3. Electronic Theses and Dissertations (ETDs) - All submissions

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    The socio-economic impact on health behaviour regarding blood pressure management amongst young adults
    (2024) Mhlaba, Mimi
    Hypertension (HTN) is a leading cause of cardiovascular disease (CVD), with hypertension prevalence among young adults (YAs) increasing on a global as well as local scale. In South Africa between 1998 and 2016, Hypertension (HTN) rates in YAs (age 15-34 years) have more than doubled. Research reports that the increasing prevalence of HTN in YAs is largely attributed to unhealthy behaviours, such as unhealthy diet, physical inactivity, smoking, drinking alcohol, and poor sleep, with YAs also perceiving themselves as invulnerable to developing HTN at a young age. Formative research has shown that lack of education, employment, and training (NEET status) presents a significant barrier to healthier behaviours in YAs. Currently, 44.7% of South African youth are NEET, indicating the increased risk of pro-HTN behaviour in this group and the need for urgent intervention. While many learnerships addressing NEET rates in the country have been implemented, few are focused on health. Therefore, this study aimed to investigate if transitioning from a NEET status to employment and health education training changes perceptions of HTN risk and health behaviour intentions. METHODS We conducted six focus group discussions (FGDs) comparing HTN-related beliefs and intention for behaviour change between NEET youth (n=20; not in employment, education, or training) and previously NEET youth on a health employment and education training initiative (HETI); n=20). All FGDs were approximately 70 minutes in duration and were recorded and transcribed verbatim. The study utilised the conceptual framework of the Health Belief Model (HBM) to inform the FGD topic guide and a deductive thematic analysis. Frequent debriefing and review sessions with research supervisors were conducted to ensure the quality of the analysis. RESULTS All youth were familiar with HTN but for NEET youth, who only knew it as “high-high” or “high blood”, this was mostly through experiences of others in their social network. While all youth viewed HTN as life-threatening if left untreated and expressed fear of lifelong medication use if diagnosed, only HETI youth felt empowered to implement positive health behaviours for disease prevention. Intention for behaviour change was related to personal relevance resulting from the practical application of HTN knowledge in their daily lives. In contrast, NEET youth felt chronic disease was inevitable at an older age and demonstrated no intention for behaviour change. Past negative experiences in local clinics and the fear of distress in the event of a possible diagnosis were described as major deterrents to blood pressure (BP) screening. CONCLUSION Results suggest that engaging NEET (Not in employment, education, or training) youth in similar HETI (Health employment and education training initiative) programs can increase personal relevance of health information, which serves as a motivator to increase intentions toward healthier behaviours for chronic disease prevention. This may also result in double-duty benefits, reducing a NEET status as well as the risk for chronic illness among the YA population.
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    Interaction between low dietary potassium and high dietary sodium intake on blood pressure in adult rats
    (2016) Mokotedi, Lebogang, Palesa
    Although it is well known that an increase in sodium intake (Na+) increases BP and is involved in the development of salt-sensitive hypertension (SS-HTN), the mechanism responsible for this increase in BP is uncertain. Further while low dietary potassium (K+) is also associated with the development of SS-HTN it is uncertain to what extent dietary potassium (K+) affects Na+-induced increases in BP. The purpose of this study was to determine whether Na+-induced increases in BP and target organ changes are altered by reductions in K+ intake. Four-month-old male Sprague-Dawley (SO) rats were randomly assigned to three dietary intervention groups for six weeks: a normal Na+ (0.3%), normal K+ (1.6%) group (CON, n=12), a high Na+ (6%), normal K+ (1.6%) group (NK+-HNa+, n=12) and a high Na+ (6%), low K+ (0.01%) group (LK+-HNa+, n=12). Tail-cuff BP, body weight, food and water intake were measured weekly. At termination, urine parameters, right kidney weight as well as left ventricular dimensions and function were measured. Vascular reactivity of the mesenteric and renal arteries was also assessed using a wire-myograph. During the diet intervention, water intake was significantly higher in the NK+-HNa+ and LK+-HNa+ groups compared to the CON group (P<0.0001). Although food intake was significantly lower in the NK+-HNa+ and LK+-HNa+ groups compared to the CON group during the first week (P=0.03 and P=0.05 respectively), no significant differences in body weight were observed between the groups (P>0.05). The urinary Na+/K+ ratio was higher in the LK+ HNa+ compared to the CON and NK+ -HNa+ groups (P<0.001). Following the 6 week dietary intervention, the systolic BP was significantly higher in the NK+-HNa+ and the LK+-HNa+ groups compared to the CON group (P=0.05 and P=0.04 respectively). The diastolic BP was significantly higher in the NK+-HNa+ and LK+-HNa+ groups compared to the CON group (P=O.05 and P=O.02, respectively). The increase in BP was not different between the NK+-HNa+ and LK+-HNa+ groups (P>O.05). In the mesenteric arteries, there was a significant increase in vascular responsiveness to phenylephrine in the NK+-HNa+ group compared to the CON group (P=O.02). However the vascular responsiveness to phenylephrine in the mesenteric arteries was similar between the NK+-HNa+ and LK+-HNa+ groups (P=O.82). No significant differences in vascular reactivity were observed in the renal arteries between the three groups. No significant differences were observed in the left ventricular dimensions and function between the different diet groups (P>O.05). In conclusion, 6 weeks of high Na+ intake increases BP, induces greater phenylephrine-induced contractions in mesenteric arteries but does not affect heart dimensions and function. The greater phenylephrine-induced contractions with a high Na+ intake may be responsible for the increase in BP. However a reduction in dietary K+ intake does not have any effect on the high Na+-induced changes in BP or mesenteric artery reactivity.
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    Mode of Impact of Genetic Determinants of Hypertension in People of African Descent
    (2006-11-10T11:37:30Z) Ngwenchi, Nkeh Benedicta
    Blood pressure (BP) is a heritable trait. However, the loci responsible and the mechanisms by which these genes determine BP are uncertain. Based on widely published data regarding frequent phenotypic characteristics that exemplify essential hypertension (EHT) in persons of African ancestry, in the present thesis I explored the role of gene candidates most likely to contribute to BP in this group. In this regard a high frequency of persons of African descent experience increases in BP in response to an enhanced salt intake (salt-sensitive hypertension). In addition, many patients of African origin with EHT fail to respond to inhibition of angiotensin-converting enzyme (ACE) with an appropriate decrease in BP, a factor that cannot be explained entirely on the basis of reduced plasma renin levels in this group. Thus, I evaluated the role of several gene variants that could influence either renal salt handling or the activity and effects of the renin-angiotensin system on BP in subjects of African ancestry. Although the angiotensinogen (AGT) gene has at least 3 variants in the promoter region that influence angiotensinogen expression and which occur with a remarkably high frequency in populations of African ancestry, their role in this group is still controversial. To-date, interactions between these variants have not been considered. Using a casecontrol study design in a sample of 1325 subjects, as well as association analysis with 24 hour ambulatory BP (ABP) values in 626 hypertensives, I confirmed that an independent effect of functional AGT gene variants on the risk for EHT or 24 hour ABP was weak at best. Importantly, however, interactions between the -20A C and -217G A variants were noted to strongly impact on the risk for EHT as well as ABP. Furthermore, interactions between the -20A C and -217G A variants played a major role in iii contributing toward the variability of ABP responses to ACE inhibitors, but not calcium channel blockers in this population group, with genotype determining whether or not ACE inhibitor responses occurred. Although the 825C T polymorphism of the guanosine triphosphate (G) protein 3 subunit (GNB3) gene influences the activity of a substance that modifies renal salt handling, namely the Na+/H+ exchanger, its impact in hypertensives of African descent is controversial. In the present thesis I confirmed in a large sample that the GNB3 variant was not associated with the risk for EHT or ABP values in subjects of African ancestry. However, because the activity of the exchanger is enhanced in obesity I hypothesised that the GNB3 gene variant could mediate a clinically relevant BP effect by modifying the impact of body size on BP (type I or II genetic effect). Indeed, GNB3 genotype proved to be a strong determinant of the impact of body size on systolic BP values, with genotype determining whether or not the effect occurred. The epithelial sodium channel (ENaC) and atrial natriuretic peptide (ANP) have an important influence on renal salt handling. The T594M polymorphism of the -subunit of the ENaC gene only exists with a relatively high frequency in subjects of African ancestry. Previous studies conducted in this population group in relatively small samples have indicated that the ENaC and ANP gene variants determine BP in subjects of African descent. In a larger sample of subjects of African descent I demonstrated that the T594M polymorphism of the ENaC gene has no impact on BP in this population group. However, my results suggest that the ANP gene may be a candidate worthy of further study. In conclusion, the results described in this thesis provide evidence that lends some clarity to the role of likely gene candidates for BP control in people of African descent. iv Importantly, data from this thesis suggest that interactions between functional variants of specific loci (e.g the AGT gene), and clinically relevant type I or II genetic effects (no independent actions, but modifier gene effects, e.g, GNB3) should be considered before excluding loci as playing an important role in BP control. Moreover, this thesis provides the first substantial data to indicate that gene variants determine the variability of BP responses to pharmacological agents in hypertension in this population group.
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