Abstract
IntroductionSympathetic and Renin-Angiotensin-Aldosterone systems play crucial roles in blood pressure response to increased salt intake. This study investigated the effects of angiotensin receptor blocker (ARB) and sympathetic excitation on the responses of blood pressure (BP) and peripheral vascular resistance (PVR) in salt loaded normotensive (NT) and hypertensive (HT) Nigerian subjects.Methods16 NT and 14 HT participants, that were age-matched [39.9 ± 1.3 vs 44.1±2.1yrs (P= 0.10)], underwent 5 days each of oral administration of 200mmol NaCl, and 200mmol NaCl + 50mg Losartan, preceded by a baseline control condition. BP and PVR responses to 30% Maximum Voluntary Contraction (MVC) of handgrip (HG) for one minute were determined at baseline, after salt load and after salt + Losartan. Data were presented as Mean ± SEM, and analyzed with two-way ANOVA and paired t-test, with P<0.05 accepted as significant.ResultsBP and PVR were significantly increased by HG at baseline, after salt load and after salt + Losartan in NT and HT. Salt load augmented the HG-induced SBP (P=0.04) and MABP responses (P=0.02) in HT. While Losartan attenuated the HG- induced Systolic Blood Pressure (SBP) SBP response (P=0.007) and DBP response (P=0.003) in HT and NT respectively after salt + Losartan. HG-induced PVR response was significantly accentuated after salt load in HT (P=0.005), but it was not significant in NT (P=0.38).ConclusionThe implication of our finding is that angiotensin II receptor blockade possibly attenuates salt-induced sympathetic nerve excitation in black hypertensive patients.
Highlights
Studies have shown that salt intake plays a key role in the regulation of blood pressure [1] and in the pathophysiology of hypertension [2,3] Sympathetic Nervous System (SNS) and Renin Angiotensin Aldosterone System (RAAS) are both involved in short and long term regulation of blood pressure respectively [4,5]
Mean Arterial Blood Pressure (MABP) responses to Handgrip contraction after salt-loading and after salt + losartan administration in NT and HT (Table 2): shows that in both groups, MABP increased significantly (P
In the NT, MABP increased from baseline by (8.25 ± 1.58)mmHg in response to HG; by (10.88 ± 2.21)mmHg after salt load, and by (7.39 ± 2.25)mmHg after salt + losartan
Summary
Studies have shown that salt intake plays a key role in the regulation of blood pressure [1] and in the pathophysiology of hypertension [2,3] Sympathetic Nervous System (SNS) and Renin Angiotensin Aldosterone System (RAAS) are both involved in short and long term regulation of blood pressure respectively [4,5]. Abnormal regulation of these dual systems by salt may result in hypertension. The prevalence of hypertension rose from 16%, as reported by Cooper in 1997 [11], to values around 32.8% and 36.6%, between the year 2008 and 2012 [12,13]
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