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

scholarly journals Nifedipine-Sensitive Blood Pressure Component in Hypertensive Models Characterized by High Activity of Either Sympathetic Nervous System or Renin-Angiotensin System

2014 ◽  
pp. 13-26 ◽  
Author(s):  
J. ZICHA ◽  
Z. DOBEŠOVÁ ◽  
M. BEHULIAK ◽  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Spontaneously Hypertensive ◽  
Renin Angiotensin ◽  
Wide Range ◽  
Voltage Dependent ◽  
Sympathetic Nervous

High blood pressure (BP) of spontaneously hypertensive rats (SHR) is maintained by enhanced activity of sympathetic nervous system (SNS), whereas that of Ren-2 transgenic rats (Ren-2 TGR) by increased activity of renin-angiotensin system (RAS). However, both types of hypertension are effectively attenuated by chronic blockade of L-type voltage-dependent calcium channel (L-VDCC). The aim of our study was to evaluate whether the magnitude of BP response elicited by acute nifedipine administration is proportional to the alterations of particular vasoactive systems (SNS, RAS, NO) known to modulate L-VDCC activity. We therefore studied these relationships not only in SHR, in which mean arterial pressure was modified in a wide range of 100-210 mm Hg by chronic antihypertensive treatment (captopril or hydralazine) or its withdrawal, but also in rats with augmented RAS activity such as homozygous Ren-2 TGR, pertussis toxin-treated SHR or L-NAME-treated SHR. In all studied groups the magnitude of BP response to nifedipine was proportional to actual BP level and it closely correlated with BP changes induced by acute combined blockade of RAS and SNS. BP response to nifedipine is also closely related to the degree of relative NO deficiency. This was true for both SNS- and RAS-dependent forms of genetic hypertension, suggesting common mechanisms responsible for enhanced L-VDCC opening and/or their upregulation in hypertensive animals. In conclusions, BP response to nifedipine is proportional to the vasoconstrictor activity exerted by both SNS and RAS, indicating a key importance of these two pressor systems for actual L-VDCC opening necessary for BP maintenance.

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.

Parabrachial nucleus modulation of vasopressin release

1990 ◽  
Vol 258 (2) ◽  
pp. R358-R364 ◽  
Author(s):  
L. E. Ohman ◽  
R. E. Shade ◽  
J. R. Haywood
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Hypertonic Saline ◽  
Parabrachial Nucleus ◽  
Vasopressin Release ◽  
Renin Angiotensin ◽  
Significant Difference ◽  
Electrolytic Lesions ◽  
Sympathetic Nervous

The present studies examine the contribution of the ventrolateral lateral parabrachial nucleus (VLLPBN) to the regulation of plasma arginine vasopressin (PAVP) release in response to either a baroreceptor or osmotic stimulus. These studies were carried out in rats with bilateral electrolytic lesions of the VLLPBN. Baroreceptor-induced stimulation of PAVP was achieved by decreasing blood pressure with combined blockade of the renin-angiotensin system with captopril (3 mg/kg iv) and the sympathetic nervous system with chlorisondamine, (11 mg/kg sc). Osmotic release of vasopressin was elicited by a 2-h intravenous infusion of hypertonic saline, (3.0 meq/ml, 0.01 ml/min). Blood pressure and heart rate were monitored throughout the experiments. Blood samples for determination of PAVP, plasma osmolality (posm), plasma sodium (PNa), and plasma potassium (PK) were taken before (base line) and after treatment in each study. The VLLPBN-lesioned rats secreted significantly more vasopressin in response to hypotension produced by combined renin-angiotensin and sympathetic nervous system blockade than did control rats. There was no significant difference between groups in Posm, PNa, or PK, or cardiovascular changes. In contrast, hypertonic saline infusion did not produce any differential changes between groups.

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.

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system

1995 ◽  
Vol 268 (6) ◽  
pp. H2267-H2273 ◽  
Author(s):  
A. Zanchi ◽  
N. C. Schaad ◽  
M. C. Osterheld ◽  
E. Grouzmann ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Sympathetic Nervous

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

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