scholarly journals The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

2016 ◽  
Vol 311 (2) ◽  
pp. H498-H507 ◽  
Author(s):  
Emma S. Darios ◽  
Brittany M. Winner ◽  
Trevor Charvat ◽  
Antoni Krasinksi ◽  
Sreenivas Punna ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Superior Mesenteric Artery ◽  
Sympathetic Nerve ◽  
Mesenteric Artery ◽  
Sympathetic Innervation ◽  
Electrical Field ◽  
Perivascular Adipose Tissue ◽  
Sympathetic Nervous

The adipokine chemerin causes arterial contraction and is implicated in blood pressure regulation, especially in obese subjects with elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that surrounds the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) amplifies the sympathetic nervous system in mediating electrical field-stimulated (EFS) contraction. The superior mesenteric artery, with or without PVAT and with endothelium and sympathetic nerve intact, was mounted into isolated tissue baths and used for isometric contraction and stimulation. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3–20 Hz) caused a frequency-dependent contraction in isolated arteries that was reduced by the chemerin receptor ChemR23 antagonist CCX832 alone (100 nM; with, but not without, PVAT), but not by the inactive congener CCX826 (100 nM). Exogenous chemerin-9 (1 μM)-amplified EFS-induced contraction in arteries (with and without PVAT) was blocked by CCX832 and the α-adrenergic receptor antagonist prazosin. CCX832 did not directly inhibit, nor did chemerin directly amplify, norepinephrine-induced contraction. Whole mount immunohistochemical experiments support colocalization of ChemR23 with the sympathetic nerve marker tyrosine hydroxylase in superior mesenteric PVAT and, to a lesser extent, in arteries and veins. These studies support the idea that exogenous chemerin modifies sympathetic nerve-mediated contraction through ChemR23 and that ChemR23 may be endogenously activated. This is significant because of the well-appreciated role of the sympathetic nervous system in blood pressure control.

Abstract MP07: Endogenous Chemerin Amplifies Nerve-Dependent Arterial Contraction

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Emma Darios ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Sympathetic Innervation ◽  
Pressure Control ◽  
Perivascular Adipose Tissue ◽  
Sympathetic Nervous ◽  
Isolated Arteries

The adipokine chemerin causes contraction of isolated arteries and is implicated in blood pressure regulation, especially in the obese population that have elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that facilitates the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) would amplify the effects of the sympathetic nervous system in mediating electrical field stimulated (EFS) contraction. The model was the superior mesenteric artery with PVAT, mounted into tissue baths for isometric contraction. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3-20 Hz) caused a frequency-dependent, prazosin-sensitive contraction that was reduced (~40%) by the chemerin receptor ChemR23 antagonist CCX832 (100 nM; figure) but not by the inactive congener CCX826 (100 nM). Exogenous chemerin (1 μM) amplified EFS-induced contraction in a manner that was also blocked by CCX832. Chemerin did not directly modify contraction of the superior mesenteric artery (-PVAT) to cumulative concentrations of norepinephrine (1 nM - 10 μM), supporting that contractile amplification by chemerin was not at the level of smooth muscle. These studies raise the interesting possibilities that endogenous chemerin and/or ChemR23 modifies nerve-mediated contraction. This is significant because of the well appreciated role of the sympathetic nervous system in blood pressure control.

Correlations of attended and unattended blood pressure with sympathetic nervous system activity in essential hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Manta ◽  
M Kouremeti ◽  
N Kakouri ◽  
A Kasiakogias ◽  
D Konstantinidis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Left Ventricular ◽  
Hypertensive Group ◽  
Oscillometric Device ◽  
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 appraise the relation of BP levels in the attended and unattended setting with MSNA in patients with essential hypertension. Methods We studied 117 patients with essential hypertension (age: 58±11 years, 60 males, office BP: 142/85±17/10 mmHg, 24-hour BP: 133/80±11/9 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=70) compared to those with attended hypertension (n=47) 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 (43.7±9.9 vs 37.7±9.7 bursts per minute, p=0.032). In all participants, sympathetic nerve traffic as assessed by resting MSNA was related to attended systolic BP (r=0.270, p=0.003), attended diastolic BP (r=0.344, p=0.001), unattended systolic BP (r=0.263, p=0.004) and unattended diastolic BP (r=0.274, p=0.003). 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. Funding Acknowledgement Type of funding source: None

scholarly journals Endogenous Chemerin from PVAT Amplifies Electrical Field-Stimulated Arterial Contraction: Use of the Chemerin Knockout Rat

2020 ◽  
Vol 21 (17) ◽  
pp. 6392
Author(s):  
Emma D. Flood ◽  
Stephanie W. Watts
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Sympathetic Nerve ◽  
Mesenteric Artery ◽  
Female Rats ◽  
Electrical Field ◽  
Perivascular Adipose Tissue ◽  
Rat Mesenteric Artery ◽  
Arterial Contraction ◽  
Isolated Rat

Background: We previously reported that the adipokine chemerin, when added exogenously to the isolated rat mesenteric artery, amplified electrical field-stimulated (EFS) contraction. The Chemerin1 antagonist CCX832 alone inhibited EFS-induced contraction in tissues with but not without perivascular adipose tissue (PVAT). These data suggested indirectly that chemerin itself, presumably from the PVAT, facilitated EFS-induced contraction. We created the chemerin KO rat and now test the focused hypothesis that endogenous chemerin amplifies EFS-induced arterial contraction. Methods: The superior mesenteric artery +PVAT from global chemerin WT and KO female rats, with endothelium and sympathetic nerve intact, were mounted into isolated tissue baths for isometric and EFS-induced contraction. Results: CCX832 reduced EFS (2–20 Hz)-induced contraction in tissues from the WT but not KO rats. Consistent with this finding, the magnitude of EFS-induced contraction was lower in the tissues from the KO vs. WT rats, yet the maximum response to the adrenergic stimulus PE was not different among all tissues. Conclusion: These studies support that endogenous chemerin modifies sympathetic nerve-mediated contraction through Chemerin1, an important finding relative in understanding chemerin’s role in control of blood pressure.

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.

Acute elevation of plasma non-esterified fatty acids increases pulse wave velocity and induces peripheral vasodilation in humans in vivo

2007 ◽  
Vol 113 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Niels P. Riksen ◽  
Marlies Bosselaar ◽  
Stephan J.L. Bakker ◽  
Robert J. Heine ◽  
Gerard A. Rongen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Adenosine Receptor ◽  
Pulse Wave ◽  
Adenosine Receptor Antagonist ◽  
Sympathetic Nervous ◽  
Control Infusion

Plasma NEFA (non-esterified fatty acid) concentrations are elevated in patients with obesity. In the present study we first aimed to provide an integral haemodynamic profile of elevated plasma NEFAs by the simultaneous assessment of blood pressure, pulse wave velocity, FBF (forearm blood flow) and sympathetic nervous system activity during acute elevation of NEFAs. Secondly, we hypothesized that NEFA-induced vasodilation is mediated by adenosine receptor stimulation. In a randomized cross-over trial in healthy subjects, Intralipid® was infused for 2 h to elevate plasma NEFAs. Glycerol was administered as the Control infusion. We assessed blood pressure, pulse wave velocity, FBF (using venous occlusion plethysmography) and sympathetic nervous system activity by measurement of noradrenaline and adrenaline. During the last 15 min of Intralipid®/Control infusion, the adenosine receptor antagonist caffeine (90 μg·min−1·dl−1) was administered into the brachial artery of the non-dominant arm. Compared with Control infusion, Intralipid® increased pulse wave velocity, SBP (systolic blood pressure) and pulse pressure, as well as FBF (from 1.8±0.2 to 2.7±0.6 and from 2.3±0.2 to 2.7±0.6 ml·min−1·dl−1 for Intralipid® compared with Control infusion; P<0.05, n=9). Although in a positive control study caffeine attenuated adenosine-induced forearm vasodilation (P<0.01, n=6), caffeine had no effect on Intralipid®-induced vasodilation (P=0.5). In conclusion, elevation of plasma NEFA levels increased pulse wave velocity, SBP and pulse pressure. FBF was also increased, either by baroreflex-mediated inhibition of the sympathetic nervous system or by a direct vasodilating effect of NEFAs. As the adenosine receptor antagonist caffeine could not antagonize the vasodilator response, this response is not mediated by adenosine receptor stimulation.

Dissociation of sympathetic nervous system and adrenal medullary responses

1984 ◽  
Vol 247 (1) ◽  
pp. E35-E40 ◽  
Author(s):  
J. B. Young ◽  
R. M. Rosa ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Adrenal Medulla ◽  
Sympathetic Nerve ◽  
Relative Importance ◽  
Peripheral Tissues ◽  
Experimental Animals ◽  
Sympathetic Nervous

The relative importance of sympathetic nerve (SNS) activity and adrenal medullary secretion in various physiological situations has generally been inferred from measurements of norepinephrine (NE) and epinephrine (E), respectively, in urine or plasma. Increasing evidence, however, indicates that under certain conditions the adrenal medulla may release substantial amounts of NE as well as E. In several of these circumstances, estimates of SNS activity based on the measurement of NE turnover in peripheral tissues of experimental animals indicate diminished SNS function, a reduction that is independent of adrenal medullary secretion. These reciprocal alterations in SNS and adrenal medullary activity fall into two patterns. First, when SNS activity is suppressed by fasting, adrenal medullary responses to various stimuli are enhanced. Second, for certain stimuli the SNS response is biphasic, with an initial suppression followed by subsequent stimulation; during the first phase adrenal medullary secretion is markedly increased. The physiological contribution of the adrenal medulla, therefore, would be particularly important under conditions of SNS suppression.

scholarly journals Role of Sympathetic Nervous System in Cyclosporine-Induced Rise in Blood Pressure

Hypertension ◽  
1999 ◽  
Vol 34 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Mario J. Carvalho ◽  
Anton H. van den Meiracker ◽  
Frans Boomsma ◽  
Joao Freitas ◽  
Arie J. Man in ‘t Veld ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

Abstract 291: Antihypertensive Effect Of Bia 5-1058 a New Selective Peripheral Dopamine β-hydroxylase Inhibitor

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Bruno Igreja ◽  
Nuno M Pires ◽  
Lyndon C Wright ◽  
Patrío Soares-da-Silva
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Receptor Antagonist ◽  
Antihypertensive Effect ◽  
Antihypertensive Drugs ◽  
Radio Telemetry ◽  
Sympathetic Nerves ◽  
Maximum Reduction ◽  
Sympathetic Nervous

The sympathetic nervous system can alter blood pressure by modulation of cardiac output, peripheral vascular resistance and renal function. One strategy for controlling sympathetic nerve function is to reduce the biosynthesis of norepinephrine (NE) via inhibition of dopamine β-hydroxylase (DβH; EC 1.14.17.1 ), the enzyme that catalyses the conversion of dopamine (DA) to NE in sympathetic nerves. BIA 5-1058 is a reversible DβH inhibitor that decreases NE levels in peripheral sympathetically innervated tissues slowing down sympathetic nervous system drive, without effect in brain tissues. In freely moving SHR implanted with radio-telemetry transmitters single administration of BIA 5-1058 showed a dose (3, 30 and 100 mg/Kg) and time dependent effect on blood pressure with no significant effect on heart rate (HR) and total activity monitored over a 96-hour period. The maximum reduction on systolic blood pressure (SBP) was -10.8, -21.1 and -35.2 mmHg for 3, 30 and 100 mg/Kg, respectively and the maximum reduction on diastolic blood pressure (DBP) was -9.9, -18.4 and -24.8 mmHg for 3, 30 and 100 mg/Kg, respectively. The antihypertensive effect of BIA 5-1058 (30 mg/Kg) was further evaluated in combination with efficacious doses of well-known antihypertensive drugs, like the ACE inhibitor captopril, the AT1 receptor antagonist losartan, the diuretic hydrochlorothiazide, beta-blocker metoprolol, the alpha-1 receptor antagonist prazosin, and the calcium channel blocker diltiazem. All drugs were administered orally (single dose) in a cross-over design and the effect was monitored for 72 hours. The combination of BIA 5-1058 with any of the tested antihypertensive drugs caused a stronger and prolonged blood pressure decrease than any of the compounds alone.In conclusion, peripheral DβH inhibitors can be used, alone or in combination with others antihypertensive drugs, to reduce blood pressure.

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