DOI: 10.4172/2167-1095.1000e106
Despite overwhelming evidence linking increased salt intake to hypertension, the relation is still disputed in some circles. Viewing the introduction of salt to human diet on an evolutionary time scale would help us better understand the role of salt in hypertension. Humans and related species evolved in a salt-free environment over millions of years with intense evolutionary pressure for the selection of salt conserving genes. The recorded history confirms how rare and inaccessible salt has been until recently. Thrusting the species that has exquisitely adapted to very low salt intake into salt surfeit conditions represents evolutionary mismatch with catastrophic health consequences. More than a quarter of human populations suffer from hypertension. World Health Organization (WHO) and many governments have now taken action to reduce dietary intake of salt in an effort to reduce the incidence of hypertension and the associated cardiovascular morbidity and mortality.
Seter Siziya, Emmanuel Rudatsikira, Olusegun Babaniyi, Peter Songolo, David Mulenga and Adamson S Muula
DOI: 10.4172/2167-1095.1000105
Background: Hypertension is a major risk factor for cardiovascular disease. The trend towards a higher burden of non-communicable chronic diseases in developing countries is of great concern as it adds to the burden of communicable diseases. The aim of this study was to estimate the prevalence and correlates of hypertension among adults in the City of Kitwe, Zambia.
Methods: A modified WHO STEPs (STEPwise Approach to Surveillance) method was used to collect data through a community-based survey among persons aged 25 years or older living in urban Kitwe, Zambia. Prevalence of hypertension was estimated and compared between males and females. Odds ratio (OR) and adjusted odds ratio (AOR) and their 95% confidence intervals were used to establish associations between exposure factors and hypertension.
Results: Altogether, 1627 persons participated in the survey of which 57.7% were females. Overall, 32.3% (33.5% of males and 31.1% of females, p=0.350) were hypertensive. Age and body mass index were significantly associated with hypertension. Compared to participants who were of age 45 years or older, participants who were below the age of 45 years were less likely to have hypertension (AOR=0.53, 95% CI [0.45, 0.62]) for 25-34 years age group, and AOR=0.61, 95% CI [0.50, 0.74]) for 35-44 years age group). Participants who had BMI of less than 18.5 kg/m2 were 50% (AOR=0.50, 95% CI [0.32, 0.77]) less likely to have hypertension compared to participants who had BMI of 30 kg/m2 or more. Meanwhile, participants who had BMI of 25.0-29.9 kg/m2 were 33% (AOR=1.33, 95% CI [1.05, 1.69] more likely to have hypertension compared to participants who had BMI of 30 kg/m2 or more.
Conclusions: Our findings indicate that hypertension is prevalent among urban residents in Kitwe, Zambia.
Effective prevention strategies including interventions to ensure lower BMIs, should be implemented, taking into considerations the risk factors identified in this study.
LU Chengzhi, WANG Li, Aubdool-Essackjee, Nima Sherpa and LUO Di
DOI: 10.4172/2167-1095.1000106
Reactive oxygen species (ROS) play an important role in the development and maintenance cardio vascular
diseases, especially hypertension. The relationship between ROS and hypertension has been demonstrated in several models of experimental hypertension. Accumulating evidence has suggested that the key mechanism through which Angiotensin II (Ang II) influences blood pressure is via its ability to activate ROS signaling pathways. Ang II, by stimulating angiotensin AT1 receptors, involved in the activation of NAD(P)H oxidase, which is a major source of ROS production. Despite many elegant studies that have been accumulated regarding ROS/Ang II signaling, there is still much to be elucidated in the role of ROS in neurogenic hypertension. The present review mainly discussed some recent findings documenting about the signaling mechanisms of Ang II-induced ROS in neurogenic hypertension and therapeutic target.
Alynne S. Carvalho, Drielle D. Guimaraes, Bruna P. V. Dantas, Juliana N. Carreiro, Leonidas G. Mendes-Junior, Maria S. França-Silva, Matheus M.O. Monteiro, Naiane F.B. Alves, Suênia K.P. Porpino, Thyago M. Queiroz and Valdir Andrade Braga
DOI: 10.4172/2167-1095.1000107
Hypertension and its relation to free radicals have been matter of continuous research worldwide. This review is based on the premise that some forms of neurogenic hypertension is, in part, caused by the formation of Angiotensin- II (Ang II)-derived reactive oxygen species within the brain, especially in areas along the Subfornical Organ- Paraventricular Nucleus of the Hypothalamus-Rostral Ventrolateral Medulla pathway (SFO-PVN-RVLM pathway). Here we will discuss the recent contribution of our laboratory and others regarding the mechanisms by which neurons in the Rostral Ventrolateral Medulla (RVLM) are activated by Ang II, how they communicate with the SFO and PVN and more importantly, how Ang II-derived Reactive Oxygen Species (ROS) participate along the SFO-PVN-RVLM pathway in the pathogenesis of neurogenic hypertension.
Maria Jonsson, Ulf Hanson, Christer Lidell and Solveig Nordén-Lindeberg
DOI: 10.4172/2167-1095.1000108
Background: Electrocardiogram changes suggestive of myocardial ischemia, ST depressions, have been reported to be associated with oxytocin administration in healthy women undergoing cesarean section in regional anesthesia. We investigated whether there was a difference in the occurrence of ST depressions on electrocardiograms in preeclamptic women randomized to five or ten units of oxytocin during cesarean section with regional anesthesia.
Methods: Double-blind randomized controlled trial. Twenty-five women with preeclampsia delivered by cesarean section under spinal anesthesia were allocated to 5 or 10 units of oxytocin, given as an intravenous bolus. A Holter monitor was used to record electrocardiograms. Non-invasive blood pressure and heart rate were monitored. The main outcome measure was depression of the ST segment on electrocardiogram related to oxytocin bolus; the secondary outcomes were changes in mean arterial pressure and heart rate related to oxytocin bolus.
Results: ST depressions associated with oxytocin administration occurred in two women (8%), one in each group. The decrease in mean arterial pressure from baseline to 2 minutes after the oxytocin bolus differed within groups, with 12 mmHg in the five unit group and 16 mmHg in the ten unit group (p<0.01). The increases in mean heart rate from baseline to 2 minutes after the oxytocin bolus did not differ.
Conclusion: ST depressions on electrocardiograms were uncommon in patients with preeclampsia undergoing cesarean section in regional anesthesia, although the hemodynamic changes associated with an oxytocin bolus were substantial.
Journal of Hypertension: Open Access received 614 citations as per Google Scholar report