Hypertension and its related factors among patients with type 2 diabetes mellitus - a multi-hospital study in Bangladesh.

BACKGROUND: Hypertension and type 2 diabetes are associated with each other, and their coexistence is linked to diabetes-related complications such as stroke, coronary artery disease, kidney disease, retinopathy and diabetic foot. This study aimed to determine the prevalence, awareness and control of hypertension and factors associated with hypertension among people with type 2 diabetes mellitus (T2DM) in Bangladesh. METHODS: A cross-sectional and retrospective study was conducted in 2017, and data from 1252 adults with T2DM were collected from six hospitals that specialise in diabetes care. These hospitals provide primary, secondary and tertiary healthcare and cover the rural and urban populations of Bangladesh. Cross-sectional data were collected from patients via face-to-face interviews, and retrospective data were collected from patients' past medical records (medical passport), locally known as the patients' guidebook or record book. The associations between hypertension and its related factors were examined using the bootstrapping method with multiple logistic regression to adjust for potential confounders. RESULTS: The mean age of participants was 55.14 (± 12.51) years. Hypertension was found to be present among 67.2% of participants, and 95.8% were aware that they had it. Of these, 79.5% attained the blood pressure control. The mean duration of diabetes was 10.86 (± 7.73) years. The variables that were found to be related to hypertension include an age of above 60 years, physical inactivity, being overweight or obese, a longer duration of diabetes and chronic kidney disease. CONCLUSION: The prevalence of hypertension as well as its awareness and control were very high among people with known type 2 diabetes. As there is a strong relationship between hypertension and diabetes, patients with diabetes should have their blood pressure regularly monitored to prevent major diabetes-related complications.

Increased aortic intimal proliferation due to MasR deletion in vitro.

A growing body of evidence suggests that the vascular actions of Ang-(1-7) appear to involve increased production of nitric oxide (NO), an important vasodilator, through the activation of MasR, thus indicating the involvement of the MasR in preventing endothelial dysfunction. However, it is unknown whether the MasR could be involved in the progression of the next step in atherosclerosis, neo-intimal formation. To determine whether the deletion of the MasR is involved in the development of intimal thickening in an in vitro model. Mice [three background controls (C57Bl/6) and 3 MasR (-/-)] were killed and the aortas excised and cleaned of connective tissue and cut into 3 mm rings. Rings were placed in an organ culture medium for 5 weeks, embedded in paraffin, cut at 5 µm and stained with haematoxylin and eosin and Masson's trichrome. In addition, aortic reactivity was measured in organ baths. After 5 weeks of culture, the intima:media ratio increased in the aortas from MasR (-/-) mice compared to the control group by 4.5-fold (P < 0.01). However, no significant difference in nuclei area count (cell proliferation) between the MasR (-/-) mice and control group was observed (0.87 ± 0.29% vs. 0.94 ± 0.18%, respectively, P = ns). Functional studies showed only a minor vasoconstrictive and full vasodilative response. This study shows that the deletion of the MasR causes marked increase in the aortic intima:media ratio, which is not due to generalized cellular proliferation. These results provide a functional role for the MasR in atherogenesis.

Reduction of angiotensin A and alamandine vasoactivity in the rabbit model of atherogenesis: differential effects of alamandine and Ang(1-7).

Novel treatments are necessary to reduce the burden of cardiovascular disease (CVD). Alamandine binds to MrgD and is reported to induce vasodilation via stimulation of endothelial nitric oxide synthase (eNOS), but its role in atherogenic blood vessels is yet to be determined. To determine the vasoactive role of alamandine and its precursor AngA in diseased aorta, New Zealand White rabbits were fed a diet containing 1% methionine + 0.5% cholesterol + 5% peanut oil for 4 weeks (MC, n = 5) or control (n = 6). In abdominal aorta, alamandine (1 µM) was added 30 min before a dose-response curve to angiotensin II or AngA (1 nM-1 µM), and immunohistochemistry was used to identify MrgD receptors and eNOS. The thoracic aorta, renal, carotid and iliac arteries were mounted in organ baths. Rings were precontracted with phenylephrine, then a bolus dose of alamandine (1 µM) was added 10 min before a dose-response curve to acetylcholine (0.01 µM-10 µM). The MrgD receptor was localized to normal and diseased aorta and colocalized with eNOS. In control but not diseased blood vessels, alamandine enhanced acetylcholine-mediated vasodilation in the thoracic aorta and the iliac artery (P < 0.05) and reduced it in the renal artery (P < 0.05). In control abdominal aorta, AngA evoked less desensitization than AngII (P < 0.05) and alamandine reduced AngA-mediated vasoconstriction (P < 0.05). In MC, AngA constriction was markedly reduced vs. control (P < 0.05). The vasoactivity of alamandine and AngA are reduced in atherogenesis. Its role in the prevention of CVD remains to be validated.