Stroke is the second most common cause of death worldwide and of adult disability, but in the near future the global burden of cerebrovascular diseases will rise due to ageing and adverse lifestyle changes in populations worldwide. The risk of stroke increases at blood pressure levels above 115/75 mm Hg and high blood pressure (BP) is the most important modifiable risk factor for stroke, associated with 54 % episodes of stroke worldwide. There is strong evidence from clinical trials that antihypertensive therapy reduces substantially the risk of any type of stroke, as well as stroke-related death and disability. The risk attributed to BP is associated not only with absolute values but also with certain parameters describing BP diurnal pattern as well as short-term and long-term variability. Many studies reported that certain features of BP like nocturnal hypertension, morning surge or increased variability predict an increased stroke risk. However, there is no accepted effective modality for correction of these disturbances (chronotherapy, certain classes of antihypertensive drugs). In the elderly, who are mostly affected by stroke, the primary prevention guidelines recommend treatment with diuretics and calcium channel blockers to lower blood pressure to the standard level.

Previous studies have shown that hyperoxia-induced deactivation of carotid body chemoreceptors reduces sympathetic activity in hypertensive patients but it does not affect blood pressure. The maintenance of blood pressure can be explained by the direct, vasoconstrictive effect of hyperoxia, which offsets diminished sympathetic activity. This study compares the effect of acute hyperoxia on hemodynamic parameters between hypertensive and normotensive subjects. Twelve males with hypertension (age 39.4±2.4 years; body mass index 27.4±1.1 kg m⁻²) and 11 normotensive males (age 39.9±2.7 years; body mass index 25.4±0.7 kg m⁻²) received, via non-rebreathing mask ventilation, ambient air, followed by 100% oxygen for 20 min. The stroke volume, heart rate, cardiac output, blood pressure, total peripheral resistance, respiratory rate, baroreceptor control of heart rate and oxygen saturation were recorded continuously. Several 30 s periods were analyzed before, during and after inducing hyperoxia. At baseline, the hypertensive subject’s blood pressure was higher and their baroreflex control of heart rate was lower when compared with the normotensive control group. After the first 30 s of hyperoxia, systolic, diastolic and mean blood pressures, as well as the total peripheral resistance, decreased significantly in hypertensives but not in normotensives. After 20 min of 100% oxygen ventilation, systolic and mean blood pressures and total peripheral resistance was increased in hypertensive patients, and the cardiac output and stroke volume had decreased in both groups. The results of this study confirm that deactivation of carotid body chemoreceptors can acutely decrease blood pressure in humans.

Beyond their hypolipidemic effect, statins reduce cardiovascular risk in hypertensive subjects via various mechanisms; one suggested mechanism is that they reduce sympathetic activity. We investigated the hypothesis that simvastatin decreased muscle sympathetic nerve activity (MSNA) in 31 hypertensive subjects with hypercholesterolemia (aged 38.7±10 years). In this randomized, placebo-controlled, double-blinded study, patients were treated with simvastatin (40 mg day⁻¹; n=15) or placebo (n=16) for 8 weeks. Before and after treatment, we measured MSNA, blood pressure and heart rate. Baroreceptor control of the heart rate, or baroreceptor sensitivity (BRS), was computed by the sequence method, a cross-analysis of systolic blood pressure and the electrocardiogram R–R interval. Blood samples were tested for plasma levels of catecholamines, neuropeptide Y, aldosterone, endothelin and renin activity. Simvastatin significantly reduced MSNA (from 36.5±5 to 27.8±6 bursts per min, P=0.001), heart rate (from 77±6.7 to 71±6.1 beats per min, P=0.01) and both total and low-density lipoprotein cholesterol (from 249±30.6 to 184±28.3 mg dl⁻¹, P=0.001 and from 169±30.6 to 117±31.2 mg dl⁻¹, P=0.01, respectively). Simvastatin also improved BRS (from 10.3±4.1 to 17.1±4.3 ms per mm Hg, P=0.04). No changes were observed in systolic or diastolic blood pressures, or in plasma levels of catecholamines, neuropeptide Y, endothelin, aldosterone and renin activity. After simvastatin therapy, MSNA and BRS were inversely related (r=−0.94, P<0.05). In conclusion, we found that, in patients with hypertension and hypercholesterolemia, simvastatin reduced MSNA, and this was related to increased baroreceptor sensitivity.

The association between elevated resting heart rate (RHR) as a cardiovascular risk factor and lowering of systolic blood pressure (SBP) to currently recommended values remain unknown. Systolic Blood Pressure Intervention Trial (SPRINT) data obtained from the NHLBI were used to describe the relationship between RHR and SBP reduction to <120 mmHg compared to SBP reduction to <140 mmHg. The composite clinical endpoint (CE) was defined as myocardial infarction, acute coronary syndrome, decompensation of heart failure, stroke, or cardiovascular death. Increased RHR was associated with a higher CE risk compared with low RHR in both treatment arms. A more potent increase of risk for CE was observed in subjects who were allocated to the SBP < 120 mmHg treatment goal. A similar effect of intensive and standard blood pressure (BP) reduction (p for interaction, 0.826) was observed in subjects with RHR in the 5th quintile (hazard ratio, 0.78, with 95% confidence interval (CI), 0.55–1.11) and in other quintiles of baseline RHR (hazard ratio, 0.75, with 95% CI, 0.62–0.90). Lower in-trial than baseline RHR was associated with reduced CE risk (hazard ratio, 0.80, with 95% CI, 0.66–0.98). We concluded that elevated RHR remains an essential risk factor independent of SBP reduction.

Objective. To compare the effect of ARB and ACE inhibitor on sympathetic activity in 32 hypertensives. Design and Methods. After a four-week wash-out period, patients were randomized to four weeks of therapy with enalapril or telmisrtan, with crossover to another drug for another four weeks. Blood pressure (BP), NPY, and catecholamine levels and HRV (frequency analysis) were measured during wash-out, in basal condition, and after postural stimulation test (PST). Results. Both drugs significantly reduced BP and NPY as compared to initial values, while no differences in BP and NPY between drugs were observed. Increase in NPY during PST was significantly higher in the enalapril than in the telmisartan group and during the wash-out period. No differences between enalapril and telmisartan in plasma catecholamines were observed. Telmisartan decreased low frequency/high frequency ratio as compared to initial values and enalapril values. Conclusions. Despite similar BP control, telmisartan attenuated autonomic balance more effectively than enalapril.

Background: Hypertension is the most prevalent and leading risk factor for stroke. SPRINT (The Systolic Blood Pressure Intervention Trial) assessed the effects on cardiovascular event risk of intensive compared with standard systolic blood pressure reduction. In this secondary analysis of SPRINT data, we investigated how low on‐treatment diastolic blood pressure ( DBP ) influenced risk for stroke events. Methods and Results: For this analysis, we used SPRINT _ POP (Primary Outcome Paper) Research Materials from the National Heart, Lung and Blood Institute (NHLBI) Biologic Specimen and Data Repository Information Coordinating Center. Data for 8944 SPRINT participants were analyzed from the period after target blood pressure was achieved until the end of the trial. Overall, there were 110 stroke events, including 49 from the intensive‐treatment arm and 61 in the standard‐treatment group. In participants with DBP <70 mm Hg, stroke risk was higher than with DBP ≥70 mm Hg (hazard ratio, 1.467; 95% CI 1.009–2.133; P =0.0445). Univariable Cox proportional hazard risk analysis showed that in the whole group, age and cardiovascular and chronic renal diseases were stroke risk factors. These risk factors were related to lower DBP and higher pulse pressure, however, not to study arm. Multivariable Cox proportional hazard analysis revealed that only age, history of cardiovascular disease, current smoking status and on‐treatment systolic blood pressure were significantly related to stroke risk. Conclusions: Low on‐treatment DBP is not related to the risk for the first stroke, in contrast to older age, the history of cardiovascular disease, current smoking status, and on‐treatment systolic blood pressure. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT 01206062.