(Hypertension. 1996;28:953-960.)
© 1996 American Heart Association, Inc.
Articles |
Arterial Baroreceptor-Cardiac Reflex Sensitivity in the Elderly
the University Departments of Medicine for the Elderly, Glenfield Hospital, and Medical Physics, Leicester Royal Infirmary (R.B.P.), Leicester, UK.
Correspondence to Dr Martin A. James, University Department of Medicine for the Elderly, Glenfield Hospital, Leicester, LE3 9QP, UK.
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Abstract |
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Uncertainty still remains regarding the differing effects of blood pressure and age on baroreceptor-cardiac reflex sensitivity in elderly individuals; these differences are at least partly due to the differing methods and subject groups used in previous studies. We sought to resolve these issues by examining baroreflex sensitivity in 54 subjects aged 70±1 years (mean±SE; range, 60 to 81) divided into groups with combined systolic-diastolic hypertension (CH group, n=16), isolated systolic hypertension (ISH group, n=16), or normotension (NT group, n=22). Baroreflex sensitivity was quantified from the pulse interval and blood pressure responses to the Valsalva maneuver and pressor (phenylephrine) and depressor (sodium nitroprusside) stimuli. Baroreflex sensitivity was significantly reduced in the two hypertensive groups but did not differ between them (Valsalva maneuver: CH group, 1.9±0.3 ms/mm Hg; ISH group, 2.8±0.5; NT group, 4.4±0.4; phenylephrine: CH group, 3.1±0.6; ISH group, 3.5±0.7; NT group, 7.7±1.0; sodium nitroprusside: CH group, 2.1±0.3; ISH group, 3.6±0.8; NT group, 5.4±0.3; all P<.05 for comparison with the NT group). Thus, this study demonstrated reductions in baroreflex sensitivity with hypertension in elderly subjects consistent across all methods but with no difference between subjects with combined hypertension and isolated systolic hypertension matched for similar systolic pressure. Baroreflex sensitivity was related only to the level of systolic pressure independent of diastolic pressure or age. If elderly subjects with isolated systolic hypertension have a greater reduction in large-artery compliance than combined hypertensive subjects with similar systolic pressure, this does not appear to lead to further reductions in baroreflex sensitivity in these individuals.
Key Words: pressoreceptors • baroreflex • aged • phenylephrine • nitroprusside • Valsalva's maneuver
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Introduction |
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The arterial baroreflex is the principal mechanism of short-term BP homeostasis in humans and has been the focus of much interest regarding the role of dysfunction of the reflex in the pathogenesis of hypertension.1 In established human hypertension, the baroreflex is both reset at a higher pressure and reduced in gain.2 3 This reduction in gain may be a result of a diminished sensitivity of the arterial baroreceptor itself, but modulation of BRS by central mechanisms in humans has been demonstrated, for instance, by arousal, exercise, and mental stress.4 5 6 7
The function of the arterial baroreflex could be theoretically disrupted by aging at a number of levels. Most obviously, this could occur in the afferent component of the reflex loop, with changes affecting the baroreceptors in the arterial wall, with medial thickening and rigidity, and with the formation of atheromatous plaques in the intima. Most but not all of the available evidence indicates a progressive decline in BRS with increasing age among younger subjects.3 8 9 10 11 12 However, there are comparatively few data on BRS in elderly subjects: Two studies on the effect of aging on baroreflex function3 13 have included a total of three individuals older than 60 years, and these results cannot necessarily be extrapolated to the elderly in general. A small number of studies have included some form of assessment of BRS in the elderly,14 15 16 17 18 and the evidence from these is somewhat conflicting. One study using the phenylephrine pressor method18 showed BRS to be lower in elderly hypertensive than normotensive individuals; another16 found no difference in BRS with hypertension by the phenylephrine method but did find that in response to a depressor stimulus, BRS was lower in elderly hypertensive than normotensive subjects. The study of McGarry et al14 (also using a depressor stimulus) suggested that BRS was not different between young and elderly hypertensive subjects, but they did not include a comparison with elderly normotensive subjects. BRS from phase 4 of the Valsalva maneuver has been found to be reduced in young hypertensive compared with normotensive subjects19 but was not different between hypertensive and normotensive subjects in the one study that used this technique in the elderly.17
Our primary purpose in the present study was therefore to clarify the evidence regarding arterial BRS in hypertension in elderly subjects but also to address the special case of isolated systolic hypertension, which represents a majority of all hypertension in the elderly.20 If BRS were largely a function of the distensibility of the arterial wall, then it could be hypothesized that the reduced compliance observed in isolated systolic hypertension18 21 would lead to a further reduction in BRS. We also set out to measure BRS using several of the currently accepted methods to allow as broad an assessment of the baroreflex control of heart rate in the elderly as possible, given that the level of agreement among the various methods has previously been shown to be low in younger subjects, with a particular disparity between results from pressor and depressor stimuli.16 22
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Methods |
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Study Subjects
This study involved 54 elderly subjects (age, 69.6±0.7 years [mean±SE]), of whom 32 were hypertensive and 22 normotensive. Hypertensive subjects were recruited from among outpatients who were having their hypertension assessed at two large teaching hospitals and through a liaison with several large local general practices. Normotensive subjects were recruited from among the spouses and friends of the hypertensive subjects and from respondents to a local newspaper advertisement. All subjects gave written informed consent to participate in the study, which received local ethics committee approval. All subjects were active and ambulant and living independently in the community. All subjects had a normal physical examination with no evidence of target-organ damage, all were in sinus rhythm with a normal electrocardiogram, and all had normal routine biochemistry including renal function (serum creatinine <125 µmol/L). Subjects with a history of other cardiovascular diseases, including atrial fibrillation; other disorders associated with autonomic dysfunction; or other major illness were excluded. No subject in the normotensive group had any history of hypertension or preeclampsia. Any subject taking medication with cardiovascular or autonomic effects was excluded. The majority of subjects (n=34) had never previously received antihypertensive treatment, but in those currently on treatment (n=20) when recruited to the study, antihypertensive medication was progressively withdrawn, leaving a minimum 1-month drug-free period before BP values used for the study were determined.
Study Protocol
Subjects attended the morning research clinic on three separate occasions at least 1 week apart. Subjects' height, weight, and body mass index (weight in kilograms divided by height in meters squared) were recorded. Supine BP (Korotkoff phase V) and heart rate were recorded three times on each visit, after the subject had rested at least 5 minutes, with the use of a standard mercury sphygmomanometer and a cuff of appropriate size. Subjects were allocated to one of three groups according to the final average of the nine BP readings obtained over the three clinic visits. The first group comprised 16 subjects with sustained combined systolic-diastolic hypertension (CH group; SBP 
160 mm Hg and DBP 90); the second group was a further 16 subjects of similar age with sustained isolated systolic hypertension (ISH group; SBP 160 mm Hg, with DBP <90); and the third group consisted of 22 age-matched normotensive subjects (NT group; clinic SBP <160 mm Hg and clinic DBP <90). The CH and ISH groups were also matched for similar levels of SBP. None of the subjects in the ISH group had a history of raised DBP; therefore, subjects with "burnt out" combined hypertension were excluded as far as possible.
Laboratory Studies
Within 2 weeks, subjects attended the cardiovascular laboratory for a morning session, having emptied the bladder, eaten a light breakfast, and refrained from smoking, alcohol, and caffeine-containing products for at least 12 hours. Subjects wore light clothing; the laboratory temperature was constant between 20°C and 22°C. Subjects rested supine for a minimum of 30 minutes after the insertion of a cannula into a dorsal hand vein. Each subject was fitted with chest leads for recording of the continuous surface electrocardiogram (model CR7, Cardiac Recorders Ltd), and the appropriately sized finger cuff of the Finapres 2300 noninvasive beat-to-beat BP recording device (Ohmeda Monitoring Systems) was fitted to the middle finger (or in five cases the thumb) of the nondominant hand, which rested throughout on an adjustable support at the level of the heart.
After a satisfactory BP signal was achieved from the Finapres and BP was stabilized at the same level for at least 10 minutes, subjects performed the following tests of cardiovascular autonomic function: (1) deep breathing at six breaths per minute for 1 minute in order to vary RR interval, and (2) the Valsalva maneuver. After several practices, subjects blew into a modified sphygmomanometer to maintain a pressure of 40 mm Hg for 15 seconds while seated. The manometer contained a small air leak so that subjects had to maintain a constant respiratory effort. The maneuver was repeated three times and the average response taken.
BRS testing was performed by the following pharmacological methods: (1) BP and pulse interval responses to phenylephrine injection4 5 : An initial bolus dose of 50 µg phenylephrine was progressively increased in 50-µg steps as necessary (up to a maximum of 200 µg) to achieve a peak BP rise of 20 to 40 mm Hg, and the effective dose was repeated to obtain a minimum of three adequate responses. Bolus injections of 0.9% saline were interspersed at random between the drug injections. The subject was blinded to the nature of each injection. (2) BP and pulse interval responses to graded SNP infusion12 14 23 : SNP infusion was begun at 0.25 µg·kg-1·min-1 and increased (by 0.25 µg·kg-1·min-1 each minute) until a fall in BP of at least 20 mm Hg was observed.
Data Analysis
The analog outputs from the Finapres device and the simultaneous electrocardiographic signal were routed to a dedicated personal computer fitted with an analog-to-digital converter sampling at 200 Hz per channel. A third channel recorded pressure from a transducer and amplifier connected to the sphygmomanometer used for the Valsalva maneuver. Dedicated software allowed the recording, calibration, and editing of the digitized signal and derivation for later off-line analysis of beat-to-beat data for SBP, mean arterial BP, and DBP, together with the pulse interval from the Finapres and electrocardiographic signals and the Valsalva pressure.
RR variability during timed respiration (as a measure of vagal efferent function) was assessed from the mean of the inspiratory-expiratory differences in heart rate averaged over six deep breaths in 1 minute. The data from the three Valsalva maneuvers were first analyzed to obtain the mean Valsalva ratio, ie, the ratio of the shortest RR interval during the strain part of the maneuver to the longest RR interval occurring after release.24 The BP and pulse interval data were then analyzed to derive an index for BRS from phase 4 of the maneuver according to the method of Smith et al.25 Two figures were derived: BRSV1 describes the BRS from the linear regression of pulse interval on BP for the whole of phase 4 (from the lowest SBP recorded immediately after release of the strain to the peak value observed several seconds later) with the "lag" (in beats) between stimulus (BP) and response (pulse interval) that achieved the highest correlation (optimal r); BRSV2 describes the results of a similar analysis confined to that portion of phase 4 in which arterial pressure exceeded that before the maneuver, that is, the pressure overshoot.
BRS was derived from the phenylephrine injection technique also by two methods. The first involved the linear regression of pulse interval on BP for the immediately preceding beat for the "ramp" portion of the BP response, including both inspiratory and expiratory beats, ie, from the first beat during which a sustained rise in BP was observed (usually 15 to 25 seconds after injection) to the maximal value (ramp BRSPE).4 5 The linear regression method for the analysis of BRS from the BP ramps is illustrated in Fig 1
. The second method took account of the observation that subjects with a very low BRS would have a nonsignificant correlation between pulse interval and BP for the ramp response and instead compared baseline values recorded over the 10 to 15 seconds immediately before drug injection with values obtained during the later, sustained part of the BP response, the modified "steady-state" method (steady-state BRSPE).8 Values for ramp BRSPE and steady-state BRSPE were obtained for each (minimum of three) of the effective phenylephrine doses and were averaged to derive a final value for each subject. BRS was derived from the SNP depressor response by the same methods; this yielded values for each subject for ramp BRSSNP and steady-state BRSSNP.
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Statistical Methods
Data are expressed as mean±SE. Student's two-tailed paired t test was used for within-subject comparisons. Differences between groups for the BRS data were examined with ANOVA and Tukey's pairwise correction for multiple comparisons. Pearson's correlation coefficient and least-squares regression analysis were used for examination of the linear association between continuous variables, and the simultaneous effects of a number of variables studied were examined with multiple linear regression. A value of P<.05 was regarded as indicating statistical significance.
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Results |
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Subject Characteristics and Clinic and Ambulatory BPs
Of the 54 subjects in the study, 16 had combined systolic-diastolic hypertension (CH group), 16 had sustained isolated systolic hypertension (ISH group), and 22 were normotensive (NT group). Age, weight, height, and body mass index did not differ between the three groups (Table 1
). Table 1 also shows BP data for the three groups. The two hypertensive groups were matched for similar levels of clinic SBP, but DBP was highly significantly different between the ISH and CH groups. A significantly higher clinic heart rate was seen in the CH group than in the other two groups.
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Laboratory Cardiovascular Tests
Baseline BP in the laboratory was significantly higher in the two hypertensive groups, and baseline heart rate was higher in the CH group (198±4/98±3 mm Hg, 77±2 beats per minute; ISH group: 183±7/86±3, 66±2; NT group: 144±4/84±3, 66±2). Heart rate (RR) variability with respiration for the three groups was not significantly different (CH group, 10.0±1.1 beats per minute; ISH group, 9.7±1.2; NT group, 12.1±1.5; P>.4).
The mean Valsalva ratio for the entire study group was 1.38±0.03. The Valsalva ratio did not differ between the three groups (Table 2) and was not related to age (r=.07, P>.2). A typical response to the Valsalva maneuver in a study subject is shown in Fig 2. The hypertensive subjects demonstrated a greater BP rise than the normotensive subjects during phase 4. BRS from the whole of phase 4 of the maneuver (BRSV1) was significantly lower in the CH and ISH groups than in the NT group (Table 2). If analysis was limited to the overshoot part of phase 4 only (BRSV2), the results were broadly similar (Table 2), with BRS again lower in the two hypertensive groups but not different between them.
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BRSV1 was significantly correlated with clinic SBP (r=-.66, P<.001), and this relation persisted even after correction for DBP and age (regression equation: BRSV1=15.0-0.044 Age-0.045 SBP-0.02 DBP; R2=45.2%, P=.001). Similarly, BRSV2 was related to clinic SBP (r=-.57, P<.001), again independent of age and DBP (BRSV2=27.3-0.048 Age-0.074 SBP-0.062 DBP; R2=32.5%, P=.02). Neither parameter for BRS was independently related to age.
Pharmacological BRS Tests
Phenylephrine drug injection was not associated with any side effects. However, a mild flushing sensation, usually confined to the face, was sometimes reported at the lowest point of the BP response to SNP infusion.
A typical response to phenylephrine bolus injection in a study subject is shown in Fig 3. Steady-state BRSPE was significantly lower in the CH and ISH groups than in the NT group but was not different between them (Table 3). Similar observations were made with the analysis of the BP ramps, although in seven subjects, ramp BRSPE could not be obtained because of nonsignificant correlations between pulse interval and BP. The mean BP rise during the ramp responses was 31±1.4 mm Hg, and there was a tendency toward a slightly lower BP response in the NT group to an equivalent dose of phenylephrine (P=.10). BRSPE was not correlated with age but was significantly correlated with clinic SBP independent of age and DBP (regression equations: Steady-state BRSPE=23.0-0.104 Age-0.086 SBP-0.035 DBP; R2=27.5%, P=.005; Ramp BRSPE=14.2+0.072 Age-0.11 SBP+0.05 DBP; R2=32.7%, P<.001).
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BRS findings with SNP infusion were broadly similar in pattern (Table 3
). Both steady-state and ramp BRSSNP were significantly lower with hypertension, but there were no differences between the CH and ISH groups. There was a smaller BP reduction in the NT group with an equivalent maximum dose of SNP (maximum doses: CH group, 0.63±0.05 µg·kg-1·min-1; ISH group, 0.75±0.07; NT group, 0.77±0.04; P>.10). There was no significant correlation between BRSSNP and age, but there was a significant relation between BRSSNP and clinic SBP independent of both age and DBP (regression equations: Steady-state BRSSNP=8.93+0.06 Age-0.06 SBP+0.003 DBP, R2=29.1%, P=.003; Ramp BRSSNP=9.77+0.05 Age-0.06 SBP+0.0007 DBP, R2=31.1%, P=.002).
Fig 4 summarizes the BRS findings. BRS was consistently reduced by any method in the groups with hypertension (ISH and CH groups) compared with the NT group, but there were no significant differences between subjects in the CH group and ISH group. The study had 80% power to detect differences between the CH and ISH groups of 1.5 ms/mm Hg in BRSV1, 3.1 in BRSV2, 2.5 in BRSSNP, and 2.7 in BRSPE at the 5% significance level. BRS responses to the pharmacological pressor or depressor stimuli within the CH and ISH groups did not differ, but BRSPE was significantly greater than BRSSNP in the NT group (P=.03).
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On univariate analysis, BRS by all methods was strongly inversely correlated with the level of clinic BP; the correlation coefficients are shown in Table 4. Values for the univariate correlations between SBP and BRS were always higher than those between DBP and BRS; the relation between clinic SBP and BRS by the four methods is shown in Fig 5. This observation was borne out by the multivariate analyses, which showed SBP to be the single significant predictor of BRS by any method, independent of both age and DBP. The univariate correlations between age and BRS were at most only weak and were not independent of the changes seen in BP with age.
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Discussion |
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This study provides a comprehensive evaluation of cardiovascular neural control of heart rate in elderly subjects and the relation to BP. The study design permits analysis of the differences in the baroreceptor-cardiac reflex (including responses to both a pressor and depressor stimulus) between elderly subjects with combined hypertension, isolated systolic hypertension, and "normal" BP. In this regard, the study achieved this division in terms of clinic BP, with the two hypertensive groups being matched for similar levels of clinic SBP, with a highly significant (both statistically and clinically) average difference of 17 mm Hg in clinic DBP. As far as was possible, we excluded from the study subjects with isolated systolic hypertension but with a history of elevated DBP to establish separation of the groups, but we cannot be certain that contamination between the groups did not occur. What is more, although baseline laboratory DBP was not different between the ISH and NT subjects, clinic DBP was still significantly higher in the ISH group than in the NT group, indicating that these subjects did not strictly have "isolated" elevation of systolic pressure but rather "predominant" systolic hypertension.26
Baroreceptor-Cardiac Reflex Sensitivity
In this study, the vagal efferent arc was demonstrated to be unaffected by hypertension, with no difference in RR interval variation with respiration between the three groups. Furthermore, the Valsalva ratio was also similar between the three groups. Study of the baroreceptor-cardiac reflex, however, identified a consistent reduction in BRS with hypertension, irrespective of the method used for study (phase 4 of the Valsalva maneuver, phenylephrine pressor or SNP depressor method; Tables 2 and 3). BRS in the CH and ISH groups was significantly lower than in the NT group, but there were no differences between the two hypertensive groups. This observation is also borne out by the multiple regression analysis, which identified SBP as the single predictor of BRS, independent of age and DBP.
The present study is in agreement with that of Sumimoto et al,18 who found reduced BRS in elderly subjects (assessed only by the pressor method) categorized as having either diastolic hypertension (continuing from middle age) or recently diagnosed isolated systolic hypertension, although after 7 days of hospitalization, most of the subjects in their study were in fact normotensive. However, the current findings contrast with those of Jansen and Hoefnagels,16 who found no difference in BRS with the phenylephrine method between elderly hypertensive and normotensive subjects. Where the current findings do agree with those of Jansen and Hoefnagels, however, is that BRS when assessed by the depressor method is impaired with hypertension in elderly subjects. This discrepancy may have been because the study of Jansen and Hoefnagels had insufficient power to test the observed difference between the groups in BRSPE. In the study of Kawamoto et al,17 BRS was measured from the BP and pulse interval responses during both phase 2 and phase 4 of the Valsalva maneuver.22 They found that BRS from phase 2 of the Valsalva maneuver was not different between young and old normotensive individuals but was significantly lower in the elderly hypertensive group. By contrast, they found that BRS from phase 4 was not different between the two elderly groups but both were significantly lower than in the young group. This suggested no effect of age with one method and no effect of hypertension with the other. The authors concluded that hypertension had a marginal, if any, further influence on BRS in elderly subjects whose regulatory mechanisms were already substantially affected by advanced age. There are methodological differences between the present study and that of Kawamoto and colleagues, but otherwise, it is difficult to account for the disparity in the results from the two studies. However, the present study has identified a distinct and independent reduction in BRS from phase 4 of the Valsalva maneuver with hypertension that is entirely consistent with the results observed with the pharmacological tests of BRS.
Atherosclerosis of large arteries, which causes loss of arterial compliance and contributes to a preferential elevation of SBP and thus to isolated systolic hypertension,21 has previously been proposed as a cause of reduced BRS in such individuals. Studies in elderly subjects have identified significant differences in large-artery compliance between elderly subjects with combined and isolated systolic hypertension.18 The present study indicates no difference in BRS between elderly subjects with combined and isolated systolic hypertension matched for similar SBP levels, suggesting that changes in arterial wall compliance at sites such as the aortic arch and carotid sinus may contribute less to reduced baroreceptor function in the elderly than has been previously thought, in contrast to what may be the case in the young.27 Results from experimental models of hypertension have failed to demonstrate a consistent relation between arterial compliance and baroreflex function.28 Furthermore, the observed association between increasing SBP levels and orthostatic hypotension has often been attributed to afferent baroreflex dysfunction related to loss of arterial compliance.29 30 If subjects with isolated systolic hypertension are indeed more prone to orthostatic hypotension than their counterparts with combined hypertension matched for similar SBP levels, this study presents no evidence that this is due to differences between these two groups in arterial baroreceptor-cardiac reflex function.
BRS and Age
The absolute values for BRS seen in the present study of elderly subjects are lower than those reported for younger subjects by both the pharmacological and Valsalva methods.2 25 Previous cross-sectional studies of the relation between BRS and age have included very few subjects older than 60 years.3 13 The present study of subjects older than 60 years (range, 60 to 81) indicates that beyond this point any relation with age is diminished or lost. Across the age range of the present study, a slight effect of age on BRS cannot be entirely ruled out, but this could account for no more than 7% of the observed variance. Thus, SBP remained the main predictor of changes in BRS independent of age and DBP, accounting for between 27% and 45% of the observed variance in BRS. The original work by Gribbin and colleagues,3 by use of the phenylephrine method, demonstrated a logarithmic rather than a linear decline in BRS with increasing age in 81 subjects, and in their study, age and BRS were not significantly related beyond the age of 40 years, similar to the present study beyond 60 years. This would suggest that the majority of the reduction seen in BRS with age has already occurred by the fifth decade, before the majority of the rise seen in BP with aging.31 32 This observation, admittedly based on cross-sectional data, is in contrast to the position which states that impaired baroreflexes are seen only as the result of the effects of a raised BP.33 Nonetheless, it would be wrong to assume that the two factors of aging and hypertension are mutually exclusive, and it remains quite possible that an elevated BP may also confer a further impairment of baroreceptors due to both a mechanical effect and local paracrine factors.34 For example, recent evidence shows the modulation of mechanical-electrical transduction in arterial baroreceptors by several endothelial factors. Chapleau and colleagues35 have demonstrated increased BRS in animal models of hypertension and atherosclerosis after treatment with exogenous prostacyclin or the free-radical scavengers superoxide dismutase and catalase as well as the inhibition of baroreceptors by aggregating platelets. These processes may affect areas of endothelial damage (either structural or functional) at sites prone to shear stress, such as the carotid sinus or aortic bifurcations,36 and may account for baroreceptor impairment long before it could be attributed to structural modification related to higher BP levels or atheroma. Alternatively, local paracrine factors may have effects on the central integration of baroreflexes. Animal studies have shown that sympathetic nerve activity is released from baroreceptor-mediated inhibition in older animals despite a similar level of afferent baroreflex activity to younger animals.37 This observation would be consistent with a degree of comparative sympathoexcitation in elderly subjects due to loss of the inhibitory effects of the baroreflex on sympathetic efferents through either afferent or central failure.10 36 38 39
Study Limitations
Interpretation of the present results needs to take into account the study limitations. The methods used for assessment of the baroreceptor-cardiac reflex are at their most accurate when used to study subjects with higher BRS levels; the "ramp" techniques cannot be used in subjects in whom pulse interval changes little in response to substantial BP changes because a significant regression will not be found. The alternative method involving a modification of the "steady-state" technique first described by Korner et al8 can avoid this obstacle, and a figure for BRS could thus be obtained for all subjects. It must be remembered, however, that observations concerning the ramp methods have excluded seven subjects from among those with lower BRS values. Notably, these considerations have not been featured in other studies of subjects who have exhibited similarly low BRS values,15 22 40 although the problem is referred to in the original description of the phenylephrine method by Smyth et al.4 The present study has described BRS only under conditions of supine rest and did not attempt to quantify BRS under other circumstances, such as exercise, mental stress, or sleep, all shown to modify the baroreflex in younger subjects.4 6 7 Furthermore, the present study has measured only the sensitivity of the baroreceptor-heart rate reflex, which cannot be regarded as descriptive of the entire baroreflex homeostatic mechanism. In particular, no assessment has been made of the sympathetically mediated baroreceptor-vascular reflex, which cannot be assessed by the pharmacological methods used in the present study.
In conclusion, the study we report here has demonstrated that reduced arterial BRS in elderly hypertensive subjects is principally related to SBP level and that this observation is consistent irrespective of the method of BRS testing used. Furthermore, arterial BRS does not differ between elderly hypertensive subjects with combined systolic-diastolic hypertension and isolated systolic hypertension matched for similar SBP levels. If elderly subjects with isolated systolic hypertension do indeed have more rigid arteries than those with combined hypertension with similar SBP, this would not appear to lead to a further reduction in afferent BRS in these individuals. Finally, and in contrast to what has been described in younger subjects, in subjects ranging in age from 60 to 81 years, there is no independent relation between increasing age and declining BRS.
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Acknowledgments |
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This research was supported by a project grant from the Sir Jules Thorn Trust.
Received May 7, 1996;
first decision May 24, 1996; first decision July 31, 1996;
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References |
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