ANG II receptor blockade and arterial baroreflex regulation of renal nerve activity in cardiac failure

DiBona, Gerald F.; Jones, Susan Y.; Brooks, Virginia L.

doi:10.1152/ajpregu.1995.269.5.r1189

Cited by 112 publications

(135 citation statements)

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“…In rats with CHF, intracerebroventricular losartan had no effect on arterial pressure but decreased the basal level of RSNA and improved both the arterial and cardiopulmonary baroreflex control of RSNA, and chronic intraperitoneal losartan administration produced an improvement in the ability to excrete both acute and chronic sodium loads. 32,33 This led to an examination of the effect of physiological changes in the activity of the renin-angiotensin system on arterial baroreflex control of RSNA in normal rats by using the intervention of alterations in dietary sodium intake. Intracerebroventricular losartan, although not affecting arterial pressure, decreased the basal level of RSNA and shifted the arterial baroreflex control of RSNA to a lower arterial pressure in proportion to the degree of activation of the renin-angiotensin system.…”

Section: The Presentmentioning

confidence: 99%

Neural Control of the Kidney

DiBona

2003

Hypertension

158

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Abstract-This article provides a chronological perspective on the development of knowledge concerning the neural control of renal function and is divided into three parts: the past, the present, and the future. The PastResearch in the area of the neural control of renal function was not very active for the first half of the 20th century. This can be attributed to 2 factors. First, the renowned renal physiologist, Homer Smith, rendered an opinion that the renal nerves were of little functional consequence. [1][2][3] This was based on his interpretation of experiments involving renal denervation in anesthetized and surgically operated animals. He criticized this approach, as he believed that the starting level of renal sympathetic nerve activity (RSNA) would be quite elevated, owing to the associated stress, so that "denervation hyperemia and diuresis appear to be a release from enhanced vasoconstriction engendered by anesthesia and traumatic operative procedures." 3 Second, there was a lack of convincing evidence that the renal innervation extended beyond the renal vasculature to either the tubules or the juxtaglomerular apparatus. The demonstration by Luciano Barajas 4 that all segments of the renal tubule (as well as the juxtaglomerular apparatus) were innervated by norepinephrine-containing renal sympathetic nerve terminals that make contact with the renal tubular epithelial cell basement membrane paved the way for increased research activity in this area. This critical observation reconfirmed once again the important relationship between structure and function.Given the powerful influence of changes in renal hemodynamics (ie, arterial pressure, glomerular filtration rate [GFR] and renal blood flow [RBF]) on urinary sodium excretion (U Na V), it was evident that the influence of changes in RSNA on U Na V must be examined in experimental protocols in which these variables remained constant. By using electrical stimulation of the efferent renal sympathetic nerves at frequencies just subthreshold for decreases in RBF, it was shown that a reversible decrease in U Na V occurred in the absence of changes in GFR (ie, filtered sodium load), RBF, and arterial pressure. 5 These results indicated that lowfrequency renal sympathetic nerve stimulation increased overall renal tubular sodium reabsorption via a direct action on the renal tubule, independent of changes in renal hemodynamics. Additional experiments demonstrated that this effect occurred in the proximal convoluted tubule, the thick ascending limb of Henle's loop, the distal convoluted tubule, and the collecting duct. 6,7 Subsequent work (reviewed in DiBona and Kopp 8 ) showed that this was owing to the release of norepinephrine from renal sympathetic nerve terminals with stimulation of postsynaptic ␣ 1 -adrenoceptors located on the basolateral membrane of renal tubular epithelial cells throughout the nephron. Subsequent intracellular signaling events resulted in an increase in activity of the sodium pump (Na ϩ ,K ϩ -ATPase), with increased transepithelial sod...

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Section: The Presentmentioning

confidence: 99%

Neural Control of the Kidney

DiBona

2003

Hypertension

158

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“…All rats showed increased heart/body weight ratio compared with normal values of Ϸ0.40% in sham or control rats in our laboratory. 14,15,17 All rats had increased LVEDP compared with normal values of Ϸ3.0 mm Hg in sham or control rats in our laboratory. 14,15,17 At autopsy, all rats had bilateral hydrothorax and ascites, which reflects their avid Figure 1.…”

Section: Discussionmentioning

confidence: 69%

“…A previously described technique [13][14][15][16][17] involving ligation of the left coronary artery was used to produce chronic CHF. Rats were anesthetized with methohexital sodium (50 mg/kg IP); an oral endotracheal tube was inserted, and mechanical ventilation with room air was instituted.…”

Section: Congestive Heart Failurementioning

confidence: 99%

Effect of Metoprolol Administration on Renal Sodium Handling in Experimental Congestive Heart Failure

DiBona

Sawin

1999

Circulation

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Background-Long-term metoprolol therapy improves cardiac performance and decreases mortality in patients with chronic congestive heart failure (CHF). This study examined the effect of long-term metoprolol therapy on renal sodium handling in an experimental rat model of CHF. Methods and Results-Rats with left coronary ligation and myocardial infarction-induced CHF were treated with metoprolol (1.5 mg ⅐ kg Ϫ1 ⅐ h

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“…Muitas substâncias humorais estão elevadas na IC, das quais podemos citar a angiotensina II, conhecida há algum tempo por modular a descarga simpática, pois quando se efetua bloqueio dos receptores AT1 para a angiotensina II, percebe-se uma redução do tônus simpático no estado de IC [49][50][51][52][53][54] .…”

Section: Autorunclassified

Insuficiência cardíaca e atividade física: o aumento de enzimas antioxidantes e a melhora da atividade nervosa simpática

Gonçalves

Valenti

Ferreira

et al. 2010

Arq. Bras. Ciên. Saúde

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ResumoA insuficiência cardíaca vem se tornando um problema cada vez maior em saúde pública, e uma das principais causas de internações hospitalares em todo o mundo.Mesmo com os progressos médicos e os avanços tecnológicos atuais, a prevalência da doença aumentou nas últimas cinco décadas. Estudos recentes com animais mostraram que existe uma relação entre hiperatividade simpática na insuficiência cardíaca e aumento do estresse oxidativo sistêmico e central. Este trabalho tem como objetivo analisar, por meio de revisão bibliográfica, os benefícios produzidos pela atividade física em pacientes portadores de insuficiência cardíaca. Foram revisados estudos relacionados ao estresse oxidativo, controle neural da circulação, insuficiência cardíaca e exercício físico entre outubro de 2009 e abril de 2010 nas bases de dados: Medline, Pubmed e Lilacs. As referências eram datadas de 1986 a 2010. Utilizaram-se os seguintes termos: "Oxidative Stress", "Chronic Heart Failure", "Baroreflex", "Nervous System" and "Exercise". Ratos com insuficiência cardíaca induzida possuem um aumento de espécies reativas de oxigênio na região rostroventrolateral do bulbo, assim como comprometimento na atividade simpática. Alguns estudos sugerem que a atividade física normaliza a atividade simpática por meio de seus mecanismos antioxidantes em seres humanos. Outro aspecto interessante é que a atividade física reduz os níveis plasmáticos de angiotensina II, regula a disfunção do baroreflexo arterial e promove o aumento de enzimas antioxidantes no músculo esquelético de pacientes com insuficiência cardíaca. Portanto, conclui-se que a atividade física é um regime terapêutico não-farmacológico de extrema importância para pacientes com insuficiência cardíaca.Palavras-chave: Insuficiência cardíaca; estresse oxidativo; exercício físico; sistema neural. AbstractHeart failure is an increasing problem in public health, and a major cause of hospitalization worldwide. Even with the medical progress and technological advances in the present, the prevalence of the disease increased in the last five decades. Recent animal studies have shown that there is a relationship between sympathetic hyperactivity in heart failure and increased oxidative stress, systemic and central. This paper aims to examine, through literature review, the benefits of physical activity in patients with heart failure. We reviewed studies related to oxidative stress, neural control of circulation, heart failure and exercise between October 2009 and April 2010, on the databases: Medline, Pubmed e Lilacs. The references dated from 1986 to 2010, and we used the following terms: "oxidative stress", "chronic heart failure", "baroreflex", "nervous system" and "exercise". Rats with induced heart failure have an increase of reactive oxygen species in the rostroventrolateral medula, and impairment of sympathetic activity. Some studies suggest that physical activity normalizes the sympathetic activity through its antioxidant mechanisms in the rostroventrolateral medulla. Some studies suggest that ...

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ANG II receptor blockade and arterial baroreflex regulation of renal nerve activity in cardiac failure

Cited by 112 publications

References 0 publications

Neural Control of the Kidney

Neural Control of the Kidney

Effect of Metoprolol Administration on Renal Sodium Handling in Experimental Congestive Heart Failure

Insuficiência cardíaca e atividade física: o aumento de enzimas antioxidantes e a melhora da atividade nervosa simpática

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