[Can determination of catecholamines in the blood reflect slight changes in sympathetic activity?].
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Biomedical subjects
Publications and source records attributed to G Parati.
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1. Slight decreases and increases in carotid baroreceptor activity were induced in subjects with essential hypertension by slight alterations in carotid transmural pressure (variable pressure neck-chamber technique) in order to obtain limited increases and reductions in sympathetic adrenergic activity. 2. When sympathetic activity was reflexly increased there was a rise in arterial pressure but no significant increase in plasma catecholamines. Likewise when sympathetic activity was reflexly reduced there was a fall in arterial pressure but no significant reduction in plasma catecholamines. 3. Plasma noradrenaline and adrenaline significantly and markedly increased in the same subjects when sympathetic activity was increased by activation of both arterial and low pressure baroreceptor reflexes with tilting. 4. It is suggested that measurements of catecholamines in systemic plasma may reveal marked degrees of sympathetic activation but may not be a sensitive index of more moderate changes in sympathetic tone.
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The antihypertensive effect of a slow-release (SR) clonidine preparation was evaluated in hypertensive patients not confined to bed using a 24-h intraarterial blood pressure monitoring (Oxford) method. The monitoring was carried out during placebo administration and after 7-10 days of daily administration of SR clonidine in a single oral dose (250 or 500 microgram). An analysis of all the blood pressure values obtained was performed by computer. The results were as follows: (a) SR clonidine significantly reduced the 24-h systolic and diastolic arterial pressure by 16 and 10 mm Hg, respectively (mean +/- SE). (b) The reduction was well evident throughout the 24-h period, the average decrease in mean arterial pressure observed during the first, second, and third 8-h period after the administration of the drug being 11, 14, and 14 mm Hg, respectively. (c) The blood pressure reduction was similar during the daytime and the nighttime, despite the lower base-line value that occurred in the latter condition. (d) There was no consistent change in blood pressure variability, as measured in each patient by the standard deviation of the blood pressure values, with SR clonidine. SR clonidine caused a reduction in heart rate that, as that in blood pressure, was well evident throughout the 24 h. It is concluded that SR clonidine is an effective antihypertensive agent and that a single administration of this drug can produce a clear-cut reduction in the blood pressure values of hypertensive patients for a 24-h period.
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Previous studies indicate that arterial baroreceptor modulation of heart rate is drastically reduced during static or dynamic exercise. We have investigated whether this reduction also occurs with regard to blood pressure modulation by the baroreflex. The study was performed in 19 subjects with uncomplicated untreated essential hypertension in whom blood pressure was measured intraarterially, and R-R interval was obtained by an electrocardiogram. The carotid baroreceptors were stimulated by neck suction of 30 seconds' duration, and equal stimuli were applied at rest and during hand-grip exercise performed at 40% of the subjects' maximal strength. Baroreceptor stimulation at rest increased R-R interval and reduced blood pressure. During hand-grip, the R-R interval responses to the baroreceptor stimulus were diminished by 61%. In contrast, the blood pressure responses were not significantly altered. Similar results were obtained when two subgroups of subjects with a lesser or greater degree of hypertension were separately considered. Thus, the carotid baroreceptor influence on blood pressure is largely preserved during exercise in contrast to the carotid baroreceptor influence on the sinus node, which is markedly impaired.
The effect of nadolol (N) on 24-hour blood pressure (BP) and heart rate (HR) values and on their variability was examined in ambulant patients with essential hypertension, using the Oxford method to obtain continuous intraarterial recording and a computer to have a beat-to-beat analysis of the data. The recording was carried out without treatment and after 10 days' administration of N once daily by mouth (dose range: 80-320 mg). After N, 24-hour BP and HR were reduced by 17 +/- 3% and 27 +/- 4% respectively as compared to before N, the effect being similar for both systolic and diastolic BP. The hypertension and bradycardia were significantly more marked during the day than during the night, neither showing any attenuation in the hours furthest from the administration of the drug. During N, there was a reduction in the 24-hour variation coefficient for HR but the reduction was limited to the longer term component of this phenomenon, the moment-to-moment variations remaining unaffected. The long- and short-term variation coefficients for BP were not modified under N. These findings suggest that N once a day can reduce BP for 24 hours in ambulant hypertensive patients. The lack of alteration in variability of BP and moment-to-moment HR suggests that the hypotension is achieved without interfering with the mechanisms involved in cardiovascular homeostasis.
Intermittent noninvasive blood pressure monitoring is becoming increasingly popular because of the belief that a daytime blood pressure profile can provide a better clinical evaluation of hypertension than that provided by casual blood pressure measurements. This approach has potential limitations, however, one of which is that the cuff inflations permitting blood pressure to be repeatedly measured may induce an alerting reaction and a pressor response in the patients and lead to an overestimation of their daytime blood pressure. Blood pressure in 22 subjects was invasively recorded for 24 hours by the Oxford method. During the day of the recording blood pressure was also measured by a noninvasive device (Vita-Stat 901), which had its cuff applied to the opposite arm from which the intra-arterial signal was derived. For 2 hours the device provided automatic cuff inflations at 10-minutes intervals. For another 2 hours it was programmed to provide cuff inflations only following patients' commands, also at 10-minute intervals. Analysis of the intra-arterial blood pressure trace during the periods preceding and following the automatically or semiautomatically induced cuff inflations showed that these procedures caused no increment in systolic and diastolic blood pressure. This finding applied not only to the mean data but also to each individual measurement considered separately, including the initial one. Our results indicate that automatic and semiautomatic blood pressure monitorings do not induce an alarm reaction and a blood pressure rise and thus do not overestimate daytime blood pressure values.
This paper will briefly summarize the available evidence on the diagnostic and prognostic relevance of a number of parameters derived from the analysis of 24 hour ambulatory blood pressure recordings. These parameters include the 24 h average blood pressure values, the difference between daytime and nighttime blood pressure, the difference between clinic blood pressure and daytime average blood pressure as a surrogate measure of the "white coat effect", and 24 hour blood pressure variability as quantified by the standard deviation of the 24 hour average value.
Ambulatory blood pressure is more closely related to the end organ damage of hypertension than clinic blood pressure is. This is the case not only for left ventricular hypertrophy, but also for an index of renal involvement such as microalbuminuria. The closer correlation of ambulatory blood pressure with end organ damage characterises not only the 24 hour average value but also, to a similar extent, day-time and night-time average blood pressure, while the clinical importance of the difference between day and night blood pressure is still a matter of controversy. A more promising index derived from ambulatory blood pressure recordings seems to be blood pressure variability, which in preliminary studies has been shown to display an independent correlation with the end organ damage of hypertension.