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Objective: Important climate related variations of clinic and ambulatory blood pressure (BP) have been repeatedly reported. However, notwithstanding the wide use of indoor climate control systems, specially in winter, no information is available regarding the role of air temperature values measured proximally to the patient, in particular when focussing on specific components of the 24 h BP profile, such as the morning BP surge (MBPS). Design and Methods: To investigate whether MBPS is affected by outdoor air temperature or by the air temperature measured proximally to the patient, 2120 hypertensives underwent 24 h ambulatory blood pressure (ABP) monitoring with a battery-powered "HOBO" temperature data logger fitted to the carrying pouch of the ABP monitor. Predictors of MBPS were investigated with a multivariate stepwise regression model including age, gender, body mass index, office systolic BP, 24 h average ABP, mean 24 h outdoor atmospheric pressure and mean 24 h air temperature measured both outdoor and by HOBO as independent variables. Results: Stepwise multiple regression analysis carried out in the 1728 subjects included in the final analysis selected outdoor air temperature(beta = -0.09;p < 0.0001), 24 h ABP(beta = -0.72;p < 0.0001), and age(beta = -0.06;p < 0.002) as negative independent predictors of MBPS, with systolic office BP selected as a positive independent predictor (beta = 1,04;p < 0.0001)(r = 0.610); no significant effect of HOBO air temperature was observed. When subjects were stratified according to age, the effect on MBPS of outdoor air temperature was detectable in subjects >65 yrs (beta = -0.086; p < 0.002), whereas the only determinants of MBPS in subjects < 50 yrs were office SBP (positive) and 24 h average SBP(negative). Conclusions: These results confirm and extend previous observation on the occurrence of seasonal changes in 24 h BP profiles, by providing new evidence that only air temperature measured outdoor affects BP morning surge in addition to office BP, 24 h ABP and age, whereas no role appears to be played by air temperature measured proximally to the patient. The clinical implications of these findings for BP control would need to be further tested by ad hoc studies.

Background— The degree of pulmonary hypertension in healthy subjects exposed to acute hypobaric hypoxia at high altitude was found to be related to increased plasma endothelin (ET)-1. The aim of the present study was to investigate the effects of ET-1 antagonism on pulmonary hypertension, renal water, and sodium balance under acute and prolonged exposure to high-altitude–associated hypoxia. Methods and Results— In a double-blind fashion, healthy volunteers were randomly assigned to receive bosentan (62.5 mg for 1 day and 125 mg for the following 2 days; n=10) or placebo (n=10) at sea level and after rapid ascent to high altitude (4559 m). At sea level, bosentan did not induce any significant changes in hemodynamic or renal parameters. At altitude, bosentan induced a significant reduction of systolic pulmonary artery pressure (21±7 versus 31±7 mm Hg, P 2 OCl/glomerular filtration rate) were significantly reduced versus placebo after 2 days of ET-1 antagonism (1100±200 versus 1610±590 mL; −6.7±3.5 versus −1.8±4.8 mL/min, P Conclusions— The present results indicate that the early beneficial effect of ET-1 antagonism on pulmonary blood pressure is followed by an impairment in volume adaptation. These findings must be considered for the prevention and treatment of acute mountain sickness.

A downward titration of antihypertensive drug regimens in summertime is often performed on the basis of seasonal variations of clinic blood pressure (BP). However, little is known about the actual interaction between outdoor air temperature and the effects of antihypertensive treatment on ambulatory BP. The combined effects of aging, treatment, and daily mean temperature on clinic and ambulatory BP were investigated in 6404 subjects referred to our units between October 1999 and December 2003. Office and mean 24-hour systolic BP, as well as morning pressure surge, were significantly lower in hot (>90th percentiles of air temperature; 136±19, 130±14, and 33.3±16.1 mm Hg; P P P P

Drs Dhar and Lambert1 correctly note that the potential relationship between sunlight and seasonal blood pressure (BP) changes is not investigated in our study.2 We agree that this interaction, possibly mediated, at least in part, by changes in brain monoamine concentration, should not be neglected. In addition, the UV-dependent cholecalciferol formation is a potential modifier of …