Impaired baroreflex changes in muscle sympathetic nerve activity in adolescents who have a family history of essential hypertension

Yamada, Yutaka; Miyajima, Eiji; Tochikubo, Osamu; Matsukawa, Tetsuya; Shionoiri, Hiroshi; Ishii, Masao; Kaneko, Yoshihiro

doi:10.1097/00004872-198812040-00165

Cited by 53 publications

(38 citation statements)

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“…This study showed that BN.GH18 rats had a significantly lower baroreceptor reflex response, compared with normotensive BN controls, suggesting that we may have captured a major locus responsible for altered baroreceptor sensitivity. Several studies suggest that baroreflex function is strongly influenced by genetic factors (55,56), but the level of the genetic contribution is not completely known (57). Given that many studies suggest that baroreflex abnormalities are an important contributing factor to the pathogenesis of hypertension (58-62), we consider this result to suggest that baroreceptor sensitivity can be considered a sub-phenotype in the BN.GH18 rat strain, not secondary to hypertension itself.…”

Section: Discussionmentioning

confidence: 84%

Genetically Hypertensive Brown Norway Congenic Rat Strains Suggest Intermediate Traits Underlying Genetic Hypertension

et al. 2008

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Aim To determine the independent and combined effects of three quantitative trait loci (QTL) for blood pressure in the Genetically Hypertensive (GH/Omr) rat by generating and characterizing single and combined congenic strains that have QTL on rat chromosomes (RNO) 2, 6, and 18 from the GH rat introduced into a hypertension resistant Brown Norway (BN) background.Methods Linkage analysis and QTL identification (genome wide QTL scan) were performed with MapMaker/EXP to build the genetic maps and MapMaker/QTL for linking the phenotypes to the genetic map. The congenic strains were derived using marker-assisted selection strategy from a single male F1 offspring of an intercross between the male GH/Omr and female BN/Elh, followed by 10 generations of selective backcrossing to the female BN progenitor strain. Single congenic strains generated were BN.GH-(D2Rat22-D2Mgh11)/Mcwi (BN.GH2); BN.GH-(D6Mit12-D6Rat15)/Mcwi (BN.GH6); and BN.GH-(D18Rat41-D18Mgh4)/Mcwi (BN.GH18). Blood pressure measurements were obtained either via a catheter placed in the femoral artery or by radiotelemetry in the single and combined congenics. Responses to angiotensin II (ANGII), norepinephrine (NE), and baroreceptor sensitivity were measured in the single congenics.Results Transferring one or more QTL from the hypertensive GH into normotensive BN strain was not sufficient to cause hypertension in any of the developed congenic strains. There were no differences between the parental and congenic strains in their response to NE. However, BN.GH18 rats revealed significantly lower baroreceptor sensitivity (β = -1.25 ± 0.17), whereas BN.GH2 (β = 0.66 ± 0.09) and BN.GH18 (β = 0.71 ± 0.07) had significantly decreased responses to ANGII from those observed in the BN (β = 0.88 ± 0.08). ConclusionThe failure to alter blood pressure levels by introducing the hypertensive QTL from the GH into the hypertension resistant BN background suggests that the QTL effects are genome backgrounddependent in the GH rat. BN.GH2 and BN.GH18 rats reveal significant differences in response to ANGII and impaired baroreflex sensitivity, suggesting that we may have captured a locus responsible for the genetic control of baroreceptor sensitivity, which would be considered an intermediate phenotype of blood pressure.

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Section: Discussionmentioning

confidence: 84%

Genetically Hypertensive Brown Norway Congenic Rat Strains Suggest Intermediate Traits Underlying Genetic Hypertension

et al. 2008

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“…Yamada Y et al, [23] reported that the baroreflex inhibition of the muscle sympathetic nerve activity was reduced in normotensive adolescents with a family history of hypertension. A reduced reflex sympatho-inhibition could lead to the development of hypertension due to an increase in the sympathetic vasomotor tone.…”

Section: Discussionmentioning

confidence: 99%

The Isometric Handgrip Exercise As a Test for Unmasking Hypertension in the Offsprings of Hypertensive Parents

Garg

Malhotra²,

Dhar³

et al. 2013

JCDR

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Background: A familial history of hypertension increases the risk of hypertension in the offsprings. Aims and objectives:The present study was undertaken to assess the underlying hypertension by using the Isometric Handgrip (IHG) exercise test in the offsprings of hypertensive parents and to compare it with age-matched controls of normotensive parents. Material and Methods:The isometric handgrip test was performed in the study and control groups. The resting blood pressure was recorded before exercise and afterwards the subjects were asked to perform the isometric handgrip exercise with the dominant hand for 2 minutes. Then the blood pressure was recorded in the sitting position during and 5 minutes after the completion of the exercise.Statistical Analysis: The analysis of the results was done by ANOVA with SPSS, version 17.0, by using the unpaired 't' test. Results:The results showed that the Resting Systolic (SBP), Diastolic (DBP) and the Mean (MBP) Blood Pressures were higher (p <0.001) in the offsprings of the hypertensive parents as compared to those in the control subjects of normotensive parents. During the isometric handgrip exercise test, the rise in the systolic, diastolic and the mean blood pressures was significantly higher (p<0.001) in the offsprings of the hypertensive parents. After 5 minutes of exercise, the SBP, DBP and the MBP were found to be significantly higher (p<0.001) in the study group as compared to those in the control group.Conclusions: An early and a regular screening of the children of hypertensive parents is necessary to prevent any future cardiovascular complications.

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“…One, in normotensive subjects with a family history of HT, sympathetic nerve traffic may be increased. 12 Two, subjects with borderline HT display a number of sympathetic bursts over time (or corrected for heart rate values) that is greater than that found in normotensive controls. 3,13,14 Three, sympathetic nerve traffic increases progressively from the normotensive to the moderately and more severe essential-hypertensive state ( Figure 1).…”

Section: Evidence For Sympathetic Activationmentioning

confidence: 95%

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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Impaired baroreflex changes in muscle sympathetic nerve activity in adolescents who have a family history of essential hypertension

Cited by 53 publications

References 0 publications

Genetically Hypertensive Brown Norway Congenic Rat Strains Suggest Intermediate Traits Underlying Genetic Hypertension

Genetically Hypertensive Brown Norway Congenic Rat Strains Suggest Intermediate Traits Underlying Genetic Hypertension

The Isometric Handgrip Exercise As a Test for Unmasking Hypertension in the Offsprings of Hypertensive Parents

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

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