Oral Yohimbine Increases Blood Pressure and Sympathetic Nervous Outflow in Hypertensive Patients

1993 ◽  
Vol 22 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Ehud Grossman ◽  
Talma Rosenthal ◽  
Edna Peleg ◽  
Courtney Holmes ◽  
David S. Goldstein
Keyword(s):  
Blood Pressure ◽  
Hypertensive Patients ◽  
Sympathetic Nervous

Abstract 2458: Atorvastatin Reduces Sympathetic Activity in Hypertensive Patients

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Marc E Gomes ◽  
Cees J Tack ◽  
Freek W Verheugt ◽  
Paul Smits ◽  
Jacques W Lenders
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Moderate Hypertension ◽  
Plasma Cholesterol ◽  
Plasma Norepinephrine ◽  
Hypertensive Patients ◽  
Nervous System Activity ◽  
Sympathetic Nervous ◽  
Coa Reductase ◽  
Central Level

Background In hypertension, a state of increased (central) sympathetic activity exists. This high sympathetic activity is associated with worse prognosis and refractoriness to pharmacological interventions. Animal experimental data suggest that HMG CoA reductase inhibitors (statins) can reduce sympathetic activity at a central level. We hypothesized that atorvastatin 80 mg/day could reduce sympathetic activity in human patients with hypertension. Methods Using a prospective, randomized, placebo-controlled, double-blind, cross-over design, patients were randomly assigned to atorvastatin 80 mg/day or placebo, for 3 weeks. Sympathetic nervous system activity was measured at the end of each treatment period, in 13 patients with mild to moderate hypertension by microneurography for direct muscle sympathetic nerve recording (MSNA) and plasma norepinephrine concentrations. Effects on blood pressure were assessed by 24 hour ambulatory blood pressure measurement. Results Atorvastatin significantly reduced MSNA (atorvastatin: 58.5±2.0 vs. placebo: 64.7±3.0 bursts/100 beats, P=0.02). Although MSNA values and plasma cholesterol levels were correlated, reduction in MSNA was independent of the degree of reduction in plasma cholesterol. Atorvastatin had no effect on plasma norepinephrine levels nor on daytime and night time blood pressure. Conclusion: In patients with mild to moderate hypertension, atorvastatin treatment reduces central sympathetic nervous outflow. This finding supports the concept that HMG CoA reductase regulates sympathetic nervous system activity at the central level and indicates a sympathoinhibitory role for atorvastatin in human hypertensive patients.

Humoral Effects of the Oral Converting-Enzyme Inhibitor Sq 14 225 in Hypertensive Patients in Supine and Tilted Position

1979 ◽  
Vol 57 (s5) ◽  
pp. 149s-152s ◽  
Author(s):  
A. Morganti ◽  
T. G. Pickering ◽  
J. Lopez-Ovejero ◽  
J. H. Laragh
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Hypertensive Patients ◽  
Sympathetic Nervous

1. To evaluate the effects of converting-enzyme inhibition on the sympathetic nervous system, on renin and on the other known regulators of aldosterone secretion, we measured blood pressure, heart rate, plasma noradrenaline, adrenaline, renin activity, aldosterone, cortisol and serum potassium in 15 sodium-repleted hypertensive patients in supine position and during 30 min of 65° head-up tilt before and during treatment with SQ 14 225. 2. SQ 14 225 produced significant decreases in supine blood pressure and plasma aldosterone and significant increments in plasma renin activity and potassium; in contrast, heart rate, noradrenaline, adrenaline and cortisol were unchanged. 3. While in control tilt studies blood pressure was always maintained, during treatment three of 15 patients had vasovagal syncopes. In the remaining 12 blood pressure was maintained during tilt on SQ 14 225; however, while the tilt-induced responses in heart rate and adrenaline were as in control studies, the 30 min increments in noradrenaline were significantly higher. 4. Both before and during treatment the responses of plasma renin activity and aldosterone to tilt were parallel, and correlated with each other, and cortisol and potassium changed only slightly. 5. It is concluded that the SQ 14 225-induced fall in blood pressure occurs without a concomitant rise in sympathetic nervous activity; thus the increase in supine plasma renin activity, being a reflection of the interruption of the angiotensin feedback mechanism on renin release, indicates an effective suppression of angiotensin II formation. 6. During SQ 14 225 the persistence of aldosterone response to tilt and its relationship with renin activity suggest that the enzymatic blockade is over-ridden; however, in the presence of a reduced formation of angiotensin II a more pronounced response of the sympathetic nervous system is required to defend blood pressure against postural changes.

P802Interrelationships of sympathetic nervous system activity with attended and unattended blood pressure levels in essential hypertensive patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E Manta ◽  
C Tsioufis ◽  
K Dimitriadis ◽  
M Kouremeti ◽  
N Kakouri ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Left Ventricular ◽  
Hypertensive Patients ◽  
Hypertensive Group ◽  
Sympathetic Nervous

Abstract Background/Introduction Measurement of unattended blood pressure (BP) may provide additional information over conventionally attended BP. Moreover, hypertension is related to sympathetic drive while there are scarce data on the diverse links of attended and unattended BP with muscle sympathetic nerve activity (MSNA) in hypertensive patients. Purpose The aim of this study was to assess the relation of BP levels in the attended and unattended setting with MSNA in patients with essential hypertension. Methods We studied 38 patients with essential hypertension (age: 59±11 years, 20 males, office BP: 142/86±19/11 mmHg, 24-hour BP: 137/80±14/12 mmHg). In all participants sympathetic drive was assessed by MSNA estimations based on established methodology (microneurography). Both unattended BP (patient alone in the room, an oscillometric device programmed to perform 3 BP measurements, at 1-minute intervals, after 5 minutes) and attended BP were measured with the same device, on the same day of MSNA recording, in random order. Patients were divided into the combined attended and unattended hypertensive group when BP≥140/90 mmHg in both attended and unattended BP estimations and to the attended hypertensive group when only attended BP≥140/90 mmHg. Results Patients with combined attended and unattended hypertension (n=18) compared to those with attended hypertension (n=20) were older (61±11 vs 57±11 years, p=0.03), whereas did not differ regarding 24-h ambulatory BP levels, glucose levels, renal function and left ventricular mass index (p=NS for all). Moreover, patients with combined attended and unattended hypertension compared to those with attended hypertension were characterized by greater levels of MSNA (41.2±11.6 vs 32.2±10.1 bursts per minute, p=0.031). In all participants, sympathetic nerve traffic as assessed by resting MSNA was related to attended systolic BP (r=0.459, p=0.004), attended diastolic BP (r=0.503, p=0.001), unattended systolic BP (r=0.433, p=0.007) and unattended diastolic BP (r=0.423, p=0.008). Conclusions The phenotype of combined attended and unattended hypertension compared to attended hypertension is accompanied by higher sympathetic nervous system activation. Moreover, the close association of MSNA with attended and unattended BP levels in essential hypertension, further supports the key role of sympathetic drive in modulating BP.

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