Journal of Preventive Medicine

Abstract

Since the late 1990s, a number of drugs have been developed that have been shown to be effective in phase 3 randomised controlled trials, despite the fact that pulmonary arterial hypertension is a rare condition. The prognosis for pulmonary arterial hypertension remains poor despite significant advancements in treatment. With vasodilation and anti-proliferative effects, current treatments target pulmonary endothelial dysfunction. Urgently needed are new treatments that affect important outcomes and target proliferative vascular remodelling. In order to conduct thorough research on each and every emerging candidate therapy, additional advancements in the design of clinical trials are required. The primary endpoint of pulmonary arterial hypertension trials is now larger clinical event-driven trial outcomes rather than short-term submaximal exercise capacity. Due to the need for larger sample sizes and longer follow-up periods, which would be problematic in such a rare disease, event-driven pulmonary arterial hypertension trials may face feasibility and efficiency issues in the future. Enhancement strategies, novel trial endpoints, and novel trial designs all have the potential to boost the efficiency of upcoming studies on pulmonary arterial hypertension while maintaining robustness and clinically relevant evidence. The gasotransmitter family includes Hydrogen Sulfide (H2S), carbon monoxide, and nitric oxide. By regulating vascular tone, sympathetic nervous system activity, and renal sodium excretion, H2S is involved in controlling blood pressure. Mice that lack the enzyme Cystathionine -Lyase (CSE), which is involved in the production of H2S in the cardiovascular system, develop moderate age-dependent hypertension as well as endothelial dysfunction. In the most common animal models of hypertension, such as spontaneously hypertensive rats, Dahl salt-sensitive rats, chronic administration of NO synthase inhibitors, angiotensin II infusion, and two-kidney-one-clip hypertension, the model of renovascular hypertension, decreased H2S concentration, as well as the expression and activities of H2S-producing enzymes. In these models, H2S donors lower blood pressure, but in animals with normal blood pressure, they have no significant effect.

Erectile Dysfunction

End-organ damage like vascular and myocardial hypertrophy and remodeling, hypertension-associated kidney injury, and erectile dysfunction can all be reduced by H2S donors. Some antihypertensive medications, natural products with antihypertensive activity like garlic polysulfides or plant-derived isothiocyanates, and non-pharmacological interventions can alter H2S level and signaling. The novel therapeutic strategy that has the potential to treat hypertension is to alter H2S signaling; nonetheless, additional experimental clinical studies investigating the role of H2S in hypertension are required.Ca2+-activated chloride channels (CaCCs) are based on TMEM16A, a member of the TMEM16 family, which is involved in numerous physiological and pathological processes. Diseases and tumors related to the respiratory system have been the primary focus of previous research. However, TMEM16A has recently been shown to play a significant role in cardiovascular diseases, particularly pulmonary hypertension. TMEM16A plays a role in the development of pulmonary hypertension because it is expressed in both smooth muscle cells and endothelial cells of the pulmonary artery. The pathogenesis of pulmonary hypertension, the structure and function of TMEM16A, and the role and mechanism of TMEM16A in pulmonary hypertension are all discussed in this paper, along with the controversies surrounding this topic and the similarities between hypertension and portal hypertension. It is hoped that this study will show how TMEM16A plays a unique role in pulmonary hypertension and spark ideas for future research. It is difficult to manage hypertension in older people who are hospitalized. Hypertension is common multiple comorbidity among older adults. When elderly patients with community-acquired pneumonia are admitted to the hospital with hypertension, nurse practitioners are essential. It is challenging to select the ideal blood pressure goal for these vulnerable patients due to the disparity between the national guidelines for managing hypertension and the lack of guidelines for managing hypertension in inpatient settings. The management of hypertension in older adults hospitalized with community-acquired pneumonia is the subject of this report. Preterm birth appears to be a risk factor for adult hypertension and Cardiovascular Disease (CVD), according to increasing evidence. It is unknown whether hypertension has any effect on CVD risk. We used data from the Women's Health Initiative on 2,303 women between the ages of 50 and 79 who self-reported being born preterm to see if there were any correlations between preterm birth, hypertension, and incident CVD.

Prevalence of Hypertension

By birth status (preterm, full-term), prevalence of hypertension at enrollment, age at hypertension diagnosis, and antihypertensive medication use were compared using multivariable logistic regression. Multivariable Cox proportional-hazard models were used to evaluate the risk of CVD, incident hypertension, and coronary heart disease. Age, race/ethnicity, education, smoking, physical activity, BMI, and diabetes were all taken into account in both models. Premature birth and prevalent hypertension were found to be significantly correlated (37 percent vs. 33.1%; p = 0.0001), early-onset hypertension (50 years) (14.7% vs. 11.7%; adjusted odds ratio 1.26; 95 percent confidence interval (CI) 1.15 to 1.28; incident hypertension. Antihypertensive use was found to be higher in preterm-born women (2.9% vs. 2.6%, p = 0.04). Women born preterm without hypertension had an elevated CVD risk compared to women born full term without hypertension when stratified by prevalent hypertension. However, the association between preterm birth and CVD risk was nonsignificant. Both preterm and full-term women with prevalent hypertension had similar increases in cardiovascular disease risk. In conclusion, preterm birth raises the risk of heart disease and hypertension. Birth history should be considered as a CVD risk factor because 10% of babies are born prematurely. Plasma renin activity is lower and volume responsive hypertensive patients respond better to diuretic monotherapy than other hypertensive patients. We hypothesized that hormones like vasopressin and antidiuretic hormone (ADH), which influence extracellular volume, might make it possible to develop a straightforward test to identify people with volume-related hypertension. The Black population, which is thought to have a higher prevalence of volume-related and responsive hypertension, might particularly benefit from such a test. As a result, we investigated whether people with and without volume-responsive hypertension had different levels of this hormone by employing copeptin, a surrogate marker for ADH. The renin-angiotensin-aldosterone system, natriuretic peptides, endothelial pathways, sympathetic nervous system, and immune system all play a role in regulating blood pressure. Over the course of the past five decades, our understanding of the genomic basis of hypertension has progressed from monogenic causes to polygenic associations, encompassing approximately 30 rare monogenic variants and more than 1500 single nucleotide variants. The unexpected early benefits of blood pressure genomics include a deeper comprehension of the intricate causes of hypertension; through Mendelian randomization, improvement of bidirectional causal estimates between blood pressure, risk factors, and outcomes; stratification of risk based on polygenic risk scores; and opportunities for drug repurposing and precision medicine.