Effects Of Sympathetic Nervous Activity Research Articles

Association of Resting Heart Rate With Blood Pressure and Incident Hypertension Over 30 Years in Black and White Adults: The CARDIA Study.

Few studies have assessed the association of resting heart rate (RHR) through young adulthood with incident hypertension by middle age. We investigated the association between RHR measured over 30 years with incident hypertension in a cohort of young Black and White men and women. A joint longitudinal time-to-event model consisting of a mixed random effects submodel, quadratic in follow-up time, and a survival submodel adjusted for confounders, was used to determine hazard ratios for a 10 bpm higher RHR. Race-sex specific effects were examined in a single joint model that included interactions of race-sex groups with longitudinal RHR. Out of 5115 participants enrolled in year 0 (1985-1986), after excluding prevalent cases of hypertension at baseline, 1615 men and 2273 women were included in the analytic cohort. Hypertension event rates per 1000 person-years were 42.5 and 25.7 in Black and White men, respectively, and 36.2 and 15.3 in Black and White women, respectively. The hazard ratios for a 10 bpm higher RHR were 1.47 (95% CI, 1.23-1.75), 1.51 (95% CI, 1.28-1.78), 1.48 (95% CI, 1.26-1.73), and 1.02, (95% CI, 0.89-1.17) for Black men, White men, White women, and Black women, respectively. Higher RHR during young adulthood is associated with a greater risk of incident hypertension by middle age. The association is similarly strong in Black men, White men, and White women, but absent in Black women, which may suggest racial differences in the effect of sympathetic nervous activity on hypertension among women.

Favorable Effect of Sympathetic Nervous Activity on Rehabilitation Outcomes in Frail Elderly

ObjectivesPrevious studies have suggested the relationship between physical function, mortality, and autonomic nervous activity in frail elderly and that maintaining sympathetic nervous activity might lead to improved physical function and mortality in the elderly population. The aim of this study was to investigate the utility of sympathetic nervous activity measured by heart rate variability in frail elderly patients undergoing inpatient rehabilitation, further focusing the nervous activity on the effect of rehabilitation therapy. DesignProspective cohort study. ParticipantsSixty-one subjects aged 75 years or older were recruited after treatment of acute phase illness. MeasurementsBefore undergoing rehabilitation, data of 24-hour Holter monitoring and a blood venous sample were obtained. From RR intervals in the electrocardiogram, heart rate and SDs of all NN intervals in all 5-minute segments of the entire recording, power spectral density, low frequency (LF), high frequency (HF), and low frequency/high frequency (LF/HF) were calculated. Functional Independence Measure (FIM) and Barthel index were used to measure physical function. ResultsFIM score and Barthel index were 46.8 ± 25.4 and 32.8 ± 31.7, respectively. Serum total protein, albumin, hemoglobin, and total cholesterol were all significantly related to FIM score and Barthel index before rehabilitation. Heart rate variability indices did not show a significant relationship with physical function, whereas the high LH/HF group showed significant improvement in physical function compared with the low LH/HF group. Moreover, LF/HF frequency was a predictive factor for improvement of physical function after 2 months of rehabilitation. ConclusionA favorable effect of preserved LF/HF on rehabilitation outcome was observed in elderly undergoing rehabilitation. Preservation of sympathetic nervous activity may lead to improved physical function in the elderly.

Reduced blood flow to contracting skeletal muscle in ageing humans: is it all an effect of sand through the hourglass?

The ability to sustain a given absolute submaximal workload declines with advancing age, likely to be due to a lower level of blood flow and O2 delivery to the exercising muscles. Given that physical inactivity mimics many of the physiological changes associated with ageing, separating the physiological consequences of ageing and physical inactivity can be challenging; yet, observations from cross-sectional and longitudinal studies on the effects of physical activity have provided some insight. Physical activity has the potential to offset the age-related decline in blood flow to contracting skeletal muscle during exercise where systemic blood flow is not limited by cardiac output, thereby improving O2 delivery and allowing for an enhanced energy production from oxidative metabolism. The mechanisms underlying the increase in blood flow with regular physical activity include improved endothelial function and the ability for functional sympatholysis - an attenuation of the vasoconstrictor effect of sympathetic nervous activity. These vascular adaptations with physical activity are likely to be an effect of improved nitric oxide and ATP signalling. Collectively, precise matching of blood flow and O2 delivery to meet the O2 demand of the active skeletal muscle of aged individuals during conditions where systemic blood flow is not limited by cardiac output seems to a large extent to be related to the level of physical activity.

Effects of sympathetic nervous activity on alveolar bone loss induced by occlusal hypofunction in rats

Effects of sympathetic nervous activity on alveolar bone loss induced by occlusal hypofunction in rats

The Effect of Cilnidipine and CPAP on Morning Hypertension Complicated With Sleep Apnea

PURPOSE: To assess the effects of N-type calcium channel blocker (CCB), Cilnidipine, which has an inhibitory effect of sympathetic nervous activity, and continuous positive airway pressure (CPAP) on morning hypertension complicated with more than moderate degree of sleep apnea (SA).

Effect of sympathetic nervous activity on alveolar bone loss induced by occlusal hypofunction in rats

ObjectiveTo elucidate the effect of sympathetic nervous activity on alveolar bone loss induced by occlusal hypofunction in rat molars. DesignOcclusal hypofunction in the molar area was produced by attaching appliances to rat maxillary and mandibular incisors. In addition, a non-selective β-adrenergic receptor antagonist, propranolol, was administered orally to rats in drinking water to pharmacologically suppress sympathetic nervous activity. After 1 week, alveolar bones in all groups were examined by micro-CT, histomorphometry and histology to determine their trabecular bone phenotypes and histological changes. ResultsThe marrow spaces of the interradicular alveolar bone of rat mandibular first molars (M1) increased in the occlusal hypofunction group (Group H) but not in the control group (Group C), whilst these decreased in rats in the occlusal hypofunction group that were administered propranolol (Group HB). Bone volume/tissue volume (BV/TV), trabecular thickness (Tb.Th) and trabecular number (Tb.N) for interradicular alveolar bone in M1 in Group H were significantly lower than those in Group C, whereas those in Group HB remained as high as those in Group C. The number of TRAP-positive cells in Group H increased compared to that in Group C, whereas it significantly decreased in Group HB. ConclusionsThese results suggest that sympathetic nervous activity may influence the alveolar bone loss induced by occlusal hypofunction.

The sympathetic nervous system modulates perception and reflex responses to gut distention in humans

Background/Aims : Intestinal distention induces perception and gut reflexes via sympathetic and vagal pathways, but the modulatory mechanisms of such responses remain obscure. The aim of this study was to determine the effects of sympathetic nervous activity on sympathetic and vagal reflexes as well as on intestinal and somatic perception. Methods : In 9 healthy volunteers, proximal duodenal distentions were produced in 4-mL increments and hand transcutaneous electrical nerve stimulation was produced in 3-mA increments. Increasing stimuli of 1-minute duration were randomly performed at 10-minute intervals both with and without sympathetic activation (induced by means of lower body negative pressure). Intestinal and somatic perception was scored by specific questionnaires; vagal enterogastric and sympathetic intestinointestinal relaxatory reflexes were simultaneously measured by gastric and distal duodenal barostats. Results : Sympathetic activation significantly heightened perception of intestinal distention without modifying perception of somatic stimuli (perception scores increased by 41% and −2%, respectively). The reflex responses to duodenal distention significantly increased during sympathetic activation both in the stomach and in the intestine (relaxation increased by 91% and 69%, respectively; P < 0.05 for both). Conclusions : Activation of the sympathetic nervous system selectively increases visceral but not somatic sensitivity and enhances both vagally and sympathetically driven reflexes in the gut.

Plasma norepinephrine and age as determinants of systemic hemodynamics in men with established essential hypertension.

Two primary predictor variables, age and supine plasma norepinephrine, were studied with respect to their influences on supine hemodynamic variables in 52 white men with essential hypertension who were 23 to 67 years of age and had been off active therapy for at least 4 weeks. Plasma norepinephrine was related to age (r = 0.39, p less than 0.01), correlated closely with mean arterial pressure (MAP; r = 0.54, p less than 0.0002) and systemic vascular resistance (r = 0.49, p less than 0.0005), and was related inversely to cardiac output (r = -0.26, p less than 0.06) and stroke volume (r = -0.31, p less than 0.05). Age correlated weakly with MAP (r = 0.31, p less than 0.05) and more strongly with systemic vascular resistance (r = 0.46, p less than 0.005) but was negatively related to cardiac output (r = -0.41, p less than 0.005) and heart rate (r = -0.33, p less than 0.05). Weight did not correlate with any of the hemodynamic variables. Partial regression techniques yielded significant residual correlations between age-adjusted plasma norepinephrine and MAP (r = 0.42, p less than 0.005) or systemic vascular resistance (r = 0.38, p less than 0.005). Residual correlations with cardiac output (r = -0.34, p less than 0.05), heart rate (r = -0.36, p less than 0.02), and systemic vascular resistance (r = 0.33, p less than 0.05) remained after adjusting age for the corresponding plasma norepinephrine values. These correlations demonstrate the independent effects of sympathetic nervous activity and the aging process on the systemic vasoconstriction and decreased cardiac function observed in essential hypertension.

Studies on the integrated extrinsic nervous control of rectal motility in the cat.

The effect of sympathetic nervous activity on rectal motility induced by pelvic nerve stimulation (PNS) was studied in anaesthetized cats. Division of the sympathetic lumbar colonic and hypogastric nerves or alpha-adrenoreceptor blockade, both of which reduced rectal tone, also reversed a predominantly relaxatory pelvic nerve response into a pure contraction. Contractions to pelvic nerve stimulation were reduced by simultaneous lumbar colonic nerve stimulation. This lumbar colonic nerve-induced inhibition was augmented by alpha-adrenoceptor blockade and abolished by beta-blockade. Close intra-arterial injection of a beta-adrenergic agonist reduced contractions to PNS, while an alpha-adrenergic agonist had no effect. Stimulation of the hypogastric nerves enhanced rectal contractions to simultaneous PNS. The apparent similarity with the arrangement of extrinsic nervous control of the internal anal sphincter suggests that the rectum is functionally involved in continence mechanisms.

Cerebral circulation in acute arterial hypertension—protective effects of sympathetic nervous activity

The cervical sympathetic chain was stimulated electrically at 6 or 3 Hz on one side in anesthetized cats. Acute arterial hypertension was induced by ligation of the aorta. Evans blue was given as tracer for protein leakage. The regional blood flow in the brain was determined by using labelled microspheres. At high blood pressures there was a multifocal breakdown of the blood-brain barrier. The regions with breakdown had 10-20 times the normal flow rates. With a maintained hypertension regions which were overperfused at 5 min were still overperfused at 10 min, but there was little addition of new overperfused areas. Normalization of the pressure resulted in almost twice the normal flow rates in previously overperfused regions. The breakdown of the blood-brain barrier was restricted to the non-stimulated side, or more marked on that side. The protective effect of the sympathetic stimulation lasted more than 10 min. The results indicate that acute arterial hypertension tends to cause forced and long-lasting vasodilation in some areas in the brain but regions which are resistant to the acute rise have an increase in the vascular tone. Sympathetic activity helps in developing this tone. Normalization of the blood pressure results in partial recovery of the vascular tone in previously overperfused regions and normalization in other areas.

Potentiation of the effects of noradrenaline and of sympathetic stimulation of the perfused rat caudal artery by angiotensin.

Abstract The isolated perfused caudal artery of the rat develops tachyphyllaxis rapidly to the direct constrictor action of angiotensin but not towards the potentiation of responses to submaximally effective periarterial stimulation or to noradrenaline. These potentiations persist in the presence of maximally effective concentrations of cocaine, are unaffected by increased sodium concentration and are enhanced by raised concentrations of calcium. Thus, angiotensin potentiates the effects of sympathetic nervous activity by an influence on the role of calcium in the contractile process. Hydrochlorothiazide did not affect arterial tone, the responses of the artery, or the potentiation to noradrenaline caused by angiotensin.

Vascular reactivity in hypertension.

N ESTABLISHED human hypertension, there has never been any real doubt that the baroreceptor mechanisms remain active, hut regulate the arterial pressure to a new high level. The upward setting of these baroreeeptors occurs not only in essential hypertension but also in hypertension secondary to renal disease of various sorts. 1 There is also evidence from the effects of ganglion blocking drugs that, in most hypertensive patients, a substantial part of the elevated blood pressure is maintained by the sympathetic nervous system and that blocking sympathetic ganglia leads to a larger fall of blood pressure in hypertensive than in normal subjects. In most patients with established hypertension, however, catecholamine excretion is within normal limits 2 so that, if the neurogenically maintained part of the blood pressure is increased in hypertension, it probably results from an increased effect of sympathetic nervous activity rather than from an increase in the activity itself. One possible way in which this could occur is by an increase in sensitivity of the blood vessels to the endogenous norepinephrine produced by sympathetic nerve endings. An alternative explanation would be that blood vessels already constricted by other means respond more vigorously to nervous stimulation. There have been numerous efforts to elucidate this problem in man. Most have involved the systemic administration of pressor amines, with assessment of the effect in terms of change in blood pressure or peripheral resistance. It is known, however, that in hypertension, as in health, stimuli that tend to alter blood pressure are opposed by homeostatic mechanisms, so that the changes in blood flow or in peripheral resistance that follow the systemic administration of pressor substances represent the resultant of the effects