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 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.

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.

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

Sustained sympathetic nervous system support of arterial blood pressure during repeated brief umbilical cord occlusions in near-term fetal sheep

2014 ◽  
Vol 306 (11) ◽  
pp. R787-R795 ◽  
Author(s):  
Robert Galinsky ◽  
Ellen C. Jensen ◽  
Laura Bennet ◽  
Clinton J. Mitchell ◽  
Eleanor R. Gunn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Umbilical Cord ◽  
Prolonged Exposure ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Significant Difference ◽  
Sympathetic Nervous

Sympathetic nervous system (SNS)-mediated peripheral vasoconstriction plays a key role in initial maintenance of blood pressure during rapid-onset asphyxia in the mammalian fetus, but it is attenuated after the first few minutes. It is unclear whether the SNS response is sustained during the brief, but frequently repeated, episodes of asphyxia characteristic of labor. In the present study, 14 fetal sheep at 0.85 of gestation received either chemical sympathectomy with 6-hydroxydopamine (6-OHDA; n = 7) or sham injection (control; n = 7), followed 4–5 days later by repeated 2-min episodes of complete umbilical cord occlusion every 5 min for up to 4 h or until mean arterial blood pressure (MAP) fell to <20 mmHg for two successive occlusions. In controls, umbilical cord occlusions were associated with a rapid initial fall in fetal heart rate (FHR) and femoral blood flow (FBF), with initial hypertension, followed by progressive development of hypotension during ongoing occlusions. Sympathectomy was associated with attenuation of the initial rise in MAP during umbilical cord occlusion, and after the onset of hypotension, a markedly more rapid fall of MAP to the nadir, with a correspondingly slower fall in FBF ( P < 0.05). In contrast, MAP and FHR between successive occlusions were higher after sympathectomy ( P < 0.05). There was no significant difference in the number of occlusions before terminal hypotension (6-OHDA; 16.1 ± 2.2 vs. control; 18.7 ± 2.3). These data show that SNS activity provides ongoing support for fetal MAP during prolonged exposure to brief repeated asphyxia.

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