Abstract
Individuals with hypertension and sympathetic overactivity are at risk for cardiovascular events. Renin inhibitors are new while thiazide diuretics are first-class drugs used for treatment of hypertension. The purpose of this study was to determine whether 6 months of treatment with aliskiren (ALSK) or hydrochlorothiazide (HCTZ) would alter blood pressure (BP) and muscle sympathetic nerve activity (MSNA) indices in older mild hypertensives during a cold pressor test (CPT). We hypothesized that the ALSK group would demonstrate a blunted response compared to HCTZ. Nineteen (9 men, 10 women) subjects performed a CPT pre- and post treatment where heart rate (HR), systolic BP (SBP) and diastolic BP (DBP), and MSNA were measured. Blood samples were withdrawn for assessment of renal-adrenal hormones. Both medications lowered ambulatory SBP and DBP (P < 0.05). Direct renin tended to be higher in the ALSK group after treatment (P = 0.081). Aldosterone was higher in the HCTZ group after treatment (P < 0.001). As expected, both groups showed increases in HR, SBP, DBP, and MSNA during the CPT (all P < 0.05). All cardiovascular and MSNA responses were similar pre- and post treatment in both groups (peak CPT SBP: 26 ± 10 vs. 17 ± 21 and 21 ± 20 vs. 29 ± 15 mmHg for pre vs. post for HCTZ and ALSK, respectively; peak CPT MSNA burst frequency: 13 ± 8 vs. 11 ± 11 and 11 ± 17 vs. 6 ± 13 bursts/min; all P > 0.05). Treatment with these antihypertensive medications lowered BP but was not successful in lowering the responsiveness to the CPT.
Highlights
Individuals with hypertension and sympathetic overactivity are at increased risk for the occurrence of cardiovascular events (Grassi 2009)
There was an upregulation of the renin-angiotensin-aldosterone system (RAAS) with HCTZ treatment where the increase in upright muscle sympathetic nerve activity (MSNA) induced by the drug treatment was positively related to the increase in aldosterone (Okada et al 2013). These results indicate that treatment with a thiazide diuretic leads to sympathetic activation through an upregulated RAAS, despite blood pressure (BP) being well controlled
As we previously demonstrated that treatment with a thiazide diuretic may enhance MSNA and treatment with a renin inhibitor may depress MSNA (Okada et al 2013), we hypothesized that patients taking ALSK would demonstrate a blunted response due to a suppression in sympathetic outflow when compared to those taking HCTZ where sympathetic outflow might be enhanced
Summary
Individuals with hypertension and sympathetic overactivity are at increased risk for the occurrence of cardiovascular events (Grassi 2009). Older hypertensive patients possess both of these characteristics, making them vulnerable to cardiovascular events. Some studies have indicated that, while BP was lower after antihypertensive medication treatment, some medications still allowed for persistent sympathetic overactivation (Lindqvist et al 1994; Fu et al 2005; Menon et al 2009). This raises an interesting concern as to the long-term beneficial effects of some antihypertensive medications. With the many different types of antihypertensive medications available, all targeting different and specific pathways, it is important to understand how BP is lowered in hypertensive patients and whether these medications favorably alter physiological responses, to hypertensive stimuli
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