Integrated Blood Pressure Control最新文献

Obesity-related hypertension represents a condition frequently observed in current clinical practice characterized by a complex pathophysiological background and a very high cardiovascular risk profile, particularly in severely obese individuals. This explains, on the one hand, the difficulty in reducing elevated blood pressure values in this pathological state and, on the other, the need to achieve this goal in a relatively short-time period to prevent the occurrence of fatal and nonfatal cardiovascular events. Both nonpharmacological and pharmacological measures are available in the therapeutic approach for this condition. Among the pharmacological interventions, a combination of two antihypertensive drugs represents the most common recommended strategy aimed at achieving blood pressure control. This paper, after briefly examining the main pathophysiological features of obesity-related hypertension, will review the importance in the treatment of this condition of the drug combination based on a calcium channel blocker and an angiotensin-converting enzyme inhibitor, with specific focus on lercanidipine/enalapril. Following an analysis of the main pharmacological properties of the combination, the results of the studies based on this pharmacological approach in obesity-related hypertension will be critically discussed. The efficacy, safety, and tolerability profile of the lercanidine/enalapril drug combination as well as its potential limitations will also be examined.

In the US, hypertension affects one in three adults. Current guideline-based treatment of hypertension involves little diagnostic testing. A more personalized approach to the treatment of hypertension might be of use. Several methods of personalized treatment have been proposed and vetted to varying degrees. The purpose of this narrative review is to discuss the rationale for personalized therapy in hypertension, barriers to its development and implementation, some influential examples of proposed personalization measures, and a view of future efforts.

Resveratrol is reported to reduce blood pressure in animal models of hypertension, but the mechanisms are unknown. We have shown that resveratrol infusion increases sodium excretion. We hypothesized that chronic ingestion of resveratrol would reduce angiotensin II (Ang II)-induced increases in blood pressure by decreasing oxidative stress and by also decreasing sodium reabsorption through a nitric oxide-dependent mechanism. We infused rats with vehicle or 80 μg Ang II/d over 4 weeks. Vehicle or Ang II-infused rats were individually housed, pair fed, and placed on a diet of normal chow or normal chow plus 146 mg resveratrol/d. Groups included 1) control, 2) resveratrol-fed, 3) Ang II-treated, and 4) Ang II plus resveratrol. Systolic blood pressure was measured by tail cuff. During the 4th week, rats were placed in metabolic caging for urine collection. NO2/NO3 and 8-isoprostane excretion were measured. Ang II increased systolic blood pressure in the 1st week by +14±5 mmHg (P<0.05) in Group 3 and +10±3 mmHg (P<0.05) in Group 4, respectively. Blood pressure was unchanged in Groups 1 and 2. After 4 weeks, blood pressure remained elevated in Group 3 rats with Ang II (+9±3 mmHg, P<0.05), but in Group 4, blood pressure was no longer elevated (+2±2 mmHg). We found no significant differences between the groups in sodium excretion or cumulative sodium balance (18.49±0.12, 17.75±0.16, 17.97±0.17, 18.46±0.18 μEq Na+/7 d in Groups 1-4, respectively). Urinary excretion of NO2/NO3 in the four groups was 1) 1631±207 μmol/24 h, 2) 1045±236 μmol/24 h, 3) 1490±161 μmol/24 h, and 4) 609±17 μmol/24 h. 8-Isoprostane excretion was 1) 63.85±19.39 nmol/24 h, 2) 73.57±22.02 nmol/24 h, 3) 100.69±37.62 nmol/24 h, and 4) 103.00±38.88 nmol/24 h. We conclude that chronic resveratrol supplementation does not blunt Ang II-increased blood pressure, and while resveratrol has mild depressor effects, these do not seem to be due to natriuresis or enhanced renal nitric oxide synthesis.

Background: Comparative cardiovascular responses to treadmill and bicycle ergometer (bike) exercise tests in hypertensive Nigerians are not known. This study compared cardiovascular responses to the two modes of exercise testing in hypertensives using maximal exercise protocols.

Methods: One hundred and ten male subjects with mild-to-moderate hypertension underwent maximal treadmill and bike test one after the other at a single visit in a simple random manner. Paired-sampled t-test was used to compare responses to both exercise tests while chi-squared test was used to compare categorical variables.

Results: The maximal heart rate (P<0.001), peak systolic blood pressure (P=0.02), rate pressure product (P<0.001), peak oxygen uptake (P<0.001), and exercise capacity (P<0.001) in metabolic equivalents were signifcantly higher on the treadmill than on the bike.

Conclusion: Higher cardiovascular responses on treadmill in Nigerian male hypertensives in this study, similar to findings in non-hypertensives and non-Nigerians in earlier studies, suggest that treadmill may be of better diagnostic utility in our population.