Interaction of the Sympathetic Nervous System with Vasopressin and Renin in the Maintenance of Blood Pressure in Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 313s-317s ◽  
Author(s):  
Peter Hatzinikolaou ◽  
Irene Gavras ◽  
William G. North ◽  
Hans R. Brunner ◽  
Haralambos Gavras
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Close Correlation ◽  
Chemical Sympathectomy ◽  
Resting Blood Pressure ◽  
Sympathetic Nervous ◽  
Angiotensin Blockade ◽  
Stimulation Of ◽  
Intact Rats

1. Anephric and intact rats were submitted sequentially to catecholamine depletion (‘chemical sympathectomy’) vasopressin inhibition and angiotensin blockade whilst blood pressure and plasma levels of each hormone were monitored. 2. Depletion of catecholamines to 15–25% of baseline levels was associated with significant fall of blood pressure. A close correlation existed between these variables. 3. Chemical sympathectomy caused stimulation of plasma vasopressin, which reached excessively high levels in anephric animals. These were inversely correlated with the levels of depleted catecholamines. 4. Vasopressin inhibition after chemical sympathectomy caused profound and lasting hypotension in anephric rats but only a transient small fall in blood pressure in intact rats. Angiotensin blockade after chemical sympathectomy in intact rats caused a transient small fall in blood pressure; subsequent vasopressin inhibition in these rats caused profound lasting hypotension. 5. It is concluded that resting blood pressure is mainly sustained by the sympathetic nervous system, whereas renin and vasopressin are important back-up mechanisms to maintain compromised blood pressure.

Neurogenic control of pressure natriuresis in conscious dogs

1990 ◽  
Vol 259 (3) ◽  
pp. F466-F473 ◽  
Author(s):  
H. Ehmke ◽  
P. B. Persson ◽  
M. Seyfarth ◽  
H. R. Kirchheim
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renal Perfusion ◽  
Conscious Dogs ◽  
Adrenoceptor Antagonist ◽  
Resting Blood Pressure ◽  
Sympathetic Nervous ◽  
Pressure Natriuresis ◽  
The Right

In this study we investigated the interaction of the sympathetic nervous system with renal perfusion pressure (RPP) in the short-term control of sodium excretion (UNa V). Pressure natriuresis curves (PNCs) were determined in 13 conscious dogs on a normal-salt diet during control conditions, bilateral common carotid occlusion (CCO), CCO combined with an intrarenal prazosin infusion, and during an intrarenal methoxamine infusion. RPP was reduced in controlled steps by inflation of a cuff placed around the renal artery. For controls, a reduction in RPP resulted in a strong decrease in urine output and UNaV. In all dogs, the PNC was closely related to individual resting blood pressure; UNaV fell to less than 50% of control (10-20 mmHg below resting blood pressure). A baroreflex activation of the sympathetic nervous system by CCO shifted PNC to the right by 10-15 mmHg (n = 8). Sensitivity of pressure natriuresis was not affected by CCO. The shift was blocked when the selective alpha 1-adrenoceptor antagonist prazosin was infused intrarenally during CCO (n = 9). Without CCO, prazosin had no effects on urine flow rate or UNaV at the control RPP. Similar to CCO, intrarenal infusion of the selective alpha 1-adrenoceptor agonist methoxamine shifted PNC to the right by 15-20 mmHg (n = 4). Neither renal blood flow nor glomerular filtration rate was significantly different between control and any experimental condition. These results indicate that the sympathetic nervous system regulates UNaV by shifting the PNC through intrarenal alpha 1-adrenoceptors without altering the sensitivity of pressure natriuresis.

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.

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.

Role of the sympathetic nervous system in CCl4 hepatotoxicity

1960 ◽  
Vol 198 (3) ◽  
pp. 669-676 ◽  
Author(s):  
Deane N. Calvert ◽  
Theodore M. Brody
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Liver Mitochondria ◽  
Central Vein ◽  
Fat Depots ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking ◽  
Stimulation Of

An hypothesis is proposed which states that the characteristic hepatic changes seen after the administration of carbon tetrachloride are the result of stimulation of central sympathetic areas which produce a massive discharge of the peripheral sympathetic nervous system. Stimulation of the sympathetic supply to the blood vessels of the liver results in restriction of blood flow in the liver, leading to anoxia and the characteristic necrosis around the central vein of the hepatic lobule. Similarly the discharge causes the release of unesterified fatty acids from the peripheral fat depots and the consequent deposition of lipid in the liver. This hypothesis is based upon experimental evidence using the following physiologic and pharmacologic maneuvers: adrenergic blocking agents, pretreatment with reserpine, adrenalectomy and section of the spinal cord—all are effective to a greater or lesser extent in preventing the changes characteristically seen in oxidative phosphorylation of the liver mitochondria, activation of a Mg-dependent ATPase and deposition of lipid in the liver. Transection of the spinal cord is the most effective treatment and prevents entirely the characteristic changes seen in the above-mentioned functions.

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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