Effect of Sympathectomy on Mechanical Properties of Common Carotid and Femoral Arteries

Mangoni, Arduino A.; Mircoli, Luca; Giannattasio, Cristina; Mancia, Giuseppe; Ferrari, Alberto

doi:10.1161/01.hyp.30.5.1085

Cited by 112 publications

(65 citation statements)

References 18 publications

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“…These data suggest that modification of vascular compliance may be an important target of sympathetically mediated ␣ 1 -adrenergic stimulation. This observation is in agreement with previous studies that have found sympathetically mediated changes in vascular compliance, independent of diameter, in conduit vessels (11,61,76,86). Alternatively, the greater reduction in HR observed in PEvs.…”

Section: Discussionsupporting

confidence: 93%

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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Polichnowski AJ, Griffin KA, Long J, Williamson GA, Bidani AK. Blood pressure-renal blood flow relationships in conscious angiotensin II-and phenylephrine-infused rats. Am J Physiol Renal Physiol 305: F1074 -F1084, 2013. First published July 3, 2013 doi:10.1152/ajprenal.00111.2013.-Chronic ANG II infusion in rodents is widely used as an experimental model of hypertension, yet very limited data are available describing the resulting blood pressurerenal blood flow (BP-RBF) relationships in conscious rats. Accordingly, male Sprague-Dawley rats (n ϭ 19) were instrumented for chronic measurements of BP (radiotelemetry) and RBF (Transonic Systems, Ithaca, NY). One week later, two or three separate 2-h recordings of BP and RBF were obtained in conscious rats at 24-h intervals, in addition to separate 24-h BP recordings. Rats were then administered either ANG II (n ϭ 11, 125 ng·kg Ϫ1 ·min Ϫ1 ) or phenylephrine (PE; n ϭ 8, 50 mg·kg Ϫ1 ·day Ϫ1 ) as a control, ANG IIindependent, pressor agent. Three days later the BP-RBF and 24-h BP recordings were repeated over several days. Despite similar increases in BP, PE led to significantly greater BP lability at the heart beat and very low frequency bandwidths. Conversely, ANG II, but not PE, caused significant renal vasoconstriction (a 62% increase in renal vascular resistance and a 21% decrease in RBF) and increased variability in BP-RBF relationships. Transfer function analysis of BP (input) and RBF (output) were consistent with a significant potentiation of the renal myogenic mechanism during ANG II administration, likely contributing, in part, to the exaggerated reductions in RBF during periods of BP elevations. We conclude that relatively equipressor doses of ANG II and PE lead to greatly different ambient BP profiles and effects on the renal vasculature when assessed in conscious rats. These data may have important implications regarding the pathogenesis of hypertension-induced injury in these models of hypertension.hypertension; hemodynamics; blood pressure variability INCREASED ACTIVITY OF THE renin-angiotensin-aldosterone system (RAAS) (40,56,73) is postulated to be a major contributor to chronic kidney disease progression through both blood pressure (BP)-dependent and -independent mechanisms (7,28,39,73). Accordingly, chronic ANG II infusion is extensively used to investigate mechanisms that mediate renal damage in hypertensive states characterized by enhanced RAAS activation (3,20,42,65,71). Renal parenchymal injury with significant tubulointerstitial fibrosis and a propensity to develop salt-sensitive hypertension has been observed after ANG II infusions (44, 57). Both barotrauma and renal vasoconstrictionmediated tissue ischemia have been postulated to initiate the pathogenic cascades that lead to renal injury after chronic ANG II infusions. However, despite its wide use, there is a paucity of experimental data describing the BP-renal blood flow (RBF) relationships in conscious ANG II-infused animals, and the relative contribution of these two initiating mechanisms ...

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Section: Discussionsupporting

confidence: 93%

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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“…21 At the opposite end of the baroreflex arc, norepinephrine affects arterial distensibility of the carotid sinus and aorta, altering discharge of the baroreceptor organs. 22 In the present study, baroreflex function significantly improved after successful reperfusion without significant alterations in serum norepinephrine concentrations. Therefore, it is unlikely that baroreflex impairment is primarily caused by sympathetic overactivity.…”

Section: Norepinephrine Concentrations and Baroreflex In Acute MIsupporting

confidence: 57%

Reflex Cardiac Activity in Ischemia and Reperfusion

et al. 2003

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Background-Abnormal heart rate turbulence (HRT) is associated with an increased risk of mortality in the chronic phase of myocardial infarction (MI) in the prethrombolytic and thrombolytic eras. However, the impact of direct percutaneous coronary intervention (PCI) on HRT in the acute phase of MI and its association to the epicardial infarct-related arterial flow has not been examined. Methods and Results-We investigated HRT in 126 patients undergoing direct PCI for a first MI. Turbulence onset and turbulence slope were determined before reperfusion, during the initial 2 hours after reperfusion, and during hours 6 to 24 after reperfusion. HRT significantly improved after PCI. There were no significant differences in baseline clinical characteristics between Thrombolysis in Myocardial Infarction Trial classification (TIMI) 2 (nϭ28) and TIMI 3 (nϭ98) flow. After PCI, turbulence slope increased (13.2Ϯ11 to 18.1Ϯ12 ms/beat, PϽ0.001) and turbulence onset decreased (Ϫ0.008Ϯ0.04% to Ϫ0.023Ϯ0.04%, PϽ0.01) in patients with TIMI 3 flow after PCI, whereas there were no significant alterations of turbulence slope (12.2Ϯ10 to 12.8Ϯ6.5 ms/beat) and turbulence onset (Ϫ0.009Ϯ0.05% to Ϫ0.003Ϯ0.03%) in patients with TIMI 2 flow. Conclusions-The

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“…45 Two, we have shown in rats that carotid and femoral artery distensibility is increased by sympathectomy. 46 We have shown that this is also the case in humans in whom radial artery and femoral artery distensibilities were found to increase markedly after removal of adrenergic tone by anesthesia of the brachial plexus and the spinal cord, respectively. 47 This is presumably due to a sympathetically mediated contraction of vascular smooth muscle, because contracted muscle tissue is less prone to distension for intravascular pressure than is muscle tissue in a relaxed state.…”

Section: Sympathetic Activation and Organ Damagementioning

confidence: 65%

Sympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage

et al. 1999

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Abstract-Although animal models of hypertension have clearly shown that high blood pressure is associated with and is probably caused by an increase in sympathetic cardiovascular influences, a similar demonstration in humans has been more difficult to obtain for methodological reasons. There is now evidence, however, of increased sympathetic activity in essential hypertension. This article will review this evidence by examining data showing that plasma norepinephrine is increased in essential hypertension and that this is also the case for systemic and regional norepinephrine spillover, as well as for the sympathetic nerve firing rate in the skeletal muscle nerve district. Evidence will also be provided that sympathetic activation is a peculiar feature of essential hypertension, particularly in its early stages, with secondary forms of high blood pressure not usually characterized by an increased central sympathetic outflow. Humoral, metabolic, reflex, and central mechanisms are likely to be the factors responsible for the adrenergic activation characterizing hypertension, which may also promote the development and progression of the cardiac and vascular alterations that lead to hypertension-related morbidity and mortality, independent of blood pressure values. This represents the rationale for considering sympathetic deactivation one of the major goals of antihypertensive treatment. Key Words: nervous system, sympathetic Ⅲ hypertension, essential Ⅲ hypertension, secondary Ⅲ pressoreceptors Ⅲ hypertrophy Ⅲ norepinephrine N eural adrenergic factors have long been hypothesized to be important in the initiation and maintenance of high blood pressure (BP). For a long time, however, the evidence supporting this hypothesis was largely limited to the results of studies performed in different animal models of hypertension (HT), in which an enhanced sympathetic drive to the heart and peripheral circulation was shown either to trigger a persistent BP elevation or to maintain the BP elevation originally induced by nonadrenergic mechanisms. [1][2][3][4] This picture has changed in the past 20 years or so because a variety of techniques that allow indirect or direct quantification of adrenergic cardiovascular influences have all provided evidence of an activation of the sympathetic nervous system (SNS) in human HT as well. This article will review the evidence that sympathetic activity is increased in essential HT and that this increase may have a pathogenetic role. It will also discuss 2 other issues, ie, (1) the mechanisms that lead to sympathetic hyperactivity in essential HT and (2) the role exerted by this hyperactivity in the progression of the cardiovascular alterations that may complicate the hypertensive state. Evidence for Sympathetic ActivationIn the past 30 years, several techniques designed to quantify sympathetic cardiovascular influences in humans have shown them to be increased in essential HT. More than 25 years ago, for example, Julius and coworkers 5 showed that the elevated resting heart rate values of bo...

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Effect of Sympathectomy on Mechanical Properties of Common Carotid and Femoral Arteries

Cited by 112 publications

References 18 publications

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Reflex Cardiac Activity in Ischemia and Reperfusion

Sympathetic Activation in the Pathogenesis of Hypertension and Progression of Organ Damage

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