scholarly journals Bidirectional asymmetry in the neurovisceral communication for the cardiovascular control: New insights

2017 ◽  
Vol 51 (3) ◽  
pp. 157-167 ◽  
Author(s):  
I Prieto ◽  
AB Segarra ◽  
M Martinez-Canamero ◽  
M De Gasparo ◽  
S Zorad ◽  
...  
Keyword(s):  
Essential Role ◽  
Renin Angiotensin System ◽  
Cardiovascular Function ◽  
Cardiovascular Control ◽  
Functional Connection ◽  
Angiotensin System ◽  
Positive Correlations ◽  
Available Information ◽  
The Brain

AbstractThe cardiovascular control involves a bidirectional functional connection between the brain and heart. We hypothesize that this connection could be extended to other organs using endocrine and autonomic nervous systems (ANS) as communication pathways. This implies a neuroendocrine interaction controlling particularly the cardiovascular function where the enzymatic cascade of the renin-angiotensin system (RAS) plays an essential role. It acts not only through its classic endocrine connection but also the ANS. In addition, the brain is functionally, anatomically, and neurochemically asymmetric. Moreover, this asymmetry goes even beyond the brain and it includes both sides of the peripheral nervous and neuroendocrine systems. We revised the available information and analyze the asymmetrical neuroendocrine bidirectional interaction for the cardiovascular control. Negative and positive correlations involving the RAS have been observed between brain, heart, kidney, gut, and plasma in physiologic and pathologic conditions. The central role of the peptides and enzymes of the RAS within this neurovisceral communication, as well as the importance of the asymmetrical distribution of the various RAS components in the pathologies involving this connection, are particularly discussed. In conclusion, there are numerous evidences supporting the existence of a neurovisceral connection with multiorgan involvement that controls, among others, the cardiovascular function. This connection is asymmetrically organized.

Is angiotensin essential in drinking induced by water deprivation and caval ligation?

1981 ◽  
Vol 240 (1) ◽  
pp. R75-R80 ◽  
Author(s):  
M. C. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Essential Role ◽  
Vena Cava ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in drinking induced by water deprivation and caval ligation was assessed by infusion of saralasin into the lateral ventricles of rats. This technique was first validated by demonstrating its capability to specifically antagonize drinking to both systemic and central angiotensin II. However, neither the latency to drink nor the amount of water consumed following 24- or 30-h water deprivation was affected by saralasin. Furthermore, saralasin had no significant effect on the recovery of blood pressure or on the water intake following ligation of the abdominal vena cava. These observations suggest that the renin-angiotensin system alone does not play an essential role in the control of drinking following water deprivation or caval ligation in rats.

Role of the Brain Renin-angiotensin System in Blood Pressure Regulation

2007 ◽  
Vol 31 (S1) ◽  
pp. 343-346
Author(s):  
M. V. Varoni ◽  
D. Palomba ◽  
M. P. Demontis ◽  
S. Gianorso ◽  
G. L. Pais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

scholarly journals The Prorenin and (Pro)renin Receptor: New Players in the Brain Renin-Angiotensin System?

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Wencheng Li ◽  
Hua Peng ◽  
Dale M. Seth ◽  
Yumei Feng
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Future Perspectives ◽  
Vasopressin Release ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Treatment Of Hypertension ◽  
High Level ◽  
The Brain

It is well known that the brain renin-angiotensin (RAS) system plays an essential role in the development of hypertension, mainly through the modulation of autonomic activities and vasopressin release. However, how the brain synthesizes angiotensin (Ang) II has been a debate for decades, largely due to the low renin activity. This paper first describes the expression of the vasoconstrictive arm of RAS components in the brain as well as their physiological and pathophysiological significance. It then focus on the (pro)renin receptor (PRR), a newly discovered component of the RAS which has a high level in the brain. We review the role of prorenin and PRR in peripheral organs and emphasize the involvement of brain PRR in the pathogenesis of hypertension. Some future perspectives in PRR research are heighted with respect to novel therapeutic target for the treatment of hypertension and other cardiovascular diseases.

Pressor Responses to Central Sodium and Ouabain Are Attenuated in Transgenic Rats Deficient in Brain Angiotensinogen

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 728-728
Author(s):  
Bing S Huang ◽  
Detlev Ganten ◽  
Frans Hh Leenen
Keyword(s):  
Antisense Rna ◽  
Renin Angiotensin System ◽  
Dietary Salt ◽  
Transgenic Rats ◽  
Angiotensin System ◽  
Sd Rats ◽  
Pressor Responses ◽  
Freely Moving ◽  
The Brain

P195 Studies using AT 1 -blockers suggest that the brain renin-angiotensin system (RAS) contributes to sympatho-excitation and hypertension by high dietary salt or central sodium loading. To more specifically examine this role of the brain RAS, [TGR (AsrAOGEN)] transgenic rats were used. These rats express an antisense RNA against angiotensinogen mRNA specifically in the brain, and the brain angiotensinogen level is reduced by more than 90%. In freely moving TGR and SD controls, BP and HR responses to intracerebroventricular (icv) infusion (3.8 μl/min for 10 min) of artificial CSF (aCSF) and Na + -rich aCSF (containing 0.2, 0.3 and 0.45 M Na + ) as well as icv injection of ouabain (0.3 and 0.6 μg/2 μl) were assessed. The vasopressin antagonist [d(CH 2 ) 5 Tyr(Me)]AVP (30 μg/kg) was given iv before each icv infusion. Data are means±SEM (n=6, for each).* p<0.05, vs SD rats. Somewhat surprisingly, angiotensin I and II levels of not only hypothalamus but also plasma were lower in TGR vs. SD rats. The clearly attenuated sympatho-excitatory and pressor effects to ouabain and Na + -rich aCSF support the concept that the brain RAS plays an important role in the sympatho-excitatory effects of ouabain and CSF sodium.

Antisense Inhibition of Central, But not Peripheral Renin Angiotensin System Decreased Arterial Pressure in Chronic Phase of Two-Kidney, One Clip Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 729-729
Author(s):  
Shuntaro Kagiyama ◽  
S M Galli ◽  
M. Ian Phillips
Keyword(s):  
Chronic Phase ◽  
Renin Angiotensin System ◽  
Saline Group ◽  
Chronic Hypertension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Group 2 ◽  
The Brain ◽  
Group 1

P198 Introduction: The systemic renin angiotensin system (RAS) plays an important role in blood pressure (BP) regulation during the development of two-kidney, one clip hypertension (2K1C). Its contributions decrease with time after constriction of the renal artery. During the chronic phase, the peripheral RAS returns to normal, nevertheless for months the hypertension is sustained. We hypothesized that during this phase of 2K1C hypertension, the brain RAS contributes to the maintenance of high BP. Methods: Therefore, we studied in the role of brain RAS by decreasing the synthesis of angiotensinogen (AGT) and angiotensin type 1a receptors (AT1R) with intracerebroventricular (ICV) injection of antisense oligonucleotides (AS-ODN). The response of systolic BP (SBP) to AS-ODN to AGT was studied at 6 mo(Group 1) and the response to AS-ODN to AT1R at 10 mo post clipping (Group 2). Each group was divided into AS-ODN, sense or inverted ODN, and saline subgroups. All groups were implanted with ICV cannulae one week before treatment. SBP was monitored by tail cuff method. Plasma and brain angiotensin II (AngII) content was measured by radioimmunoassay in all treated 2K1C groups and in nonclipped rats. Results: The results show that in Group 1, at 6 mo post clipping, the ICV AS-ODN to AGT (200 μg/kg, n=5) significantly decreased SBP(≈−22±6 mmHg, P<0.05)compared to sense ODN and saline group (n=5). The hypothalamic AngII content in sense ODN and saline groups was significantly (P<0.05) higher than in nonclipped rats. AS-ODN to AGT reduced the elevated hypothalamic AngII level. Plasma AngII was significantly decreased in the clipped group (40±12 pg/ml) compared with nonclipped group (75±8 pg/ml). In Group 2, 10 mo post clipping, the ICV injection of AS-ODN to AT1R (250 μg/kg, n=6) significantly decreased SBP(≈−26±8 mmHg, P<0.05) for 3 days post injection, compared to inverted ODN. In contrast, intravenous AS-ODN to AT1R in dose of 250-500 μg/kg did not affect SBP. Conclusion: These results suggest that the brain RAS plays an important role in maintaining the elevated SBP in chronic hypertension phase.

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