Elevated Blood Pressure Variability Research Articles

Baroreflex, Cerebral Perfusion, and Stroke: Integrative Physiology at Its Best

To the Editor: We wish to congratulate Sykora et al for their timely review on the potential role the arterial baroreflex plays in cerebrovascular disease outcomes.1 Although it may seem intuitive that both arterial baroreflex function and cerebral blood flow (CBF) regulation are important modulators of stroke outcome, clear and consistent evidence implicating the arterial baroreflex as an independent clinical predictor of stroke-related mortality is only emerging. The authors proffer several plausible hypotheses linking baroreflex dysfunction to the etiology of acute stroke and related clinical outcomes. Among them, the proposed “cross-linked” impairment of cerebrovascular autoregulation (CA) and altered autonomic drive as part of an underlying regulatory continuum in the context of stroke require further discussion. …

Blood pressure variability is more important than blood pressure level in determination of end-organ damage in rats

This study was designed to determine how important a novel risk factor of elevated blood pressure variability (BPV) is in the determination of end-organ damage by comparison with the classic risk factor of a high blood pressure (BP) level. The effects of haemodynamics on cardiovascular morphology were evaluated by univariate and multivariate regression analysis in two different rat models with an enlarged distribution of haemodynamics. In male sham-operated and sinoaortic-denervated Wistar-Kyoto rats and spontaneously hypertensive rats (n = 34), BPV was more important than BP in cardiac and renal damage and aortic hypertrophy. BPV and BP had independent effects, explaining 59.4% of the variation in damage to these organs. In male (n = 44) and female (n = 46) F1 hybrids of Sprague-Dawley rats and spontaneously hypertensive rats, the greater importance of BPV than BP was further demonstrated in left ventricular hypertrophy, glomerular damage and aortic hypertrophy. The phenomenon was more evident in females than males for cardiovascular hypertrophy. BPV and BP or BPV alone had independent effects, explaining 46.9% (male) or 37.5% (female) of the variation in damage to these organs. BPV is a more critical determinant than BP level for cardiac damage, renal lesions and aortic hypertrophy in rats, strongly suggesting the significance of BPV control for the protection of these organs.

White-coat normotension and blood pressure variability.

The objective of this study was to assess blood pressure variability in patients with clinical normotension and ambulatory hypertension (the so-called white-coat normotension). In 58 white-coat normotensives (mean age 64.2 +/- 14.9 years; male/female ratio = 1.5:1) the authors evaluated blood pressure variability using the twenty-four-hour coefficient of variability. Fifty-eight essential hypertensives with the same age and sex distribution were recruited as a control group. The coefficient of variability in white-coat normotension was greater than in the control group (14.8/16.1 +/- 4.2/3.8% vs 13.5/15.1 +/- 3.3/3.1%), but this difference was not statistically significant. These findings suggest that white-coat normotension is the result of a specific relaxing response to medical visits and not the expression of an elevated blood pressure variability. It is probably due to the reverse of the alerting response, which causes white-coat hypertension.

Sympathetic and parasympathetic influence on blood pressure and heart rate variability in Wistar-Kyoto and spontaneously hypertensive rats.

The relative influence of sympathetic and parasympathetic nervous control of heart rate and heart rate variability, of mean arterial pressure (MAP) and MAP variability was investigated in young spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). An on-line computerized system was used for continuous intra-arterial measurements of MAP and heart rate every 2.5 min in freely moving rats with indwelling arterial catheters. Variability was expressed as the standard deviation in each rat. Heart rate and MAP showed clear diurnal rhythms, both in WKY and SHR. Blood pressure variability was clearly higher in SHR than in WKY, both during dark active hours and during light hours of relative sleep, and it did not change in response to either beta-adrenoceptor or vagal blockade. Structural vascular changes with the consequent increase in vascular reactivity may be one explanation for the elevated blood pressure variability in SHR. Heart rate variability was clearly reduced in SHR compared with WKY. This may be due to a reduced tonic vagal discharge in SHR, whereby a vagally mediated tachycardia is eliminated. The vagal withdrawal is part of the defence reaction, which is more easily elicited in SHR than in WKY.