac hypertrophy due to absence of NPRA can develop and/or persist even in the absence of elevated BP and when the local effects of hypertrophic stimuli like angiotensin II or β-adrenergic signaling are blocked (33,(60)(61)(62). Nevertheless, under the severe stress of mechanical overload Npr1 -/-mice have an exaggerated response at any total load, suggesting that these mice have a differential response to growth stimuli that are activated by pressure overload.…”

Section: Discussionmentioning

confidence: 99%

Pressure-independent enhancement of cardiac hypertrophy in natriuretic peptide receptor A–deficient mice

Knowles

Esposito²,

Mao³

et al. 2001

J. Clin. Invest.

285

196

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IntroductionThe natriuretic peptide system plays a crucial role in blood pressure (BP) and blood volume (BV) homeostasis. Increases in atrial stretch trigger the release of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which act through natriuretic peptide receptor A (NPRA) in the kidneys and vasculature to increase natriuresis, diuresis, and vasorelaxation (1-4).Elevations in circulating ANP and BNP are cardinal features of cardiac hypertrophy and heart failure in both humans and animal models (5-8), and induction of the ANP gene is one of the most robust responses to hypertrophic stimuli in the heart (9-12). Recent results suggest that these natriuretic peptides are not simply involved in BP and BV homeostasis but that they are also directly involved in moderating the cardiac growth response to hypertrophic stimuli. For example, the NPRA system has intrinsic growth inhibitory properties in noncardiac and cardiac cells in vitro (13). In endothelial and vascular smooth muscle cells (VSMCs), ANP is antimitogenic (14-17) and in cultured neonatal rat cardiomyocytes, ANP both attenuates the growth response to adrenergic stimuli (18) through a pathway that requires extracellular signal-related protein kinase (ERK) activation (19) and induces apoptosis (20). Furthermore, NPRA knockout mice (which have greatly attenuated responses to ANP and BNP) not only have increased BP, but also display marked cardiac hypertrophy and chamber dilatation by 3 months of age (21), whereas other mutant mice with similar increases in BP do not have this hypertrophic phenotype (22). These observations have led to the hypothesis that the NPRA signaling pathway plays an important autocrine role in the prevention of cardiac hypertrophy and heart failure beyond its effects on BP and BV regulation.To test the hypothesis that the NPRA pathway directly modulates the hypertrophic response we compare the response of Npr1 +/+ and Npr1 -/-mice to a pressure overload induced by transverse aortic constriction (TAC). We have also investigated the natural progression to cardiac hypertrophy that occurs in Npr1 -/-mice in the absence of TAC and the effects of chronic (3 months) BP normalization by enalapril, furosemide, hydralazine, or losartan. We conclude that the NPRA system indeed plays a primary role in moderating cardiac hypertrophy in vivo independently of its effects on BP regulation. Mice lacking natriuretic peptide receptor A (NPRA) have marked cardiac hypertrophy and chamber dilatation disproportionate to their increased blood pressure (BP), suggesting, in support of previous in vitro data, that the NPRA system moderates the cardiac response to hypertrophic stimuli. Here, we have followed the changes in cardiac function in response to altered mechanical load on the heart of NPRA-null mice (Npr1 -/-). Chronic treatment with either enalapril, furosemide, hydralazine, or losartan were all effective in reducing and maintaining BP at normal levels without affecting heart weight/body weight. In the reverse direction, we used t...

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Section: Discussionmentioning

confidence: 99%

Pressure-independent enhancement of cardiac hypertrophy in natriuretic peptide receptor A–deficient mice

Knowles

Esposito²,

Mao³

et al. 2001

J. Clin. Invest.

285

196

View full text Add to dashboard Cite

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“…These data suggest that chronic β-AR blockade can arrest the development of cardiomyopathy. The beneficial effects of β-AR blockade on cardiac fibrosis in response to hypertension (25,26), norepinephrine (27) and myocardial infarction (28) have also been shown. Even more interest-…”

Section: Discussionmentioning

confidence: 99%

β-Adrenergic receptor blockade arrests myocyte damage and preserves cardiac function in the transgenic Gsα mouse

et al. 1999

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“…These findings suggest that cardiac /3-adrenoceptors in SHR may be more sensitive to ISA-induced down-regulation of receptor number than that in WKY. It is well-established that physiologi cal conditions of hypertensive rats are quite different from those of normotensive rats (14,24,(28)(29)(30). For example, the /31 : / 2-adre noceptor ratio in the heart and lung of SHR is significantly different from that of WKY (24) and presynaptic /3-adrenoceptors may function tonically to facilitate the ralease of norepi nephrine in the renal arteries of young SHR more than that of age-matched WKY (14).…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Administration of Carteolol on .BETA.-Adrenoceptors in Spontaneously Hypertensive Rat Heart.

et al. 1991

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ABSTRACT-We studied the effects of chronic administration of 8-adrenoceptor antagonists with and without intrinsic sympathomimetic activity (ISA): carteolol (with ISA) and propranolol (without ISA), respectively, on the heart of spontaneously hypertensive rat (SHR) and Wistar Kyoto rat (WKY). Six-week-old SHRs and WKYs were orally given carteolol or propranolol for ten weeks. The heart rate was reduced in propranolol-treated SHR, but not in carteolol-treated ones. In WKY, carteolol treatment increased the heart rate. The number and affinities of 8-adrenoceptors were analyzed using [3H]dihydroalprenolol as a ligand. Propranolol at 30 mg/kg in creased the number of cardiac f8-adrenoceptors in both SHR and WKY. In contrast, 10 mg/kg carteolol significantly decreased the number of cardiac 8-adrenoceptors in SHR, but not in WKY. These data indicate that carteolol, a /3-adrenoceptor antago nist with ISA, does not cause up-regulation of the number of cardiac ,8-adrenoceptors in the rat and suggest that this fact is related to a possible lack of "rebound phe nomena" after sudden discontinuation of chronic carteolol-therapy in humans.

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Effect of long-term treatment with $beta;-blocker on cardiac hypertrophy in SHR

Cited by 20 publications

References 23 publications

Pressure-independent enhancement of cardiac hypertrophy in natriuretic peptide receptor A–deficient mice

Pressure-independent enhancement of cardiac hypertrophy in natriuretic peptide receptor A–deficient mice

β-Adrenergic receptor blockade arrests myocyte damage and preserves cardiac function in the transgenic Gsα mouse

Effects of Chronic Administration of Carteolol on .BETA.-Adrenoceptors in Spontaneously Hypertensive Rat Heart.

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