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Biomedical subjects

G Mancia

Publications and source records attributed to G Mancia.

At least 145 records · Page 8Linked to original sources
PubMed1998

The smoothness index: a new, reproducible and clinically relevant measure of the homogeneity of the blood pressure reduction with treatment for hypertension.

OBJECTIVE: To introduce a new method, the smoothness index, for assessing the homogeneity of 24 h blood pressure reduction by antihypertensive treatment and to compare it with the trough : peak ratio; and to assess the ability of both indices to predict a reduction in the left ventricular mass index induced by treatment. PATIENTS AND METHODS: In 174 patients with essential hypertension and left ventricular hypertrophy, enrolled in the Study on Ambulatory Monitoring of Pressure and Lisinopril Evaluation (SAMPLE), aged 20-65 years, we measured clinic blood pressure, 24 h ambulatory blood pressure and the left ventricular mass index (echocardiography) before and after treatment with lisinopril at 20 mg with the addition of 12.5 or 25 mg hydrochlorothiazide as needed to reach a sufficient blood pressure reduction. The following parameters were computed for systolic and diastolic ambulatory blood pressure: (1) hourly and 24 h blood pressure averages (+/- SD) at baseline and after 3 and 12 months of treatment; (2) hourly blood pressure changes from baseline after 3 and 12 months of treatment, and their average (+/- SD) over 24 h; (3) the trough : peak ratio after 3 and 12 months of treatment; and (4) the smoothness index after 3 and 12 months of treatment Similar calculations were also performed at the end of a final study month during which active treatment was withdrawn and placebo was substituted (n = 164). RESULTS: The smoothness index for systolic and diastolic ambulatory blood pressure computed after 3 months of treatment was more closely related to its corresponding values after 12 months of treatment than the trough : peak ratio values computed after the same time periods were (r = 0.68 versus 0.38 for systolic and 0.68 versus 0.42 for diastolic blood pressure, respectively). The smoothness index showed an inverse correlation with the 24 h standard deviation of systolic and diastolic blood pressure (r = -0.25 and -0.16, P < 0.01 and < 0.05, respectively, for 12 months of treatment), while the trough : peak ratio did not (r = -0.01 to -0.12, NS). A treatment-induced reduction in the left ventricular mass index was related to the smoothness index for systolic and diastolic blood pressure (r = -0.35 and -0.32, P< 0.001 with 12 months of treatment), but not to the corresponding trough : peak ratios. CONCLUSIONS: The smoothness index identifies the occurrence of a balanced 24 h blood pressure reduction with treatment and correlates with the favourable effects of treatment on left ventricular hypertrophy better than the commonly used trough : peak ratio.

Adult↗
PubMed1998

Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension.

BACKGROUND: Human studies have shown that the blood pressure lowering effects of angiotensin converting enzyme inhibitors are accompanied by a reduction in plasma norepinephrine levels. Whether this is due to central or peripheral mechanisms is unknown, however. OBJECTIVE: To evaluate the effects of chronic interference with the renin-angiotensin system on sympathetic nerve traffic and baroreflex control of vagal and adrenergic cardiovascular drive. PATIENTS AND METHODS: In 18 untreated mild to moderate essential hypertensive patients aged 48.5+/-1.9 years (mean+/-SEM), we measured mean arterial pressure (Finapres), heart rate (electrocardiogram), plasma renin activity (radioimmunoassay), plasma norepinephrine (high-performance liquid chromatography) and postganglionic muscle sympathetic nerve activity (microneurography at a peroneal nerve). In nine patients, measurements were performed before and after 2 months of oral administration of lisinopril (10 mg/day), while in the remaining nine patients they were performed before and after a 2 month observation period, without the drug administration. Measurements were performed at rest and during baroreflex stimulation and deactivation elicited by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. RESULTS: Lisinopril induced a marked increase in plasma renin activity (from 1.1+/-0.2 to 6.4+/-1.3 ng/ml per h, P< 0.01) and a reduction in mean arterial pressure (from 109.6+/-3.1 to 98.7+/-2.9 mmHg, P < 0.01) without affecting the heart rate. Plasma norepinephrine and muscle sympathetic nerve activity values were not significantly different before and after lisinopril treatment (plasma norepinephrine values changed from 290.4+/-39.2 to 308.1+/-67.1 pg/ml; muscle sympathetic nerve activity changed from 56.4+/-5.3 to 50.6+/-6.6 bursts/100 heart beats). Neither the sympathoinhibitory nor the sympathoexcitatory responses to phenylephrine and nitroprusside were affected by lisinopril, nor the concomitant bradycardia and tachycardia. The curves relating mean arterial pressure to heart rate and muscle sympathetic nerve activity values during baroreceptor manipulation were shifted to the left, indicating a resetting of the baroreflex to the lower blood pressure values achieved during treatment. CONCLUSIONS In essential hypertension, sympathetic nerve traffic is not affected by chronic angiotensin converting enzyme inhibitor treatment that effectively interferes with the renin-angiotensin system and lowers the elevated blood pressure. The baroreflex ability to modulate heart rate and central sympathetic outflow is also unaffected. These data argue against the existence of a central sympathoexcitatory effect of angiotensin II in this condition. They also indicate that antihypertensive treatment with an angiotensin converting enzyme inhibitor preserves autonomic reflex control, with favorable consequences for cardiovascular homeostasis.

Administration, Oral↗
PubMed1998

Present and future role of combination treatment in hypertension.

Both in clinical practice and in drug trials, combination treatment of hypertension plays a fundamental role. This article reviews the features that make combined therapy with two drugs valuable, i.e., additive antihypertensive efficacy, different mechanisms of action, and reciprocal side-effect minimization. Also examined are the advantages and disadvantages of a fixed combination, emphasizing that a major advantage is simplification of the treatment schedule. This is clinically relevant because complexity of treatment negatively affects patient compliance, which in hypertensive patients is poor, leading to poor long-term blood pressure control in the hypertensive fraction of the population.

Drug Therapy, Combination↗
PubMed1998

Dissociation between muscle and skin sympathetic nerve activity in essential hypertension, obesity, and congestive heart failure.

Essential hypertension, obesity, and congestive heart failure are characterized by an increase in muscle sympathetic nerve activity. Whether in these conditions skin sympathetic nerve activity is also increased has never been systematically examined, however. In 10 untreated mild essential hypertensive, 12 untreated normotensive obese, 10 mild (New York Heart Association class II) heart failure, and 10 normotensive lean healthy control subjects, we measured beat-to-beat arterial blood pressure (Finapres technique), body mass index, and postganglionic sympathetic nerve activity in skeletal muscle and skin areas (microneurographic technique, peroneal nerve). The muscle and skin nerve measurements were made in a randomized sequence. All data were obtained with the subject supine in a quiet, semidark environment at constant temperature over two periods of 30 minutes each, separated by a 20- to 30-minute interval. Blood pressure was increased only in hypertensive and body mass index only in obese subjects. Muscle sympathetic nerve activity quantified as bursts/min was markedly and significantly (P<.01) greater in essential hypertensive (33.3+/-1.7), obese (42.2+/-2.8), and congestive heart failure subjects (55.8+/-4.3) in comparison with control subjects (23.9+/-1.6). This was the case also for muscle sympathetic nerve activity, quantified as bursts per 100 heart beats. In contrast, skin sympathetic nerve activity (bursts per minute) was superimposable in hypertensive, obese, heart failure, and control subjects, its ability to increase being documented in all four groups by the marked response to an acoustic stimulus. Thus, in various diseases, muscle but not skin sympathetic activity is increased, with the sympathetic activation not being uniformly distributed over the whole cardiovascular system.

Adult↗
PubMed1998

Baroreflex control of sympathetic nerve activity in essential and secondary hypertension.

Studies performed in experimental animals and in humans have documented that high blood pressure markedly impairs baroreceptor control of heart rate. Whether a similar impairment also characterizes baroreceptor control of sympathetic activity modulating peripheral vasomotor tone is still unknown. In 28 untreated essential hypertensive subjects [14 of moderate and 14 of more severe degree, age 51.6+/-2.4 and 52.6+/-2.1 years (mean+/-SEM)] and in 13 untreated secondary hypertensives (renovascular or pheochromocytoma, age 50.1+/-4.6 years), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Data were compared with those obtained in 15 age-matched normotensive control subjects. Muscle sympathetic nerve activity (bursts per 100 heart beats) showed a progressive and significant (P<.01) increase from normotension (40.3+/-3.3) to moderate (55.6+/-4.1) and more severe essential hypertension (68.2+/-4.1), paralleling the progressive increase in blood pressure values. In contrast, muscle sympathetic nerve activity was not increased in secondary hypertensives (40.5+/-6.7) despite blood pressure values similar to or even greater than those of severe essential hypertensives. In both essential and secondary hypertensives, baroreceptor-heart rate control was displaced toward elevated blood pressure values and markedly impaired compared with normotensive subjects (average reduction, 38.5%). In contrast, the sympathoinhibitory and sympathoexcitatory responses to baroreceptor stimulation and deactivation were displaced toward elevated blood pressure values but similar in all groups. Thus, sympathetic activation characterizes essential but not secondary hypertension. Regardless of its nature, however, hypertension is not accompanied by an impairment of baroreceptor modulation of sympathetic activity.

Blood Pressure↗
PubMed1998

Hemodilution reduces clinic and ambulatory blood pressure in polycythemic patients.

Limited information is available for humans on whether blood viscosity affects total peripheral resistance and, hence, blood pressure. Our study was aimed at assessing the effects of acute changes in blood viscosity on both clinic and 24-hour ambulatory blood pressure (BP) values. In 22 normotensive and hypertensive patients with polycythemia, clinic and 24-hour ambulatory BPs were measured before and 7 to 10 days after isovolumic hemodilution; this was performed through the withdrawal of 400 to 700 mL of blood, with concomitant infusion of an equivalent volume of saline-albumin solution. Hematocrit, plasma renin activity, plasma endothelin-1, right atrial diameter (echocardiography), and blood viscosity were measured under both conditions. Plasma renin activity and right atrial diameter were used as indirect markers of blood volume changes. Plasma endothelin-1 was used to obtain information on a vasomotor substance possibly stimulated by our intervention, which could counteract vasomotor effects. Isovolumic hemodilution reduced hematocrit from 0.53+/-0.05 to 0.49+/-0.05 (P<.01). Plasma renin activity, plasma endothelin-1 and right atrial diameter were unchanged. Clinic blood pressure was reduced by hemodilution (systolic, 144.3+/-5.4 to 136.0+/-3.9 mm Hg[mean+/-SEM]; diastolic, 87.0+/-2.8 to 82.1+/-2.6 mm Hg, P<.05 for both) and a reduction was observed also for 24-hour average ABP (systolic, 133.6+/-2.9 to 129.5+/-2.7 mm Hg; diastolic, 80.0+/-2.0 to 77.3+/-1.7 mm Hg, P<.05 for both). The reduction was consistent in hypertensive patients (n = 12), whereas in normotensive patients (n = 10) it was small and not significant. Both clinic and 24-hour average heart rates were unaffected by the hemodilution. Thus, in polycythemia, reduction in blood viscosity without changing blood volume causes a significant fall in both clinic and 24-hour ambulatory BPs; this is particularly true when, as can often happen, blood pressure is elevated. This emphasizes the importance this variable may have in the determination of blood pressure and the potential therapeutic value of its correction when altered.

Blood Pressure↗
PubMed1998

Difference between clinic and daytime blood pressure is not a measure of the white coat effect.

The purpose of the present study was to evaluate whether the difference between blood pressure measured in the clinic or physician's office and the average daytime blood pressure accurately reflects the blood pressure response of the patient to the physician ("white coat effect" or "white coat hypertension"). We studied 28 hypertensive outpatients (mean age, 41.8+/-11.2 years; age range, 21 to 64 years) of 35 consecutive patients attending our hypertension clinic, in whom (1) continuous noninvasive finger blood pressure was recorded before and during the visit, (2) blood pressure was measured according to the Riva-Rocci-Korotkoff method (mercury sphygmomanometer) with the patient in the supine position, and (3) daytime ambulatory blood pressure was monitored with a SpaceLabs 90207 device. The peak blood pressure increase recorded directly during the visit was compared with the difference between clinic and daytime average ambulatory blood pressures. Compared with previsit values, peak increases in finger systolic and diastolic blood pressures during the visit to the clinic were 38.2+/-3.1 and 20.7+/-1.6 mm Hg, respectively (mean+/-SEM, P<.01 for both). Daytime average systolic and diastolic blood pressures were 135.5+/-2.5 and 89.2+/-1.9 mm Hg, with both lower than the corresponding clinic blood pressure values (146.6+/-3.6 and 94.9+/-2.2 mm Hg, P<.01). These differences, however, were <30% of the peak finger blood pressure increases during the physician's visit, to which these increases showed no relation. Although the visit to the physician's office was associated with tachycardia (9.0+/-1.6 bpm, P<.01), there was no difference between clinic and daytime average heart rates. These data indicate that the clinic-daytime average blood pressure difference does not reflect the alerting reaction and the pressure response elicited by the physician's visit and thus is not a reliable measure of the white coat effect.

Adult↗
PubMed1998

Estimation of blood pressure variability from 24-hour ambulatory finger blood pressure.

Portapres is a noninvasive, beat-to-beat finger blood pressure (BP) monitor that has been shown to accurately estimate 24-hour intra-arterial BP at normal and high BPs. However, no information is available on the ability of this device to accurately track ambulatory BP variability. In 20 ambulatory normotensive and hypertensive subjects, we measured 24-hour BP by Portapres and through a brachial artery catheter. BP and pulse interval variabilities were quantified by (1) the SDs of the mean values (overall variability) and (2) spectral power, computed either by fast Fourier transform and autoregressive modeling of segments of 120-second duration for spectral components from 0.025 to 0.50 Hz or in a very low frequency range (between 0.00003 and 0.01 Hz) by broadband spectral analysis. The 24-hour SD of systolic BP obtained from Portapres (24+/-2 mm Hg) was greater than that obtained intra-arterially (17+/-1 mm Hg, P<0.01), but the overestimation was less evident for diastolic (3+/-1 mm Hg, P<0.01) and mean (3+/-1 mm Hg, P<0.01) BP. The BP spectral power <0.15 Hz was also overestimated by Portapres more for systolic than for diastolic and mean BPs; similar findings were obtained by the fast Fourier transform, the autoregressive approach, and focusing on the broadband spectral analysis. BP spectral power >0.15 Hz obtained by the Portapres was similar during the day but lower during the night when compared with those obtained by intra-arterial recordings (P<0.01). No differences were observed between Portapres and intra-arterial recordings for any estimation of pulse interval variabilities. The overestimation of BP variability by Portapres remained constant over virtually the entire 24-hour recording period. Thus, although clinical studies are still needed to demonstrate the clinical relevance of finger BP variability, our study shows that Portapres can be used with little error to estimate 24-hour BP variabilities if diastolic and mean BPs are used. For systolic BP, the greater error can be minimized by using correction factors.

Adult↗
PubMed1998

Reproducibility and clinical value of the trough-to-peak ratio of the antihypertensive effect: evidence from the sample study.

The objectives of our study were to assess the reproducibility of the trough-to-peak ratio (T/P) and to see whether a high T/P is accompanied by more organ protection or vice versa. The study included 175 (mean+/-SD age, 51+/-9 years) subjects with mild-moderate essential hypertension who had echocardiographic evidence of left ventricular (LV) hypertrophy taken from the SAMPLE study (Study on Ambulatory Monitoring of Blood Pressure and Lisinopril Evaluation), an open-label multicenter study. The study included a 3-week washout pretreatment period, a 12-month treatment period with lisinopril (n=84) or lisinopril plus hydrochlorothiazide (n=91) once daily, and a 4-week placebo follow-up period. Results of 24-hour ambulatory blood pressure monitoring and echocardiographic determination of left ventricular mass index (LVMI) were obtained before and after 3 and 12 months of treatment. T/Ps were computed in each patient by dividing the systolic and diastolic blood pressure changes at trough (changes in the last 2 hours of the monitoring period) by those at peak (average of the 2 adjacent hours with the maximal blood pressure reduction between the 2nd and 8th hour from drug intake) after 3 and 12 months of treatment. Average 24-hour blood pressure was similarly reduced at 3 and 12 months. Trough blood pressure changes at 3 and 12 months were closely correlated, as were the corresponding peak blood pressure changes. However, the 3- and 12-month T/Ps correlated to a lesser degree (r<0.42). Furthermore, the reduction of LVMI induced by treatment was similarly correlated with the treatment-induced reduction in 24-hour average, trough, and peak blood pressures but not with the T/Ps. This was also evident when the contribution to LV hypertrophy regression by 24-hour blood pressure changes and T/Ps was assessed in a multivariate regression analysis. In patients with a T/P >/=0.5 or <0.5, the regression of LVMI was similar. In conclusion, peak and trough blood pressure changes are reproducible and predict the regression of LVMI induced by treatment as well as average 24-hour blood pressure. T/Ps are less reproducible, and their value does not predict regression of organ damage by antihypertensive treatment.

Adult↗
PubMed1998

Effects of prolonged immobilization of the limb on radial artery mechanical properties.

Physical training is associated with an increase in arterial distensibility. Whether the effect of training on this variable is evident also for ordinary levels of exercise or no exercise is unknown, however. We have addressed this issue by investigating the effect on radial artery distensibility of prolonged monolateral immobilization of the ipsilateral limb versus the following resumption of normal mobility. We studied 7 normotensive subjects (age, 25.4+/-3.0 years; systolic/diastolic blood pressure, 119+/-9/68+/-6 mm Hg, mean+/-SE) in whom 1 limb had been immobilized for 30 days in plaster because of a fracture of the elbow. At both the day after plaster removal and after 45 days of rehabilitation, radial artery distensibility was evaluated by an echo-tracking device (NIUS-02), which allows arterial diameter to be measured noninvasively and continuously over all pressures from diastole to systole (finger monitoring), with the distensibility values being continuously derived from the Langewouters formula. In both instances, the contralateral arm was used as control. Immediately after removal of the plaster, radial artery distensibility was markedly less in the previously immobilized and fractured limb compared with the contralateral limb (0.4+/-0.1 versus 0.8+/-0.1, 1/mm Hg 10(-3), P<0.05). After rehabilitation, the distensibility of the radial artery was markedly increased in the previously fractured limb (0.65+/-0.1 1/mm Hg 10(-3), P<0.05), whereas no change was seen in the contralateral limb. Thus, complete interruption of physical activity is associated with a marked reduction of arterial distensibility, indicating that even an ordinary level of activity plays a major role in modulation of arterial mechanical properties.

Adolescent↗
PubMed1998

Nitric oxide dependent vasodilation in young spontaneously hypertensive rats.

Conflicting evidence exists on the possible impairment of tonic nitric oxide (NO) mediated vasodilation as a causative factor in the genesis of human as well as experimental hypertension. We evaluated the tonic NO-dependent vasodilation from the pressor response to NO synthesis inhibition by NG-monomethyl-L-arginine (L-NMMA) in 9 conscious, chronically instrumented spontaneously hypertensive rats (SHR) at 12 weeks of age, ie, during the early established hypertensive stage. Nine age-matched Wistar-Kyoto rats (WKY) were used as controls. The pressor responses to L-NMMA (100 mg . kg-1 IV bolus plus 1.5 mg . kg-1 . min-1 infusion for 60 minutes) as well as to non NO-dependent pressor stimuli, namely, vasopressin (2, 4, and 8 ng . kg-1) and phenylephrine (0.5, 1, and 2 microg . kg-1) given as IV boluses, were assessed both under control conditions and during suppression of autonomic reflexes by hexamethonium (30 mg . kg-1 IV bolus+1.5 mg . kg-1 . min-1 infusion). Rather than being reduced, the pressor responses to L-NMMA were 39% and 71% larger in the control and areflexic conditions, respectively, than those observed in WKY (both P<0.01). A similar pattern was observed for the pressor responses to vasopressin (+37% and +68% in the control and areflexic conditions, respectively; both P<0.01) and phenylephrine, (+20% and +52%; both P<0.05). Additional groups of 6-week-old prehypertensive SHR (n=11) and age-matched WKY (n=11) were subjected to an identical protocol: in these animals, the pressor responses to L-NMMA were similar in each strain, as were the pressor responses to vasopressin and phenylephrine in both control and areflexic conditions. In conclusion, our observations indicate that during the developmental phase of hypertension in the SHR model, namely, during the prehypertensive as well as the early established hypertensive stage, NO-dependent vasodilation is preserved (if not enhanced) so that a putative impairment of this function provides no significant pathogenic contribution to the onset of hypertension in this experimental model.

Aging↗
PubMed1998

The trough:peak ratio and the smoothness index in the evaluation of control of 24 h blood pressure by treatment in hypertension.

The duration and homogeneity of the antihypertensive effect of a drug are commonly quantified by computation of the trough:peak ratio (T/P) from 24 h ambulatory blood pressure recordings [i.e. the ratio of the reduction in blood pressure at the end of the interval between doses (trough) and the reduction in blood pressure at the time of the maximal effect of a drug (peak)]. Although it is widely employed, this index has a lot of limitations: it makes use of only a small portion of a 24 h blood pressure recording; individual T/P values do not have a normal distribution, unless responders at peak are selected; it bears no relation to 24 h blood pressure variability; peak changes in blood pressure are affected by a placebo effect and thus T/P needs correction for effects of placebo; peak and trough changes in blood pressure are reproducible over time but T/P is not; and, finally, it was shown in the SAMPLE study that T/P is not correlated to changes in left ventricular mass induced by treatment, and thus has a limited clinical value.

Journal Article↗
PubMed1998

Sympathetic control of circulation in hypertension and congestive heart failure.

Adrenergic overactivity is a common hallmark of both essential hypertension and congestive heart failure. Indirect and direct measures of sympathetic function have clearly shown that sympathetic activation characterizes essential hypertension. This adrenergic overactivity appears to be related to the severity of the hypertensive state, being detectable in its early stages and showing a progressive increase with the severity of the disease. Essential hypertension is also associated with an impaired baroreflex control of vagal activity, whereas baroreceptor modulation of sympathetic nerve traffic remains unaltered, although undergoing a resetting phenomenon. In contrast, secondary hypertension is not associated with an increased adrenergic activity, thus suggesting that an enhancement in efferent sympathetic outflow is a peculiar feature of essential hypertension. Congestive heart failure is a condition also characterized by sympathetic activation, whose degree is proportional to the clinical severity of the disease. This is paralleled by an impairment in arterial baroreceptor modulation of both vagal and sympathetic activity, thus suggesting that the adrenergic overactivity in congestive heart failure is triggered by a reduced afferent restraint on the vasomotor centre. Chronic angiotensin-converting enzyme inhibition reduces the degree of both sympathetic activation and baroreflex dysfunction occurring in heart failure patients, a finding which documents that the neurohumoral abnormalities can be at least partially reversed by pharmacologic treatment.

Adrenergic Fibers↗
PubMed1998

Antihypertensive treatment: past, present and future.

THE PAST: Guidelines for pharmacological and non-pharmacological approaches to the treatment of hypertension were first published in 1977 and were subsequently revised in the 1980s. They were largely based on the approach known as 'stepped care', which suggests that antihypertensive treatment should be started with the initial use of a thiazide diuretic, followed by the addition of a second, third and fourth drug if no satisfactory therapeutic success is obtained. This approach was reviewed in the guidelines that followed, which indicated that pharmacological treatment should be started in a more liberal fashion by selecting the antihypertensive drug from among four rather than two classes (diuretics, beta-blockers, angiotensin converting enzyme inhibitors and calcium antagonists). THE PRESENT: The latest guidelines issued in 1993 by the World Health Organization/International Society of Hypertension and by the Joint National Committee contain innovative aspects on how to treat high blood pressure. They share common features, such as lifelong treatment of hypertension, attention to overall cardiovascular risk profile, initiation of treatment with lifestyle changes and subsequently with monotherapy, but they also have differences, such as goal blood pressure, initial blood pressure values to be treated and first-choice drug. For example, according to the World Health Organization/International Society of Hypertension guidelines first-choice drugs include five classes of drug, whereas the Joint National Committee guidelines advocate two classes of drug for first choice. THE FUTURE: It is likely that the 'stepped care' approach for hypertension treatment will continue to be employed in the future, although greater attention will be devoted to the need for combination drug treatment. Greater importance will be also given to the non-pharmacological antihypertensive approaches, as well as to baseline blood pressure values at which drug treatment should be started.

Antihypertensive Agents↗
PubMed1998

Early and late sympathetic activation in hypertension.

In several experimental animal models of hypertension, sympathetic factors have been shown to be involved in the development and/or maintenance of high blood pressure. Although the information available on this issue in man is more scarce, recent evidence clearly indicates the participation of adrenergic mechanisms in the early and late phases of the hypertensive process. In addition, several cardiovascular risk factors frequently associated with hypertension, such as obesity, insulin-resistance, cigarette smoking, and the atherogenic process, are also characterized by alterations in sympathetic cardiovascular drive. This contributes to a further activation of the sympathetic nervous system thus favoring the development of the end organ damage (e.g. cardiac and vascular hypertrophy) associated with the hypertensive state.

Animals↗
PubMed1998

Methods to quantify sympathetic cardiovascular influences.

This paper will critically review the main features of the various techniques (plasma noradrenaline assay, noradrenaline spillover technique, microneurographic recording of postganglionic muscle sympathetic nerve and power spectral analysis of blood pressure and heart rate signals in specific bands) currently employed to assess sympathetic cardiovascular control in humans. After highlighting the advantages and limitations of each approach, the paper will describe some of the results obtained by employing the above mentioned techniques to detect abnormalities in sympathetic cardiovascular tone in physiological and pathological conditions.

Arousal↗