• Users Online: 565
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
Year : 2014  |  Volume : 1  |  Issue : 2  |  Page : 113-119

Association of sympathovagal imbalance with arterial stiffness indices in women with risk factors for pregnancy-induced hypertension in first and third trimesters of gestation

1 Department of Physiology, Jawaharlal Institute of Medical Education and Research, Puducherry, India
2 Department of Obstetrics and Gynecology, Jawaharlal Institute of Medical Education and Research, Puducherry, India
3 Department of Pharmacology, Jawaharlal Institute of Medical Education and Research, Puducherry, India
4 Department of Biochemistry, Jawaharlal Institute of Medical Education and Research, Puducherry, India

Date of Submission30-Apr-2014
Date of Decision02-Jun-2014
Date of Acceptance10-Jun-2014
Date of Web Publication23-Jul-2014

Correspondence Address:
Pravati Pal
Department of Physiology, Jawaharlal Institute of Medical Education and Research, Pondicherry 605 006
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2348-8093.137404

Rights and Permissions

Background and Aim: Though contribution of sympathovagal imbalance (SVI) to arterial stiffness indices (ASI), and markers of CV risk in pregnancy-induced hypertension (PIH) has been reported, their association during early trimesters of gestation in PIH has not been studied. Therefore, in the present study, we have investigated the association of SVI with ASI in pregnant women with risk factors for PIH during their first and third trimesters of gestation.
Methods: Blood pressure (BP), rate-pressure product (RPP), spectral analysis of heart rate variability (HRV), and arterial stiffness indices (ASI) were assessed in subjects of control group (normal pregnant women without having risk for PIH, n = 50) and study group (pregnant women with risk factors for PIH, n = 50). Independent association of LF:HF ratio to the various parameters were determined using multiple regression analysis.
Results: It was observed that the ratio of low-frequency to high-frequency power (LF-HF ratio) of HRV, the sensitive indicator of SVI was significantly high in study group subjects starting from first trimester of pregnancy. SVI could be due to both sympathetic activation and vagal withdrawal. ASI was found to be significantly high in study group subjects compared to that of controls. LF-HF ratio had significant correlation and independent association with RPP (the marker of CV risk) and ASI.
Conclusion: SVI is associated with arterial stiffness in pregnant women having risk factors for PIH. SVI and increased arterial stiffness could contribute to CV risks in pregnant women with risk factors for PIH.

Keywords: Arterial stiffness indices, cardiovascular risks, heart rate variability, pregnancy-induced hypertension, sympathovagal imbalance

How to cite this article:
Subha M, Pal P, Pal GK, Habeebullah S, Adithan C, Sridhar M G. Association of sympathovagal imbalance with arterial stiffness indices in women with risk factors for pregnancy-induced hypertension in first and third trimesters of gestation. Int J Clin Exp Physiol 2014;1:113-9

How to cite this URL:
Subha M, Pal P, Pal GK, Habeebullah S, Adithan C, Sridhar M G. Association of sympathovagal imbalance with arterial stiffness indices in women with risk factors for pregnancy-induced hypertension in first and third trimesters of gestation. Int J Clin Exp Physiol [serial online] 2014 [cited 2019 Mar 20];1:113-9. Available from: http://www.ijcep.org/text.asp?2014/1/2/113/137404

  Introduction Top

Pregnancy-induced hypertension (PIH) is a serious complication of pregnancy that affects 3-8% [1] of all pregnancies and accounts for about 12% of maternal deaths in developing countries of south-east Asia. [2] It has been reported recently that PIH is associated with arterial stiffness (AS), [3] which is a marker of increased cardiovascular (CV) disease risk. [4] Also, there are reports of CV diseases in preeclamptic women during and years after pregnancy. [5],[6] It has been observed that both preeclampsia and CV disease share common risk factors. [7] Therefore, repeated screening of women with risk factors for PIH in the early part of pregnancy is essential for proper management and prevention of PIH.

Though the etiology of PIH is still elusive, it has been documented that the disease is characterized by low circulating volume and high vascular resistance. [8] The vascular resistance in PIH has been reported due to the increased sympathetic tone. [9],[10] Recently, we reported that along with sympathetic overactivity, there is vagal withdrawal in PIH. [11],[12],[13] From our earlier studies, we observed that women who develop PIH in later part of pregnancy, had some degree of sympathetic overactivity from the early trimester of pregnancy. [11] With the progress of pregnancy, vagal withdrawal occurs in later part of pregnancy in addition to the sympathetic overactivity that contributes to the development of SVI and PIH. [13] However, till date, no study has been conducted to assess the degree of SVI in women with risk factor for PIH. SVI has recently been reported to be associated with CV morbidity and mortality. [14],[15] Studies have demonstrated that sympathetic overactivity is implicated in the stiffening of arteries and diastolic dysfunction, which might contribute to development and progression of hypertension and its complications. [16] There are reports of increased arterial stiffness indices (ASI) in PIH [3],[4],[17] and increase in arterial stiffness is an independent predictor of CV mortality. [18],[19] Although there are evidence to suggest that arterial stiffness contributes to CV outcomes, [20],[21] studies in pregnant women in their early trimester are lacking. To the best of our knowledge, no study has been conducted till date to assess the association of SVI with ASI comparing the early trimester with late trimester of pregnancy. Therefore, in the present study we have assessed the link between arterial stiffness and SVI during early and late trimesters in pregnant women with risk factors for PIH.

  Materials and methods Top

The present study was conducted in the department of physiology, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry, India. After obtaining approval of the project plan from research and ethics committees of JIPMER, 100 subjects (50 in control group, 50 in study group) were recruited from the out-patient unit of the obstetrics and gynecology department of JIPMER. Written informed consent was obtained from all the participants prior to initiation of the study. Subjects of study group included pregnant women who had risk factors for PIH and of control group included normal pregnant women without any risk factor for PIH.

Inclusion criteria for the study group were established risk factors for PIH, [8] such as family history of preeclampsia, preeclampsia in previous pregnancy, extremes of reproductive age, body mass index (BMI) >35, diastolic blood pressure (DBP) >80 mmHg at the first visit, first pregnancy, multiple pregnancy, underlying medical conditions (diabetes mellitus, renal disease, pre-existing hypertension), etc. Subjects of control group included normal pregnant ladies who had none of the above-mentioned risk factors for PIH. Subjects receiving oral contraceptives prior to pregnancy were excluded from both the groups.

Subjects attended obstetrics OPD for their regular check-ups and also reported to polygraph laboratory of physiology department for recording of various parameters at all the three trimesters of pregnancy. The subjects reported to polygraph laboratory about two hours after a light breakfast devoid of coffee or tea. Height and weight were measured to calculate body mass index (BMI). Blood pressure (BP) was recorded using the automatic non-invasive BP monitor, (Omron, HEM 7203 model, Omron Healthcare Co., Kyoto, Japan). Heart rate, systolic BP and DBP were noted from the display screen of BP monitor, and mean arterial pressure (MAP) was calculated. Rate pressure product (RPP) was calculated. [22]

HRV recording

Following 10 minutes of supine rest in polygraph laboratory (room temperature maintained at 25°C), basal heart rate (BHR) and BP (diastolic and systolic) were recorded. For recording of short-term HRV, recommendation of the Task Force on HRV was followed. [23] For this purpose, electroencephalogram (ECG) electrodes were connected and Lead II ECG was acquired at a rate of 1000 samples/second during supine rest using BIOPAC MP 100 data acquisition system (BIOPAC Inc., USA). The data was transferred from BIOPAC to a windows-based PC with AcqKnowledge software version 3.8.2. Ectopics and artifacts were removed from the recorded ECG. RR tachogram was extracted from the edited 256-s ECG using the R wave detector in the AcqKnowledge software and saved in ASC-II format, which was later used offline for short term HRV analysis. HRV analysis was done using the HRV analysis software version 1.1 (Bio-signal Analysis group, Finland). Among the frequency-domain indices of HRV, ratio of low-frequency to high-frequency power (LF-HF ratio) was recorded.

Assessment of arterial stiffness

Arterial stiffness was assessed by measuring pulse wave velocity (PWV), following the standard procedures and the ASI was computed. [24] PWV was determined by PeriScope (M/S Genesis Medical System, Hyderabad, India) in an 8-channel real-time personal computer-based simultaneous acquisition and analysis system with an acquisition rate of 200 samples/second. In this method, BP is measured by detecting pulsation of the artery as the pressure oscillation in the cuff caused by ventricular ejection. The entire recording was carried out following 10-15 minutes of supine rest. For this purpose, electrodes were placed on the proximal end of the limbs and BP cuffs were wrapped on both upper arms 2.5 cm above the cubital fossae for recording from the brachial artery, and on both legs above the ankle for recording from the tibial artery. The cuffs were connected to a plethysmographic sensor that determines volume pulse form and an oscillometric pressure sensor that measures BP volume waveforms from the brachial and tibial arteries. Cuff pressure was controlled by a microcomputer, which activates the cuff inflation and deflation system during the measurement cycle. PWV is the speed at which the pressure pulse wave travels from the heart to the peripheral artery, after blood rushes out during contraction assesses the stiffness of the artrial wall.

Statistical analysis of data

SPSS version 13 (SPSS Software Inc., Chicago, IL, USA) was used for statistical analysis. All data were expressed as mean ± SD. Normality of data was tested by Kolmogorov Smirnov test. For parametric data, the level of significance between the groups was tested by Student's unpaired t-test and for nonparametric data Welch's corrected t-test was used. The association of LF-HF ratio with HRV, and ASI parameters were assessed by Pearson's correlation analysis. The independent contribution of various parameters to SVI (alteration in LF-HF ratio) were assessed by multiple regression analysis. P < 0.05 was considered statistically significant.

  Results Top

There was no significant difference in age, body weight, and BMI between the subjects of control group and study group at first trimester recordings [Table 1]. In the third trimester, the body weight (P = 0.0371) and BMI (P = 0.0425) of study group subjects was more than that of the control group. BHR of study group subjects was significantly more compared to the control group from early trimesters. SBP, DBP, MAP, and RPP of study group subjects were significantly more (P < 0.0001) compared to the respective values of control group both in first and third trimesters. Among the frequency-domain indices, LF-HF ratio was significantly more in study group compared to the control group in both the first and third trimester recordings [Table 1] and [Figure 1].
Figure 1: Power spectral analysis (Auto Regression model) of heart rate variability (from one of the subject for sample) depicts the ratio of low-frequency to high-frequency power (sympathovagal imbalance) in women with risk factors for pregnancy-induced hypertension in the first trimester and third trimesters of gestation. VLF: Very low-frequency power, LF: Low-frequency power, HF: High-frequency power, PSD: Power spectrum density

Click here to view
Table 1: Age, body weight, BMI and cardiovascular parameters in subjects of control and study group

Click here to view

All brachial artery PWV parameters and ASI were significantly increased in study group compared to control group in both the trimester recordings [Table 2] and [Figure 2]a and b]. In study group, BMI was not correlated with LF-HF ratio in first and third trimester recordings [Table 3]. Though BHR, MAP, RPP, PWV, and ASI were not correlated with LF-HF ratio in first trimester recordings of the study group, they demonstrated a significant correlation in third trimester [Table 3]. In third trimester, in the study group, RPP, PWV, and ASI, had significant independent contribution to the LF-HF ratio as demonstrated by multiple regression analysis [Table 4].
Figure 2: This picture depicts the numerical data recordings of the (a) Normal pregnant women and (b) In pregnant women with risk factors for pregnancy induced hypertension obtained using periscope. HR: Basal heart rate, SBP: Systolic blood pressure, DBP: Diastolic blood pressure, MAP: Mean arterial pressure, PP: Pulse pressure, PWV: Pulse wave velocity, ASI: Arterial stiffness index, ABI: Arterial brachial indices, RB: Right brachial artery; LB: Left brachial artery, RA: Right ankle; LA: Left ankle, ECG: Electroencephalogram, Prb: PWV in right brachial artery, Plb: PWV in left brachial artery, Pra: PWV in right ankle, Pla: PWV in left ankle

Click here to view
Table 2: Arterial stiffness indices in control and study groups in the first and third trimester

Click here to view
Table 3: Correlation of LF/HF ratio with BMI, BHR, SBP, DBP and ASI of subjects with risk factors for PIH

Click here to view
Table 4: Multiple regression analysis of LF-HF ratio (as dependable variable) with various parameters (as independent variables) in subjects of PIH risk group in the third trimester

Click here to view

  Discussion Top

In the present study, significantly high BHR, SBP, DBP, MAP, and RPP were seen in study group (pregnant women with risk factors for PIH) compared to the control group (women with normal pregnancy) [Table 1], which suggest that subjects having risks of developing PIH have altered CV parameters even in the early part of pregnancy. Heart rate (HR) at rest is the function of vagal tone and increase in HR represents decreased vagal activity. [23] Recently, it has been reported that increase in resting HR is a cardiometabolic risk and risk factor for all cause mortality. [25],[26] The level of BP is the function of vascular resistance that reflects the sympathetic tone. [27] Thus, the increase in HR and BP in study group subjects indicated decreased vagal tone and increased sympathetic tone in pregnant women with risk factors for PIH. RPP is a measure of myocardial work load and oxygen utilization. [28] Increased RPP, especially in individuals with high BP has been reported as a potential CV risk. [28]

LF-HF ratio is the index of SVI and increase in this ratio reflects increased sympathetic activity. [29] LF-HF ratio was significantly high in study group in comparison to the control group [Figure 1], which confirms the presence of sympathetic overactivity in subjects with risks for PIH since early part of pregnancy, that may lead to the development of hypertension in the later part of pregnancy.

Since sympathetic overactivity is involved in the stiffening of large arteries, assessment of sympathetic activity should be considered as a measure of arterial function. Increased arterial stiffness and elevated BP could be mutually and causally related, and it appears that the significance of this relationship may increase with the increase in BP, even in subjects without hypertension. [16]

MAP has been shown to be a measure of pulsatile component of BP and is a marker of increased large artery stiffness. Sympathetic overactivity may have a stiffening influence on arterial mechanical properties. [16],[20] Increased RPP, especially in individuals with high BP has been reported as a potential CV risk. [28] Thus, increased BP, resting tachycardia, and increased RPP in study group subjects could predispose them to CV risk throughout their pregnancy. There is an experimentally well-defined and physiologically plausible mechanism linking increased arterial stiffness to cardiac risk via raised pulse pressure. Prior studies have reported that MAP and pulse pressure reflects increased large artery stiffness and is a risk factor for both CV and cerebrovascular events. [20],[21]

Brachial artery PWV and ASI were significantly higher in study group compared to the control group [Figure 2]a and b], indicating that there is increased arterial wall thickness and stiffness in PIH risk subjects, which was progressively more from the first trimester. As indices of PWV and ASI were significantly correlated with LF-HF ratio in third trimester in the study group, arterial stiffness could be associated with SVI. Furthermore, all these indices had independent contribution to LF-HF in third trimester in PIH risk subjects, as demonstrated by multiple regression analysis [Table 4]. Thus, SVI appears to contribute to ASI in PIH risk subjects. Persistent increase in sympathetic tone in subjects with PIH risk subjects could be the cause of increased arterial stiffness, as chronic sympathetic stimulation has been reported to produce increase in arterial wall thickness and promote vascular resistance. [30],[31] As increased arterial stiffness is an established CV risk, [32] SVI in PIH risk women further contribute to CV risks in these subjects. PWV in women with risk factors for PIH was higher compared with that in normotensive controls.

Furthermore, studies in women with a history of PIH have demonstrated increased PWV (carotid femoral) [33] and the persistence of maternal endothelial dysfunction for several months following the index pregnancy. [34] The increased arterial stiffness and SVI [18] in PIH risk factor women observed in our study, could provide a plausible link between this condition and the increased risk of CV events that these women could experience later on in life. [35] In the present study, SVI in the form of increased LF-HF ratio and increased arterial stiffness indices were noted in the first trimester of pregnancy. Our study is the first report to assess the association of SVI with arterial stiffness in the early part of pregnancy. However, though SVI and arterial stiffness were noted in the first trimester, there was no significant correlation of LF-HF ratio with arterial stiffness indices. Therefore, it appeared that in early part of pregnancy, arterial stiffness was not directly linked to the SVI, which was not significant but marginally increased. In the later part of pregnancy, i.e. in the third trimester, SVI was more intense and was found to be significantly correlated with arterial stiffness indices. Moreover, LF-HF ratio had independent contribution to ASI as demonstrated by multiple regression analysis in the third trimester. Therefore, it is likely that SVI has to be more intense to be directly associated with the arterial stiffness. Further studies should be done to assess what factors contribute to arterial stiffness in the initial part of pregnancy, which is accentuated by increased SVI in later part of pregnancy.

Therefore, future studies should evaluate the association of maternal endothelial dysfunction to CV risks attributed by SVI during and after pregnancy in women with risk factors for PIH. Furthermore, findings of the present study demonstrate the presence of ASI in women at high risk for PIH; we suggest that all pregnant women with risk factors for PIH should be screened for SVI and ASI. Moreover, a long term follow up study measuring both ASI and SVI in all three trimesters is necessary to establish the exact mechanism of these alterations. As pregnant women with risk for PIH are at greater risk of cardiac morbidities and mortalities, studies should evaluate if sympathovagal stability by various non-pharmacological means such as yoga and relaxation therapy, [36],[37] can prevent development of PIH in these high-risk subjects.

  Conclusion Top

Our study suggests that SVI is associated with arterial stiffness in pregnant women having risk factors for PIH. Though arterial stiffness persistsed in those women in mild form in the early trimester, it was found to be very prominent in third trimester and it significantly correlated with SVI in third trimester of the women with risk factors for PIH. Therefore, from our study it was found out that SVI and increased arterial stiffness were associated with each other and might contribute to the CV risks in pregnant women with risk factors for PIH.

  Acknowledgments Top

The authors acknowledge the financial assistance from JIPMER authority through the intramural fund granted.

  References Top

1.Dekker G. Hypertension. High Risk Pregnancy, 4 th ed. London: Elsevier; 2010.p. 599-626.  Back to cited text no. 1
2.Walker JJ. Pre-eclampsia. Lancet 2000. 356:1260-1265.  Back to cited text no. 2
3.Hausvater A, Giannone T, Sandoval YH, Doonan RJ, Antonopoulos CN, Matsoukis IL, et al. The association between preeclampsia and arterial stiffness. J Hypertens 2012;30:17-33.  Back to cited text no. 3
4.Kaihura C, Savvidou MD, Anderson JM, McEniery CM, Nicolaides KH. Maternal arterial stiffness in pregnancies affected by preeclampsia. Am J Physiol Heart Circ Physiol 2009;297:H759-64.  Back to cited text no. 4
5.Kurabayashi T, Mizunuma H, Kubota T, Kiyohara Y, Nagai K, Hayashi K. Pregnancy-induced hypertension is associated with maternal history and a risk of cardiovascular disease in later life: Japanese cross-sectional study. Maturitas 2013;75:227-31.  Back to cited text no. 5
6.Skjaerven R, Wilcox AJ, Klungsoyr K, Irgens LM, Vikse BE, Vatten LJ, et al. Cardiovascular mortality after pre-eclampsia in one child mothers: Prospective, population based cohort study. BMJ 2012;345:e7677.  Back to cited text no. 6
7.Romundstad PR, Magnussen EB, Smith GD, Vatten LJ. Hypertension in Pregnancy and Later Cardiovascular Risk: Common Antecedents? Circulation 2010; 122: 579-84.  Back to cited text no. 7
8.Joydev M, Subroto LS, Geeta BB. Current concepts in PIH. In: Geeta GM, editor. Current obstetrics and gynecology. 1 st ed. New Delhi: Jaypee Publications; 2007. p. 93-100  Back to cited text no. 8
9.Hans PS, Thorsten F, Karsten H, Helmut G, Ronal ES. Preeclampsia: A state of sympathetic overactivity. New Eng J Med 1996;335:1480-5.  Back to cited text no. 9
10.Greenwood JP, Stoker JB, Walker JJ, Mary DA. Sympathetic nerve discharge in normal pregnancy and pregnancy-induced hypertension. J Hypertens 1998;16:617-24.  Back to cited text no. 10
11.Pal GK, Shyma P, Habeebullah S, Shyjus P, Pal P. Spectral analysis of heart rate variability for early prediction of pregnancy-induced hypertension. Clin Exp Hypertens 2009;31:330-41.  Back to cited text no. 11
12.Pal GK, Shyma P, Habeebullah S, Shyjus P, Pal P, Nanda N. Association of albumin-globulin ratio with sympathovagal imbalance in pregnancy-induced hypertension. Indian J Physiol Pharmacol 2011;55:128-38.  Back to cited text no. 12
13.Pal GK, Shyma P, Habeebullah S, Pal P, Nanda N, Shyjus P. Vagal withdrawal and sympathetic overactivity contribute to the genesis of early-onset pregnancy-induced hypertension. Int J Hypertens 2011;2011:361417.  Back to cited text no. 13
14.Thayer JF, Yamamoto SS, Brosschot JF. The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors. Int J Cardiol 2010;141:122-31.  Back to cited text no. 14
15.Pal GK, Pal P, Nanda N, Amudharaj D, Adithan C. Cardiovascular dysfunctions and sympathovagal imbalance in hypertension and prehypertension: Physiological perspectives. Future Cardiol 2013;9:53-69.  Back to cited text no. 15
16.Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension 1998;32:560-4.  Back to cited text no. 16
17.Yuan LJ, Xue D, Duan YY, Cao TS, Yang HG, Zhou N. Carotid intima-media thickness and arterial stiffness in preeclampsia by analysis with a radio-frequency ultrasound technique. Ultrasound Obstet Gynecol 2013;42:644-52.  Back to cited text no. 17
18.Paolo Palatini, Edoardo Casiglia, Jerzy G¹sowski, Jerzy G³uszek, Piotr Jankowski, Krzysztof Narkiewicz, et al . Arterial stiffness, central hemodynamics, and cardiovascular risk in hypertension. Vasc Health Risk Manag 2011:7 725-739.  Back to cited text no. 18
19.Vlachopoulos C, Aznaouridis K, Stefanadis C. Prediction of cardiovascular events and all-cause mortality with arterial stiffness: A systematic review and meta-analysis. J Am Coll Cardiol 2010;55:1318-27.  Back to cited text no. 19
20.Benetos A, Safar M, Rudnichi A, Smulyan H, Richard JL, Ducimetieere P, et al. Pulse pressure: A predictor of long-term cardiovascular mortality in a French male population. Hypertension 1997;30:1410-5.  Back to cited text no. 20
21.Chae CU, Pfeffer MA, Glynn RJ, Mitchell GF, Taylor JO, Hennekens CH. Increased pulse pressure and risk of heart failure in the elderly. JAMA 1999;281:634-9.  Back to cited text no. 21
22.Heart rate variability: Standard and measurement, physiological interpretation and clinical use. Task force of the European Society of Cardiology and the North American society of Pacing and Electrophysiology. Circulation 1996;93:1043-65.  Back to cited text no. 22
23.Pal GK, Pal P. Autonomic function tests. In: Textbook of Practical Physiology. 3 rd ed. Chennai: Universities Press; 2010. P . 282-90.  Back to cited text no. 23
24.Yamashina A, Tomiyama H, Takeda K, Tsuda H, Arai T, Hirose K, et al. Validity, reproducibility, and clinical significance of noninvasive brachial-ankle pulse wave velocity measurement. Hypertens Res 2002;25:359-64.  Back to cited text no. 24
25.Palatini P. Heart rate and the cardiometabolic risk. Curr Hypertens Rep 2013;15:253-9.  Back to cited text no. 25
26.Jensen MT, Suadicani P, Hein HO, Gyntelberg F. Elevated resting heart rate, physical fitness and all-cause mortality: A 16-year follow-up in the Copenhagen Male Study. Heart 2013;99:882-7.  Back to cited text no. 26
27.Ganong WF. Cardiovascular regulatory mechanisms. In: Review of Medical Physiology. 22 nd ed. San Fransisco: McGraw Hill; 2005. p. 597-602.  Back to cited text no. 27
28.White WB. Heart rate and the rate-pressure product as determinants of cardiovascular risk in patients with hypertension. Am J Hypertens 1999;12:50-5S.  Back to cited text no. 28
29.Malliani A. Heart rate variability: From bench to bedside. Eur J Intern Med 2005;16:12-20.  Back to cited text no. 29
30.Dinenno FA, Jones PP, Seals DR, Tanaka H. Age-associated arterial wall thickening is related to elevations in sympathetic activity in healthy humans. Am J Physiol Heart Circ Physiol 2000;278:H1205-10.  Back to cited text no. 30
31.Cates MJ, Steed PW, Abdala AP, Langton PD, Paton JF. Elevated vertebrobasilar artery resistance in neonatal spontaneously hypertensive rats. J Appl Physiol (1985) 2011;111:149-56.  Back to cited text no. 31
32.Francesco U.S. Mattace-Raso, Tischa J.M. van der Cammen, Albert Hofman, Nicole M. van Popele, Michiel L. Bos, et al. Arterial stiffness and risk of coronary heart disease and stroke: The Rotterdam study. Circulation 2006;113:657-63.  Back to cited text no. 32
33.Elvan-Taºpinar A, Bots ML, Franx A, Bruinse HW, Engelbert RH. Stiffness of the arterial wall, joints and skin in women with a history of pre-eclampsia. J Hypertens 2005;23:147-51.  Back to cited text no. 33
34.Chambers JC, Fusi L, Malik IS, Haskard DO, De Swiet M, Kooner JS. Association of maternal endothelial dysfunction with preeclampsia. JAMA 2001;285:1607-12.  Back to cited text no. 34
35.Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre-eclampsia and risk of cardiovascular disease and cancer in later life: Systematic review and meta-analysis. BMJ 2007;335:974.  Back to cited text no. 35
36.Monika Mourya, Aarti Sood Mahajan, Narinder Pal Singh, and Ajay K. Jain. Effect of Slow- and Fast-Breathing Exercises on Autonomic Functions in Patients with Essential Hypertension. J Altern Complem Med 2009;15:711-7.  Back to cited text no. 36
37.Pal GK, Ganesh V, Karthik S, Nanda N, Pal P. The effects of short-term relaxation therapy on indices of heart rate variability and blood pressure in young adults. Am J Health Promot  2013. [Epub ahead of print]  Back to cited text no. 37


  [Figure 1], [Figure 2]

  [Table 1], [Table 2], [Table 3], [Table 4]

This article has been cited by
1 Decreased baroreflex sensitivity is linked to sympathovagal imbalance, low-grade inflammation, and oxidative stress in pregnancy-induced hypertension
M. Subha,Pravati Pal,G. K. Pal,S. Habeebullah,C. Adithan,M. G. Sridhar
Clinical and Experimental Hypertension. 2016; 38(8): 666
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
   Materials and me...
   Article Figures
   Article Tables

 Article Access Statistics
    PDF Downloaded380    
    Comments [Add]    
    Cited by others 1    

Recommend this journal