Japan Society of Home Economics

As few epidemiological studies have investigated the effect of lifestyle factors on hypertension in the very elderly population, we conducted a cross-sectional study to examine the association of estimated salt intake and body weight with blood pressure in the very elderly population. We enrolled 288 participants aged 75years or older who were residents of Sukagawa City, Fukushima Prefecture, Japan, who attended the health checkup conducted in 2015. Salt intake was estimated from spot urine samples using the Tanaka method. The mean values for age, estimated salt intake, and body weight of all participants were 79.7years, 9.1g/d (standard deviation 2.4g), and 54.3kg (standard deviation 10.2kg), respectively. General linear models showed that salt intake and body weight were associated with higher systolic blood pressure (SBP) levels (per standard deviation higher level, adjusted difference 4.13mmHg [95% confidence interval 1.69-6.57] and 5.34mmHg [95% confidence interval 2.12-8.56], respectively). Body weight was associated with higher diastolic blood pressure (DBP) levels (per standard deviation higher level, 2.74mmHg [95% confidence interval 0.58-4.90]). However, salt intake was not associated with higher diastolic blood pressure levels (per standard deviation higher level, 1.15mmHg [95% confidence interval -0.49 to 2.79]). Our findings suggest that higher SBP is associated with both salt intake and body weight and that higher DBP is associated with body weight in the very elderly population. This study provides a rationale for lifestyle modifications to prevent hypertension as a population approach.

Objective: Rgs2 (regulator of G-protein signaling-2)-deficient mice exhibit persistent vascular constriction and severe hypertension, and genetic variations of RGS2 occur in hypertensive patients. Moreover we have known that RGS2 mRNA expression was up regulated by angiotensin II (Ang II) stimulation in vascular smooth muscle cells (VSMC). This study was to disclose the role of calcium channel blockers (CCBs) in signal transduction through RGS2. Design and method: VSMCs were isolated from thoracic aortas of male Wistar rats and cells between passages 4 to 6 were used at semi-confluence growth state. VSMC were incubated in azelnidipine, amolnidipine or cilnidipine (∼40 nM) and cells were collected. RGS2 mRNA expression was performed by real-time quantitative reverse transcription-polymerase chain reaction (QRT-PCR). Results: Azelnidipine (∼4 nM and ∼40 nM) dose-dependently increased RGS2 mRNA expression in VSMC (p < 0.01). On the other hand, RGS2 mRNA expression was increased with cilnidipine (∼40 nM) stimulation and the cells were pre-incubated with PKC inhibitor for 30 minutes, PKC inhibitor significantly decreased cilnidipine-induced RGS2 up-regulation by 50% (p < 0.05). Conclusions: These results suggest that CCBs decreased post-receptor signal transduction through the up-regulation of RGS2 mRNA expression and this upregulation of RGS2 mRNA expression possibly via N-type calcium channel.