Renal sympathetic nerve activity in the development of hypertension

Malpas, Simon C.; Ramchandra, Rohit; Guild, Sarah-Jane; McBryde, Fiona D; Barrett, Carolyn J.

doi:10.1007/s11906-006-0057-0

Cited by 14 publications

(7 citation statements)

References 46 publications

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“…Overactivity of renal sympathetic nerve is considered a major cause of the pathophysiology of hypertension [26, 27]. The splanchnic nerve is thought to influence the regulation of a number of basic functions, such as arterial blood pressure, heart rate, vascular tone [28].…”

Section: Discussion Of Specific Organs and Organ Systemsmentioning

confidence: 99%

Thresholds for thermal damage to normal tissues: An update

Yarmolenko

Moon

Landon

et al. 2011

International Journal of Hyperthermia

582

487

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The purpose of this review is to summarise a literature survey on thermal thresholds for tissue damage. This review covers published literature for the consecutive years from 2002–2009. The first review on this subject was published in 2003. It included an extensive discussion of how to use thermal dosimetric principles to normalise all time-temperature data histories to a common format. This review utilises those same principles to address sensitivity of a variety of tissues, but with particular emphasis on brain and testis. The review includes new data on tissues that were not included in the original review. Several important observations have come from this review. First, a large proportion of the papers examined for this review were discarded because time–temperature history at the site of thermal damage assessment was not recorded. It is strongly recommended that future research on this subject include such data. Second, very little data is available examining chronic consequences of thermal exposure. On a related point, the time of assessment of damage after exposure is critically important for assessing whether damage is transient or permanent. Additionally, virtually no data are available for repeated thermal exposures which may occur in certain recreational or occupational activities. For purposes of regulatory guidelines, both acute and lasting effects of thermal damage should be considered.

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Section: Discussion Of Specific Organs and Organ Systemsmentioning

confidence: 99%

Thresholds for thermal damage to normal tissues: An update

Yarmolenko

Moon

Landon

et al. 2011

International Journal of Hyperthermia

582

487

View full text Add to dashboard Cite

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“…One hypothesis suggests that renal afferent nerve input may be important in the establishment and maintenance of certain forms of experimental hypertension (12). Renal afferent nerve signals are integrated centrally and can result in an enhanced sympathetic drive, which is directed toward, not only the kidneys, but also other organ systems that have a dense sympathetic innervation, such as the heart and the peripheral vasculature, resulting in a rise in blood pressure (12,24,38). The present study is unique that RDN was initiated 4 wk after the onset of HF (chronic), making it relevant to patients who may be administered RDN as a therapeutic modality after diagnosis of the chronic HF condition.…”

Section: Discussionmentioning

confidence: 99%

Renal denervation improves cardiac function in rats with chronic heart failure: Effects on expression of β-adrenoceptors

Zheng

Liu

Sharma

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Zheng H, Liu X, Sharma NM, Patel KP. Renal denervation improves cardiac function in rats with chronic heart failure: Effects on expression of ␤-adrenoceptors. Am J Physiol Heart Circ Physiol 311: H337-H346, 2016. First published June 10, 2016; doi:10.1152/ajpheart.00999.2015.-Chronic activation of the sympathetic drive contributes to cardiac remodeling and dysfunction during chronic heart failure (HF). The present study was undertaken to assess whether renal denervation (RDN) would abrogate the sympathoexcitation in HF and ameliorate the adrenergic dysfunction and cardiac damage. Ligation of the left coronary artery was used to induce HF in Sprague-Dawley rats. Four weeks after surgery, RDN was performed, 1 wk before the final measurements. At the end of the protocol, cardiac function was assessed by measuring ventricular hemodynamics. Rats with HF had an average infarct area Ͼ30% of the left ventricle and left ventricular end-diastolic pressure (LVEDP) Ͼ20 mmHg. ␤ 1-and ␤2-adrenoceptor proteins in the left ventricle were reduced by 37 and 49%, respectively, in the rats with HF. RDN lowered elevated levels of urinary excretion of norepinephrine and brain natriuretic peptide levels in the hearts of rats with HF. RDN also decreased LVEDP to 10 mmHg and improved basal dP/dt to within the normal range in rats with HF. RDN blunted loss of ␤ 1-adrenoceptor (by 47%) and ␤2-adrenoceptor (by 100%) protein expression and improved isoproterenol (0.5 g/kg)-induced increase in ϩdP/dt (by 71%) and ϪdP/dt (by 62%) in rats with HF. RDN also attenuated the increase in collagen 1 expression in the left ventricles of rats with HF. These findings demonstrate that RDN initiated in chronic HF condition improves cardiac function mediated by adrenergic agonist and blunts ␤-adrenoceptor expression loss, providing mechanistic insights for RDN-induced improvements in cardiac function in the HF condition. renal nerve; sympathetic nerve activity; cardiac function; heart failure NEW & NOTEWORTHYThis study shows in a comprehensive way that renal denervation initiated after a period of chronic heart failure enhances cardiac contractility and the responsiveness of hearts to isoproterenol stimulation, and these effects are due in part to renal denervation-induced increase in ␤-adrenoceptor protein and function.WORLDWIDE, MORE THAN 100 MILLION people are afflicted with chronic heart failure (HF), imposing a significant burden on the health care systems throughout the world. Chronic overactivation of the sympathetic nervous system is one of the major pathophysiological soliloquy abnormalities leading to the progression of chronic HF (28,29,48). Activation of sympathetic outflow is initially a hemodynamic adaptation to compensate for decreased cardiac function and output. This adaptation also includes an increase in Na ϩ and fluid retention and activation of the renin-angiotensin-aldosterone system (11, 34). Additional adverse effects of elevated sympathetic drive directed toward the heart have been shown to result in the desensitization or downreg...

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“…Circulating ANG II affects the cardiovascular centers in the brain to enhance sympathetic nerve firing to systemic and renal blood vessels. While sympathetic innervation of systemic vessels is largely involved in moment-to-moment restoration of BP in case of a sudden decrease, sympathetic innervation of renal vessels may affect renal function and long-term regulation of BP (100,106). Also, circulating ANG II directly constricts blood vessels, leading to systemic and renal vasoconstriction and maintenance of BP.…”

mentioning

confidence: 99%

Cellular mediators of renal vascular dysfunction in hypertension

Ponnuchamy¹,

Khalil²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Ponnuchamy B, Khalil RA. Cellular mediators of renal vascular dysfunction in hypertension. Am J Physiol Regul Integr Comp Physiol 296: R1001-R1018, 2009. First published February 18, 2009 doi:10.1152/ajpregu.90960.2008.-The renal vasculature plays a major role in the regulation of renal blood flow and the ability of the kidney to control the plasma volume and blood pressure. Renal vascular dysfunction is associated with renal vasoconstriction, decreased renal blood flow, and consequent increase in plasma volume and has been demonstrated in several forms of hypertension (HTN), including genetic and salt-sensitive HTN. Several predisposing factors and cellular mediators have been implicated, but the relationship between their actions on the renal vasculature and the consequent effects on renal tubular function in the setting of HTN is not clearly defined. Gene mutations/ defects in an ion channel, a membrane ion transporter, and/or a regulatory enzyme in the nephron and renal vasculature may be a primary cause of renal vascular dysfunction. Environmental risk factors, such as high dietary salt intake, vascular inflammation, and oxidative stress further promote renal vascular dysfunction. Renal endothelial cell dysfunction is manifested as a decrease in the release of vasodilatory mediators, such as nitric oxide, prostacyclin, and hyperpolarizing factors, and/or an increase in vasoconstrictive mediators, such as endothelin, angiotensin II, and thromboxane A 2. Also, an increase in the amount/activity of intracellular Ca 2ϩ concentration, protein kinase C, Rho kinase, and mitogenactivated protein kinase in vascular smooth muscle promotes renal vasoconstriction. Matrix metalloproteinases and their inhibitors could also modify the composition of the extracellular matrix and lead to renal vascular remodeling. Synergistic interactions between the genetic and environmental risk factors on the cellular mediators of renal vascular dysfunction cause persistent renal vasoconstriction, increased renal vascular resistance, and decreased renal blood flow, and, consequently, lead to a disturbance in the renal control mechanisms of water and electrolyte balance, increased plasma volume, and HTN. Targeting the underlying genetic defects, environmental risk factors, and the aberrant renal vascular mediators involved should provide complementary strategies in the management of HTN. blood pressure; dietary salt; oxidative stress; cytokines; kidney; endothelium; vascular smooth muscle; extracellular matrix; matrix metalloproteinases THE ROLE OF THE KIDNEY IN the regulation of sodium and water balance and blood pressure (BP) is well recognized (53,55,128). A decrease in plasma volume and renal blood flow (RBF) stimulates renin release from the juxtaglomerular cells (JGCs) and activates the renin-angiotensin system (RAS). Renin transforms angiotensinogen to angiotensin I (ANG I), and angiotensin-converting enzyme (ACE) transforms ANG I to ANG II. ANG II stimulates the adrenal cortex to release aldosterone (Aldo), which acts on the rena...

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Renal sympathetic nerve activity in the development of hypertension

Cited by 14 publications

References 46 publications

Thresholds for thermal damage to normal tissues: An update

Thresholds for thermal damage to normal tissues: An update

Renal denervation improves cardiac function in rats with chronic heart failure: Effects on expression of β-adrenoceptors

Cellular mediators of renal vascular dysfunction in hypertension

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