Blood pressure in third-year students of GrSMU based on family history of hypertension

Research Article

Blood pressure in third-year students of GrSMU based on family history of hypertension

Сai M ^*
Lelevich A.V.
Bon E.I.
Satsuta P.P.
Yankovskaya E.A.
Victoria Alekseevna Demko V.A.
Pashkevich P.A.

Grodno State Medical University, Republic of Belarus.

*Corresponding Author: Сai M, Grodno State Medical University, Republic of Belarus.

Citation: Сai M, Lelevich A.V, Bon E.I, Satsuta P.P, Yankovskaya E.A, Victoria Alekseevna Demko V.A, et al. (2026). Blood pressure in third-year students of GrSMU based on family history of hypertension, Clinical Case Reports and Studies, BioRes Scientia Publishers. 12(6):1-4. DOI: 10.59657/2837-2565.brs.26.335

Copyright: © 2026 Cai M, this is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Received: June 24, 2026 | Accepted: July 08, 2026 | Published: July 20, 2026

Abstract

The study aimed to analyze blood pressure (BP) levels and the prevalence of hypertension among third-year students at GrSMU (2025/2026) with a family history of the condition. It was found that female students with parental hypertension have higher diastolic BP values (p=0.039). Among male students with a paternal history, episodes of elevated BP occur twice as often (45.0% vs. 21.74%; p=0.04). The results confirm the impact of family history on the risk of elevated BP in medical students.

Keywords: blood pressure; family history; hypertension

Introduction

The genetic component accounts for up to 30-50% of the variability in blood pressure (BP) levels [1]. Against the background of hereditary predisposition, external environmental factors exert a greater influence on the risk of developing arterial hypertension (AH) [2]. To date, over 1,000 genetic loci influencing BP have been identified [3].

One such genetic factor is the polymorphism of the α-adducin gene. Adducin is a heterodimeric cytoskeletal protein of cell membranes that plays a crucial role in the formation of spectrin-actin complexes. It also serves as a substrate for protein kinases C and A. Adducin is known to participate in cellular sodium ion transport by regulating Na+/K+-ATPase activity. Mutations in the α-adducin gene can lead to increased sodium reabsorption across the renal tubular membrane, potentially contributing to the development of arterial hypertension [4].

It is well established that the renin-angiotensin-aldosterone system (RAAS) plays a key role in blood pressure regulation. Therefore, identifying genetic defects within RAAS components is essential for understanding the pathogenesis of AH. In particular, the study of mutations in the angiotensinogen gene, which encodes the precursor of angiotensin II, is of significant interest. Most currently known mutations in this gene result in amino acid substitutions. Such changes can lead to a substantial increase in the concentration of angiotensin II in the body. By interacting with angiotensin receptors on the cell surface, angiotensin II exerts a vasoconstrictive effect, which may clinically manifest as arterial hypertension [5].

The functioning of the RAAS is closely linked to the genetic characteristics of intracellular signaling. A key marker in this context is the C825T polymorphism of the GNB3 gene, which encodes the β3 subunit of the G-protein. In carriers of the 825T variant, this protein becomes hyperactive. This leads to enhanced cellular Na+/H+ exchange, causing the kidneys to retain excessive sodium. Consequently, blood volume increases, and blood vessels become more sensitive to angiotensin II, leading to a persistent increase in blood pressure, especially with high salt intake [6].

The next genetic marker is the angiotensin-converting enzyme (ACE) gene. This enzyme plays a key role in the RAAS by catalyzing the conversion of angiotensin I to angiotensin II. Additionally, ACE participates in maintaining electrolyte balance and influences fibrinolysis, as well as platelet activation and aggregation, thereby playing a significant role in the regulation of hemostasis. Polymorphisms of the ACE gene may be associated with an increased risk of several conditions, including essential arterial hypertension, myocardial infarction, left ventricular hypertrophy, and renal diseases accompanied by hypertension [7].

One of the key targets is the aldosterone synthase gene (CYP11B2). Studies across various age groups show that the -344C/T polymorphism in the promoter region of this gene directly affects BP levels. Carriers of the T allele (especially the TT genotype) exhibit higher aldosterone secretion and elevated systolic BP compared to carriers of the CC variant. This genetic defect causes the kidneys to excessively retain sodium and water, leading to increased blood volume and a persistent rise in pressure as early as middle age [8].

The endothelin-1 gene encodes a protein that plays a substantial role in maintaining vascular tone and BP. Endothelin-1 is a potent vasoconstrictor. Mutations in the endothelin-1 gene can lead to increased synthesis of the protein, causing constant vasoconstriction and elevated BP. Increased levels of endothelin-1 can reduce the effectiveness of vasodilators, such as nitric oxide, further contributing to hypertension. It is important to note that endothelin-1 interacts with other hormonal systems, such as the RAAS, which can further exacerbate hypertension [9].

It is also necessary to note the significant influence of endothelial nitric oxide synthase (eNOS) on maintaining normal BP. This enzyme, present in endothelial cells and cardiomyocytes, is responsible for the synthesis of nitric oxide (NO) – a molecule that induces vascular smooth muscle relaxation and, consequently, vasodilation. In addition to its vasodilatory effect, nitric oxide also exhibits antiplatelet properties, preventing thrombus formation. It is important to emphasize that mutations in the eNOS gene can lead to functional impairment. This, in turn, may be accompanied by decreased gene expression, vasospasm, increased BP, and a subsequent rise in the risk of developing arterial hypertension [10].

Mutations in genes responsible for regulating sympathetic nervous system (SNS) tone can significantly affect the levels of neurotransmitters, such as norepinephrine, and other biologically active substances. These changes can trigger the development of arterial hypertension through several mechanisms. First, a mutation may lead to increased norepinephrine synthesis in sympathetic neurons. As the primary neurotransmitter of the SNS, norepinephrine is responsible for vasoconstriction and increased cardiac output, which results in elevated BP. Alterations in genes encoding enzymes involved in norepinephrine synthesis can lead to its overproduction. Second, mutations can affect the receptors to which norepinephrine binds. For instance, changes in genes encoding adrenoceptors can increase their sensitivity or their density on the cell surface. This enhances the effect of norepinephrine on the heart and blood vessels, further contributing to hypertension. Third, mutations may involve other neurotransmitters, such as dopamine and serotonin, which play important roles in regulating vascular tone and BP. Changes in their levels can disrupt the balance between sympathetic and parasympathetic activity, which may also promote the development of hypertension [11].

Aim: to study blood pressure levels, the prevalence of BP categories, and the history of elevated BP episodes among third-year students at Grodno State Medical University (2025/2026 academic year) with a parental history of arterial hypertension.

Methods

The study involved 385 female and 160 male third-year students at Grodno State Medical University (2025-2026). Voluntary informed consent was obtained from all participants. Data were collected via an anonymous survey. Students were questioned regarding a history of elevated BP episodes (responses: "yes", "no", "don't know") and parental history of hypertension (responses: "yes", "no", "don't know"). Students who responded "don't know" to these questions were excluded from the study.

BP was measured in accordance with WHO recommendations using a manual sphygmomanometer (Korotkoff method) [12]. Students who had smoked or consumed tea, coffee, or energy drinks within one hour prior to BP measurement were excluded from the analysis. Statistical analysis was performed using StatSoft STATISTICA 10.0 software. Quantitative data were presented as medians (Me) with the 25th and 75th percentiles. Comparisons of quantitative variables between two independent groups were conducted using the non-parametric Mann-Whitney U-test. Categorical variables were expressed as absolute frequencies (n) and percentages (%). Frequency distributions were compared using Pearson's chi-squared (χ²) test and Fisher's exact test. The threshold for statistical significance (p) was set at 0.05.

Results

The study found that among female students with hypertension, 17.1% (n=66) had affected fathers, 15.8% (n=61) had affected mothers, and 5.2% (n=20) had both parents with the condition.

Female students whose fathers suffer from hypertension have higher DBP values, compared to those whose fathers do not suffer from hypertension: 75.0 (70.0; 85.0) and 70.0 (65.0; 80.0) mmHg, respectively, p=0.007, table 1. Female students whose mothers suffer from hypertension have higher DBP values, compared to those whose mothers do not suffer from hypertension: 79.0 (70.0; 80.0) and 70.0 (65.0; 80.0) mmHg, respectively, p=0.04.

Table 1: Blood pressure of GrSMU third-year female students (2025/2026 academic year) based on parental history of hypertension, Me (25%; 75%)

	Arterial hypertension in the father		p-value
	absent (n=150)	present (n=60)
DBP, mm Hg	70.0 (65.0; 80.0)	75.0 (70.0; 85.0)	0.007
	Arterial hypertension in in the mother
	absent (n=138)	present (n=38)
DBP, mm Hg	70.0 (65.0; 80.0)	79.0 (70.0; 80.0)	0.039

In female students whose fathers suffer from hypertension, the frequency of occurrence of the high blood pressure category is higher than in those whose fathers do not suffer from hypertension: 17.39% (8 people) and 6.84% (8 people), respectively, p=0.048, table 2.

Table 2: Blood pressure categories by paternal history of hypertension among third-year female students of GrSMU in the 2025/2026 academic year, % (n).

	n	Low BP	Optimal BP	Normal BP	High-normal BP	High BP
Non-hypertensive father	117	11,11% (13)	36,75% (43)	31,62% (37)	13,68% (16)	6,84%(8)
Hypertensive father	46	2,17% (1)	34,78% (16)	23,91% (11)	21,74% (10)	17,39%(8)

It was found that 16.3% (n=26) of male students had fathers with arterial hypertension (AH), 7.5% (n=12) had mothers with AH, and 3.6% (n=5) had both parents affected.

Among young men, those with a paternal history of AH exhibited episodes of elevated blood pressure (BP) significantly more often than those without such a history: 45.00% (9 out of 20) versus 21.74% (15 out of 69), respectively (p=0.04), table 3.

Table 3: Frequency of elevated blood pressure episodes in third-year male students of GrSMU in the 2025/2026 academic year based on paternal history of arterial hypertension, % (n).

Paternal AH	n	No episodes of low BP	Episodes of low BP present
No	69	78.26% (54)	21.74% (15)
Yes	20	55.00% (11)	45.00% (9)

Conclusion

A family history of hypertension on both the maternal and paternal lines in third-year female students of GrSMU is associated with significant changes in hemodynamic parameters, specifically an increase in diastolic blood pressure. Furthermore, the "high-normal" blood pressure category is more prevalent among female students whose fathers have hypertension. Similarly, the presence of arterial hypertension in fathers significantly increases the risk of elevated blood pressure episodes in their sons. These findings further confirm the role of the hereditary factor in the early onset of cardiovascular disorders among young adults, necessitating targeted screening for students in these high-risk groups.

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