Hypertension is one of the most important modifiable cardiovascular risk factors and contributes substantially to cardiovascular, cerebrovascular, and renal morbidity. Its development reflects a complex interaction among genetic susceptibility, environmental exposures, behavioural factors, vascular regulation, renal mechanisms, and autonomic nervous system activity. A positive parental history of hypertension is an established marker of increased susceptibility, and physiological abnormalities may be detectable in susceptible offspring before sustained hypertension becomes clinically apparent [1,2].

The autonomic nervous system has an important role in short-term cardiovascular regulation through dynamic modulation of heart rate, cardiac contractility, vascular resistance, and blood pressure. Disturbances in the balance between sympathetic and parasympathetic cardiovascular control have consequently attracted attention as potential early features in the pathophysiology of essential hypertension. Studies involving normotensive offspring of hypertensive parents have reported differences in autonomic modulation, including altered heart rate variability and baroreflex function [3,4].

Heart rate variability represents the physiological variation in the intervals between consecutive normal heartbeats. HRV provides a non-invasive method of characterizing cardiac autonomic modulation. Time-domain indices such as the standard deviation of normal-to-normal intervals (SDNN) reflect overall variability, whereas the root mean square of successive differences (RMSSD) predominantly reflects short-term vagally mediated variability. In frequency-domain analysis, the high-frequency (HF) component is strongly influenced by parasympathetic modulation and respiration, while low-frequency (LF) power reflects more complex autonomic and baroreflex influences. The LF/HF ratio has historically been used as an index of sympathovagal balance, although its interpretation as a direct measure of sympathetic-to-parasympathetic balance requires caution [5].

Several investigations have identified autonomic alterations among normotensive individuals with a family history of hypertension. Piccirillo et al. reported altered autonomic modulation of heart rate and blood pressure among normotensive offspring of hypertensive subjects [3]. Studies in young adults have similarly demonstrated reductions in vagally related HRV indices and changes in frequency-domain parameters [6,7]. Obesity and other cardiometabolic factors may further influence these autonomic abnormalities [8].

A meta-analysis examining young adults with a family history of hypertension found lower RMSSD, SDNN, and HF values together with higher LF and LF/HF values compared with individuals without such a family history [9]. These observations suggest that altered cardiac autonomic regulation may precede clinically apparent hypertension.

Early identification of such physiological changes is potentially important because individuals at familial risk can be targeted for longitudinal observation and modification of established cardiovascular risk factors. Therefore, the present study was designed to assess resting HRV among normotensive offspring of hypertensive parents and compare it with that of normotensive offspring of normotensive parents.

This was designed as a cross-sectional comparative study conducted in the Department of Physiology of a tertiary-care teaching institution. The study population consisted of apparently healthy young adults aged 18–30 years. Institutional Ethics Committee approval should be obtained before recruitment, and written informed consent should be obtained from every participant. Study Population A total of 100 participants were divided into two groups. Group I – Study group: 50 normotensive participants having at least one biological parent diagnosed with hypertension. Group II – Control group: 50 normotensive participants whose biological parents had no known history of hypertension. The groups were frequency-matched for age and sex as far as practicable. Inclusion Criteria Participants aged 18–30 years, currently normotensive, apparently healthy, and willing to provide written informed consent were eligible. For Group I, a documented or reliable history of hypertension in at least one parent was required. For Group II, both parents were required to have no known history of hypertension. Exclusion Criteria Participants with diagnosed hypertension, diabetes mellitus, known cardiovascular disease, chronic kidney disease, thyroid disorders, neurological disorders, clinically significant arrhythmias, or other illnesses known to influence autonomic function were excluded. Individuals taking drugs known to substantially affect heart rate or autonomic function were also excluded. Acute illness at the time of examination was an additional exclusion criterion. Study Procedure Participants were instructed to avoid vigorous physical activity and caffeine-containing beverages before testing and to attend after an adequate period without smoking or other stimulants. Recordings were performed in a quiet room under comfortable environmental conditions. Height and weight were measured using standardized techniques, and body mass index (BMI) was calculated as weight in kilograms divided by height in metres squared. After resting quietly in the supine position, blood pressure was measured using a validated sphygmomanometer or automated device with an appropriately sized cuff. Multiple readings were obtained according to the study protocol, and the average was used for analysis. Heart Rate Variability Recording A continuous ECG was recorded with the participant resting supine and breathing spontaneously. A stable five-minute segment was selected for short-term HRV analysis in accordance with accepted methodological principles [5]. The ECG signal was examined for artefacts and ectopic beats before analysis. Normal-to-normal intervals were extracted and analysed using validated HRV software. The following parameters were assessed: Time-domain parameters: SDNN and RMSSD. Frequency-domain parameters: total power, LF power (0.04–0.15 Hz), HF power (0.15–0.40 Hz), LFnu, HFnu, and LF/HF ratio. Because respiration can materially influence HF power, respiratory conditions should be standardized or documented during recording. Statistical Analysis Data were entered into a spreadsheet and analysed using appropriate statistical software. Continuous variables were summarized as mean ± standard deviation when approximately normally distributed and as median with interquartile range when skewed. Categorical variables were expressed as frequencies and percentages. Between-group comparisons were performed using the independent-samples Student's t-test for normally distributed continuous variables and the Mann–Whitney U test for non-normally distributed variables. Categorical variables were compared using the chi-square or Fisher's exact test. A two-sided p-value <0.05 was considered statistically significant. Multivariable analysis may additionally be performed to account for BMI, sex, physical activity, resting heart rate, and other potential confounding variables.

A total of 100 participants were included, with 50 participants in each group. The demographic characteristics of the groups were comparable.

Table 1. Baseline characteristics of study participants

The groups did not differ significantly in age or BMI. Resting heart rate, systolic blood pressure, and diastolic blood pressure were higher in the hypertensive-parent group, although participants remained within the study's normotensive eligibility criteria.

Table 2. Comparison of time-domain HRV parameters

Both SDNN and RMSSD were lower in the hypertensive-parent group. The reduction in RMSSD was consistent with lower vagally mediated beat-to-beat variability, while lower SDNN indicated reduced overall short-term variability.

Table 3. Comparison of frequency-domain HRV parameters

HF power and HFnu were lower among offspring of hypertensive parents. LFnu and the LF/HF ratio were higher, whereas absolute LF power did not differ significantly. Taken together, the illustrative pattern suggests reduced vagal modulation rather than demonstrating a simple isolated increase in sympathetic activity.

The present study was designed to evaluate cardiac autonomic modulation in normotensive offspring of hypertensive parents using short-term HRV analysis. In the illustrative dataset, individuals with a parental history of hypertension exhibited lower SDNN, RMSSD, total power, HF power, and HFnu, together with higher LFnu and LF/HF ratio than controls. These findings would support the hypothesis that autonomic alterations can be detectable before the development of sustained hypertension. The reduction in RMSSD and HF-related indices is particularly relevant because these measurements are strongly associated with cardiac parasympathetic modulation. Reduced SDNN additionally indicates lower overall short-term variability. However, interpretation of LF and especially the LF/HF ratio should be cautious because LF power is not a pure measure of cardiac sympathetic activity and the LF/HF ratio cannot universally be interpreted as a direct numerical measure of sympathovagal balance [5]. The overall pattern is consistent with previous research. Piccirillo et al. studied normotensive offspring of hypertensive subjects and identified abnormalities in autonomic modulation and baroreflex-related cardiovascular regulation [3]. Similarly, HRV studies among young normotensive individuals with parental hypertension have reported alterations in both time- and frequency-domain measures [6,7]. Johncy et al. evaluated young normotensive offspring of hypertensive parents and found that obesity could further accentuate autonomic dysregulation. Obese offspring with parental hypertension showed higher heart rate and LF/HF ratio together with reductions in total power, HF, SDNN, RMSSD, and pNN50 [8]. This highlights the importance of considering BMI and related metabolic characteristics when studying familial hypertension. More importantly, evidence is not limited to individual small studies. A meta-analysis involving 38 studies and 2,025 young adults found that participants with a family history of hypertension had higher clinic systolic and diastolic pressures. HRV analysis demonstrated lower RMSSD, SDNN, and HF alongside higher LF and LF/HF values [9]. These pooled findings strengthen the evidence that a familial predisposition to hypertension is associated with measurable differences in cardiovascular autonomic regulation. Altered autonomic responses may also become apparent during physiological stress. Almeida et al. reported impaired cardiac autonomic modulation during isometric exercise among offspring of hypertensive parents despite similar blood pressure and heart-rate responses between groups [10]. Thus, resting HRV and autonomic responses to physiological challenges may provide complementary information. The findings have potential preventive relevance. A positive family history is non-modifiable, but many factors influencing cardiovascular risk—including excess adiposity, physical inactivity, smoking, dietary patterns, and metabolic abnormalities—are modifiable. Identifying physiological alterations in apparently healthy high-risk young adults could support longitudinal cardiovascular risk assessment.

Normotensive offspring of hypertensive parents may demonstrate altered cardiac autonomic modulation before the appearance of sustained hypertension. Lower SDNN, RMSSD, and HF-related measures would be consistent with reduced vagal modulation, while changes in LF-related measures may reflect altered autonomic and baroreflex regulation. Short-term HRV is non-invasive and relatively simple to obtain under standardized conditions, making it useful as a research tool for investigating early cardiovascular autonomic alterations in individuals with familial susceptibility to hypertension. However, HRV should not be considered a standalone diagnostic test for predicting hypertension. Prospective longitudinal studies with larger populations and control of important confounding factors are required to determine its predictive clinical value.

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