BP reactivity to public speaking in stage 1 hypertension: influence of different task scenarios.

AIM: To investigate the blood pressure (BP) reaction to public speaking performed according to different emotionally distressing scenarios in stage 1 hypertension. METHODS. We assessed 64 hypertensive and 30 normotensive subjects. They performed three speech tasks with neutral, anger and anxiety scenarios. BP was assessed with the Finometer beat-to-beat non-invasive recording system throughout the test procedure. RESULTS: For all types of speech, the systolic BP response was greater in the hypertensive than the normotensive subjects (all p < 0.001). At repeated-measures analysis of covariate (R-M ANCOVA), a significant group-by-time interaction was found for all scenarios (p ≤ 0.001). For the diastolic BP response, the between-group difference was significant for the task with anxiety scenario (p < 0.05). At R-M ANCOVA, a group-by-time interaction of borderline statistical significance was found for the speech with anxiety content (p = 0.053) but not for the speeches with neutral or anger content. Within the hypertensive group, the diastolic BP increments during the speeches with anxiety and anger scenarios were greater than those during the speech with neutral scenario (both p < 0.001). CONCLUSIONS: These data indicate that reactivity to public speaking is increased in stage 1 hypertension. A speech with anxiety or anger scenario elicits a greater diastolic BP reaction than tasks with neutral content.

Interplay between miR-155, AT1R A1166C polymorphism, and AT1R expression in young untreated hypertensives.

BACKGROUND: A silent polymorphism (+1166 A/C single-nucleotide polymorphism) localized in the 3'-UTR (untranslated region) of the human angiotensin II type-1 receptor (AT1R) has been associated with hypertension and cardiovascular complications. The +1166 A/C is recognized by a specific microRNA-155 (miR-155), which is base-pairing complementary with the +1166 A-allele but not with the mutant +1166 C allele. Aim of our study was to investigate the interplay between miR-155 and AT1R protein expression. METHODS: Sixty-four subjects were selected for the +1166 A/C from the cohort of hypertensives (n = 573) of the Hypertension and Ambulatory Recording Venetia Study (HARVEST): 25 were homozygous for the 1166 A allele, 20 heterozygous, and 19 homozygous for the 1166 C allele. RESULTS: miR-155 expression was significantly decreased in subjects with CC genotype in comparison to AA and AC genotype. AT1R protein expression was significantly increased in the CC group in comparison to AA and AC (P < 0.01) although AT1R mRNA expression was not significantly different in the three groups. AT1R protein expression was positively correlated with systolic and diastolic blood pressure and negatively correlated with miR-155 expression level. Plasma transforming growth factor-ß1 (TGF-ß1) may have a modulator role in the interplay between miR-155 and AT1R protein expression as it was correlated negatively with miR-155 expression and positively with AT1R protein expression in subjects with CC genotype. CONCLUSION: The interplay between miR-155 expression, +1166C polymorphism, and AT1R protein expression may have a role in the regulation of blood pressure.

Regular physical activity attenuates the blood pressure response to public speaking and delays the development of hypertension.

OBJECTIVES: The objective of this study was to investigate the effect of regular physical activity on the haemodynamic response to public speaking and to evaluate the long-term effect of exercise on development of hypertension. PARTICIPANTS: We assessed 75 sedentary and 44 active participants screened for stage 1 hypertension with consistent activity habits and 63 normotensive individuals as control. METHODS: The blood pressure (BP) response to public speaking was assessed with beat-to-beat noninvasive recording. Definition of incident hypertension was based either on clinic or 24-h BP measurement. RESULTS: The BP response to public speaking was greater in the hypertensive than the normotensive participants (P=0.018/0.009). Among the former, sedentary participants showed increased BP reactivity to the speech test (45.2+/-22.6/22.2+/-11.5mmHg, P<0.01/<0.001 versus controls), whereas physically active participants had a response similar to that of controls (35.4+/-18.5/18.5+/-11.5mmHg, P=not significant). During a median follow-up of 71 months, ambulatory BP did not virtually change in the active participants (-0.9+/-7.8/-0.0+/-4.7mmHg) and increased in their sedentary peers (2.8+/-9.8/3.2+/-7.4mmHg, P=0.08/0.003 versus active). Active participants were less likely to develop incident hypertension than sedentary ones. After controlling for several confounders including baseline heart rate, the hazard ratio was 0.53 [95% confidence interval (CI) 0.31-0.94] for clinic hypertension and 0.60 (95% CI 0.37-0.99) for ambulatory hypertension. Inclusion of BP response to public speaking into the Cox model influenced the strength of the association only marginally [hazard ratio=0.55 (95% CI 0.30-0.97) and hazard ratio=0.59 (95% CI 0.36-0.99), respectively]. CONCLUSION: Regular physical activity attenuates the BP reaction to psychosocial stressors. However, this mechanism seems to be only partially responsible for the long-term effect of exercise on BP.

Angiotensin II type 1 receptor gene polymorphism predicts development of hypertension and metabolic syndrome.

BACKGROUND: The aim of the study was to investigate the effect of polymorphism A1166C for AGTR1 and -1332G/A for AGTR2 on the incidence of sustained hypertension (HT) and metabolic syndrome in a cohort of young patients screened for stage 1 HT. METHODS: We assessed 420 white hypertensive subjects never treated for HT and followed up for 7.3 years in the HT and Ambulatory Recording Venetia Study (HARVEST). Incident physician-diagnosed HT, increase in ambulatory blood pressure (BP), and new onset metabolic syndrome were the outcome measures. RESULTS: For AGTR1, 37.2% of the subjects in the group with AA genotype, 47.5% in the group with AC genotype, and 66.7% in the group with CC genotype developed HT during follow-up (P = 0.001). Ambulatory systolic (P = 0.007) and diastolic (P < 0.001) BPs increased largely in the patients with CC genotype than in the rest of the group. New onset metabolic syndrome during follow-up (n = 30, P = 0.008), and the frequency of the metabolic syndrome at the end of follow-up (n = 65, P = 0.002) were also more common among the patients with CC and AC genotype. In a Cox analysis, subjects with CC genotype had an increased risk of developing HT (hazard ratio (HR) 1.6, 95% confidence interval (CI) 1.2-2.0, P = 0.000) and metabolic syndrome (HR 2.8, 1.5-5.2, P = 0.002) than AA subjects. No association was found between the AGTR2 polymorphism and any outcome measure. CONCLUSIONS: The AGTR1 A1166C polymorphism may be considered a genetic marker predisposing to an increase in BP and the development of the metabolic syndrome in subjects screened for stage 1 HT.

RGS2 C1114G polymorphism and body weight gain in hypertensive patients.

RGS2 is a negative regulator of Galpha protein signaling and promotes adipocyte differentiation. Recently, we described a polymorphism at the C1114G locus with the G allele associated with hypertension in a cross-sectional study. The aim of the present study was to assess whether the RGS2 C1114G is predictive of overweight in young subjects with grade I hypertension. We genotyped at the RGS2 C1114G locus 406 (male, n = 294; female, n = 112) white hypertensive subjects (age, 33 +/- 9 years) never treated for hypertension and at low cardiovascular risk. Median follow-up was 7.85 years. At baseline, male patients carrying the RGS2 1114G allele had higher body mass index (BMI) than patients with CC genotype (26.1 +/- 0.3 vs 25.3 +/- 0.3 kg/m2, P < .05). The frequency of male patients with BMI > or = 25 was similar between the patients with G allele and those with CC genotype (55.1% vs 47.8%, P = not significant). No significant difference between the 2 groups was observed with regard to physical activity, blood pressure, and heart rate. At the end of follow-up, BMI was higher in male patients with G allele compared with patients with CC genotype (26.8 +/- 0.3 vs 25.8 +/- 0.2 kg/m2, P < .01); and the frequency of male patients with BMI >25 kg/m2 was greater in the former (69.0% vs 52.2%, P < .01). According to Cox regression, allele G was a significant predictor of developing overweight or obesity during follow-up. These epidemiologic relations were not significant in female patients. In young male patients with grade I hypertension, RGS2 1114G allele is associated with increased BMI and with greater risk of developing overweight or obesity. The RGS2 1114G allele may be considered a genetic marker that predicts an individual's predisposition to gaining weight.