scholarly journals Altered Neural and Vascular Mechanisms in Hypertension

2011 ◽  
pp. 381-402 ◽  
Author(s):  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
G Proteins ◽  
High Blood Pressure ◽  
Calcium Current ◽  
Calcium Influx ◽  
Dominant Role ◽  
Cardiovascular Complications ◽  
Sympathetic Nervous

Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins. Although there is considerable information on the complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing.

scholarly journals An experimental rat model of salt-sensitive hypertension; biochemical and morphological parameters and sympathetic nervous system

1999 ◽  
Vol 70 (1) ◽  
Author(s):  
L.I. Somova ◽  
M.L. Channa ◽  
M.S. Khan
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
High Blood Pressure ◽  
Genetic Model ◽  
Body Weight Gain ◽  
Hypochromic Anaemia ◽  
Matrix Expansion ◽  
Sympathetic Nervous ◽  
Salt Sensitive Hypertension

The objective of the study was to outline the characteristics of the development of hypertension and some neurohumoral, haematological and morphological factors contributing to development of high blood pressure in a genetic model of salt-sensitive rat. Characteristics of Dahl salt-sensitive (DS) rats, as compared to their Dahl salt-resistant (DR) controls were as follows: 1) DS rats display higher blood pressure and lower heart rate compared to DR rats as early as 1 month of age at weaning). They gradually develop hypertension at 2 months of age, irrespective of diet. Low-Na diet (0.5%NaCl) does not prevent hypertension but delays its development and ameliorates it. High Na-diet (8 % NaCl) exacerbates hypertension. 2) DS rats have retardation in body weight gain. They develop mild hypochromic anaemia. 3) After 2 months of Na loading (3 months of age), DS rats express significantly increased Na and water retention and increased plasma volume by 15 % compared to 2.8 % increase in DR rats on high-Na diet. 4) DS rats showed renal parenchymal lesions, more pronounced after Na-loading, focal atrophy of cortical tubules, mesangial matrix expansion and glomerulosclerosis. Consistent with high blood pressure were changes in renal arterioles, fibromuscular proliferation, deposition of fibrinoid material in intima. 5) Sodium loading produced increased activity of the sympathetic nervous system (SNS), and sodium restriction reduced SNS responsiveness.

Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate–salt hypertensive rats

1987 ◽  
Vol 73 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Yutaka Takata ◽  
Yoshiaki Yamashita ◽  
Shuichi Takishita ◽  
Masatoshi Fujishima
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Calcium Influx ◽  
Hypotensive Effect ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Blood Pressure Lowering Effect ◽  
Hypotensive Action ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA–salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.

Impaired Response of Plasma Renin Activity to Tilting after Renal Transplantation

1981 ◽  
Vol 61 (1) ◽  
pp. 69-73 ◽  
Author(s):  
J. Cunningham ◽  
M. J. Vandenburg ◽  
J. M. P. Holly ◽  
F. J. Goodwin
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Plasma Renin Activity ◽  
Pulse Rate ◽  
Dominant Role ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Sympathetic Nervous

1. Changes in plasma renin activity, plasma noradrenaline, pulse rate and blood pressure after tilting were measured in normal subjects and in patients with renal transplants. 2. There was a marked difference between the renin responses in the two groups, the increases in plasma renin activity in the control subjects being much greater than those in the transplanted patients. 3. Activation of the sympathetic nervous system after tilting, as indicated by changes in pulse rate, blood pressure and plasma noradrenaline, was similar in the two groups. 4. We conclude that the ability of the transplanted kidney to increase plasma renin activity after tilting is impaired, probably as a result of sympathetic denervation of the kidney during transplantation. The results suggest a dominant role of the sympathetic nervous system in the mediation of renin release after tilting.

Renin–angiotensin and sympathetic nervous system contribution to high blood pressure in Schlager mice

2011 ◽  
Vol 29 (11) ◽  
pp. 2156-2166 ◽  
Author(s):  
Kesia Palma-Rigo ◽  
Kristy L. Jackson ◽  
Pamela J. Davern ◽  
Thu-Phuc Nguyen-Huu ◽  
Jean-Luc Elghozi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
High Blood Pressure ◽  
Renin Angiotensin ◽  
Sympathetic Nervous

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.

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.

Sign in / Sign up

Export Citation Format

Share Document