Sympathetic Nervous System and Blood-Pressure Control in Essential Hypertension

Philipp, T.; Distler, A.; Cordes, U

doi:10.1016/s0140-6736(78)92526-6

Cited by 201 publications

(57 citation statements)

References 13 publications

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“…In our N subjects, the NE pressor dose correlated positively with endogenous plasma NE (p < 0.02), pointing to a physiologic regulatory mechanism. 19 A similar relationship existed also in borderline hypertension, but it was shifted so that NE pressor response for any given basal plasma NE value was significantly (p < 0.001) increased by about 35%. Philipp et al" described a comparable disturbance of the relationship between exercise-stimulated plasma NE and NE pressor response in patients with established essential hypertension, whose diastolic BP was >100 mm Hg.…”

Section: Discussionmentioning

confidence: 65%

Pressor factors and cardiovascular pressor responsiveness in borderline hypertension.

Meier¹,

Weidmann²,

Grimm³

et al. 1981

Hypertension

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SUMMARYThe role of various pressor factors and cardiovascular responsiveness to norepinephrine or angiotensin II in the pathogenesis of borderline hypertension was evaluated. Exchangeable body sodium, blood volume, plasma renin activity, norepinephrine or dopamine levels, and norepinephrine or epinephrine excretion rates were similar between 24 patients with borderline hypertension (mean age 34 ± 4 (SEM) years and 22 normal subjects matched for age; the patients had a slight increase in supine plasma epinephrine. Pressor doses of norepinephrine or angiotensin II were significantly lower (p < 0.01 and 0.001, respectively) in the borderline hypertensive group. These findings suggest that borderline hypertension may be maintained by inappropriately increased cardiovascular response to norepinephrine and angiotensin II in the presence of normal sympathetic and renin activity and a normal body sodium-volume state.

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Section: Discussionmentioning

confidence: 65%

Pressor factors and cardiovascular pressor responsiveness in borderline hypertension.

Meier¹,

Weidmann²,

Grimm³

et al. 1981

Hypertension

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“…The relationship between body weight (BW) and some so-called metabolic risk factors', ®rstly arterial hypertension, is well documented in adults; there is also evidence that BW is able to in¯uence blood pressure (BP) levels during childhood, at least in baseline conditions (Ferrara et al, 1989). Pathophysiological speculations imply that the impairment of insulin sensitivity or adrenergic nervous system activity are responsible for the relationship observed (Julius & Johnson, 1985;Philipp et al, 1978;Ferrannini et al, 1987). The problem is even more intriguing during childhood, since the in¯uence of sexual maturation on BP levels should also be considered (Tanner & Whitehouse, 1976;Vartiainen et al, 1986;Daniels et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Sex-related influence of body size and sexual maturation on blood pressure in adolescents

Leccia¹,

Marotta

Mr³

et al. 1999

Eur J Clin Nutr

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Objective: This study is aimed at investigating the in¯uence of body size, body fat and sexual maturation on blood pressure (BP) in adolescents. Design: A cross-sectional study. Setting: A suburban student population of Southern Italy. Subjects: One hundred ninety students attending the ®rst and second year of a secondary school. Five were excluded because they were affected by major diseases. The remaining were 98 M and 87 F (mean age for either group 12.0 AE 0.8 y). Methods: Blood pressure was measured by a mercury sphygmomanometer, body weight by a platform beamscale, other measurements included height, biceps, triceps, subscapular and suprailiac skinfolds by a caliper; sexual maturation was evaluated according to Tanner. Results: Body size was greater than in Tanner's population: in particular body weight (but not height) in our sample markedly exceeded that of the children of the same age in Tanner's population. Boys had higher systolic blood pressure (SBP) than girls (BP 109a64 AE 12a10 vs 103a63 AE 11a8 mmHg, P`0.02 for SBP), while heart rate and waistahip ratio were lower.During puberty Ð evaluated on the basis of pubic hair growth Ð BP in girls was higher than in the prepubertal phase (107a66 AE 9a7 vs 99a61 AE 10a7, P`0.01). Pubertal boys showed a reduced percent of body fat (calculated from four skinfold measurements) in comparison to prepubertal ones (21.0% AE 4.5 vs 24.5% AE 7.1, P`0.01). In linear correlation analysis, height, BW, BMI and lean body mass were found to be signi®cantly associated with SBP in both sexes and to diastolic blood pressure (DBP) in girls. Percent body fat was correlated with SBP in boys, while sexual maturation was associated to SBP and DBP in girls only.Multiple regression analysis indicated a signi®cant contribution of body size to BP variability, particularly in the girls. Sexual maturation was excluded from the ®nal regression equations when height, BW or lean body mass were present. Conclusions: These data indicate that body weight in these adolescents is greater that in Tanner's population of the same age and sex. Body size appears to be a major determinant of BP, whereas sexual maturation seems to in¯uence BP levels mainly through body growth. The in¯uence of percent body fat on BP setting seems to be of limited importance.

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“…16 " 18 Age, for example, alters norepinephrine clearance." Because of individual variability in the vascular reactivity to the neurotransmitter norepinephrine, 20 comparing pressor responses to various stimuli with changes in PNE may be misleading. Finally, as Folkow et al 21 caution, activities that increase blood pressure in humans usually do so by effecting differentiated rather than generalized increases in sympathetic discharge.…”

mentioning

confidence: 99%

Failure of plasma norepinephrine to consistently reflect sympathetic activity in humans.

Floras¹,

Jones²,

Hassan³

et al. 1986

Hypertension

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SUMMARY To determine whether venous plasma norepinephrine concentrations consistently reflect changes in sympathetic nervous activity, the influence of mental arithmetic, static handgrip, and submaximal bicycle exercise on infra-arterial blood pressure, heart rate, and plasma norepinephrine was studied in 51 subjects with untreated essential hypertension (mean age, 46 years; range, 16-69 years). At rest, plasma norepinephrine was unrelated to age or blood pressure. Mental arithmetic increased mean arterial pressure from 108 ± 18 to 127 ± 18 mm Hg (mean ± S.D.; p<0.001) and heart rate from 69 ± 7 to 93 ± 13 beats/min (p<0.001) but not plasma norepinephrine (547 ± 297 to 518 ± 250 pg/ml). Isometric exercise raised mean arterial pressure from 115 ± 18 to 148 ± 21 mm Hg (p<0.001) and heart rate from 76 ± 9 to 95 ± 13 beats/min (p<0.001) but not plasma norepinephrine (683 ± 253 to 741 ± 253 pg/ml). Bicycle exercise increased mean arterial pressure from 114 ± 20 to 146 ± 26 mm Hg (p< 0.001), heart rate from 77 ± 9 to 128 ± 19 beats/min (p< 0.001), and plasma norepinephrine from 645 ± 228 to 1151 ± 462 pg/ml (p<0.001). Both the maximum mean arterial pressure and the peak heart rate attained during bicycle exercise were related to the exercise plasma norepinephrine level (r = 0.33, p<0.02 and r=0.28, p<0.03, respectively). Increases in plasma norepinephrine with exercise were not greater in older or more hypertensive subjects. In fact, the relative rise in mean arterial pressure and the absolute increase in plasma norepinephrine during cycling were greater in those with lower resting blood pressures. As only bicycle exerdse increased plasma norepinephrine, and as there was no direct relationship between plasma norepinephrine and arterial blood pressure in subjects studied supine, seated, and during these three activities, we conclude that plasma norepinephrine concentrations do not consistently reflect variations in sympathetic neuronal activity and therefore are relatively insensitive measures of sympathetic tone in humans. Received March 25, 1985; accepted January 21, 1986. Norepinephrine concentration in the venous drainage of an organ is also proportional to the rate of stimulation of its nerves. 3 In humans, physical and emotional stimuli that increase blood pressure and heart rate (HR) also increase PNE. "7 Conversely, concentrations of this catecholamine may be reduced in subjects with autonomic nervous dysfunction 8 or lowered by drugs that interfere with the action of the sympathetic nervous system. 9 Watson et al., 6 who recorded PNE and blood pressure in hypertensive subjects while they slept, lay quietly, woke, stood, walked, and cycled, described a log-linear relationship between PNE and systolic blood pressure during these activities, which suggests that PNE concentrations indeed reflect changes in sympathetic activity.Although increases in PNE with exertion may be greater in some subjects with essential hypertension, 10

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Sympathetic Nervous System and Blood-Pressure Control in Essential Hypertension

Cited by 201 publications

References 13 publications

Pressor factors and cardiovascular pressor responsiveness in borderline hypertension.

Pressor factors and cardiovascular pressor responsiveness in borderline hypertension.

Sex-related influence of body size and sexual maturation on blood pressure in adolescents

Failure of plasma norepinephrine to consistently reflect sympathetic activity in humans.

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