Renin Angiotensin System and Cardiovascular Disease


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Ang II signaling in the brain modulates reflex control of heart rate and sympathetic outflow Dampney et al. Power spectral analysis of heart rate and blood pressure indicates an altered autonomic nervous system activity with a dominance of vagal tone over sympathetic tone and exaggerated spontaneous baroreflex sensitivity Baltatu et al.

The brain RAS — sympathetic nervous system connection is important in the development of left ventricular dysfunction after myocardial infarction Huang and Leenen, Sympathetic activity surges in parallel with the progress of damage in cardiac performance, contributing to the progression of the heart failure Packer, Lower cardiac TH levels may represent a mechanism contributing to the lower pathological elevation of norepinephrine.

Not only does peripheral Ang II interact with the brain RAS to activate the sympathetic nervous system in chronically overactive conditions, but also the brain RAS appear to influence renal renin release.

Antihypertensive Drugs (Part 05)- Renin-Angiotensin System Inhibitors (RAAS Mechanism) Hindi

The sympathetic nervous system, which is involved in the fight-or-flight reaction, is one of the main stimulators of renal renin release. During the stress reaction, there is an increase in blood levels of renin in addition to epinephrine. We provided evidence that brain RAS is an important player involved in the stress-induced renin release.

Therefore, inhibition of the brain RAS may represent a protective strategy against chronic and generalized activation of both endocrine and local systems in disease. Brain RAS modulates the cardiovascular and fluid—electrolyte homeostasis not only by interacting with the autonomic nervous system but also by modulating hypothalamic—pituitary axis and vasopressin release Baltatu et al. Therefore, we studied the Ang II-induced hypertension in vasopressin-deficient Brattleboro rats, as well. Heart hypertrophy measured as heart weight per body weight was evident neither in LE nor in Brattleboro rats, probably due to the mild hypertension levels.

These results together with our previous results Baltatu et al.

Function of renin angiotensin system on heart failure

Figure 1. Data are extracted from telemetry recording and data acquisition as day mean. The start of Ang II infusion is at the end of day 0. Circadian variability of blood pressure may constitute another mechanism through which brain RAS may participate to the hypertensive target organ injury and cardiovascular events. It is also helpful to assess patients with apparent drug resistance, hypotensive symptoms with antihypertensive medications, episodic hypertension, and autonomic dysfunction.

Our group was the first to determine that slow-pressor Ang II infusion may induce a shift in BP circadian rhythm, making it a convenient and reproducible experimental model of Ang II-induced non-dipping hypertension Baltatu et al. These alterations in BP circadian rhythm are not synchronized with alterations of heart rate or locomotor activity, contributing to the concept that the circadian variability of blood pressure and heart rate are differentially regulated Baltatu et al.

Ang II not only induces alterations in the circadian rhythm of BP but also its local production in the brain modulates the synthesis of both melatonin and vasopressin, which are important hormones regulating circadian rhythms Baltatu et al. Furthermore, melatonin itself may alter the short-term variability of cardiovascular parameters, including the baroreflex Campos-Santos et al.

With these studies we demonstrated that the brain RAS is an important regulator of circadian rhythm of blood pressure. The experimental model of Ang II-induced hypertension might be useful to further dissect the pathophysiology and molecular biology of non-dipping hypertension. In summary, several lines of evidence indicate that the brain RAS is involved in cardiovascular diseases including heart failure contributing to pathophysiological alterations Figure 2.

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Chronically overactive RAS is thus recruiting tissue RASs through a positive biofeedback in order to maintain a state of alert diseased conditions. A circadian pattern becomes quite obvious in the occurrence of acute cardiovascular diseases, such as ischemia, infarction, stroke, and sudden death, and new chronotherapeutic approaches in antihypertensive therapy are trying to exploit the knowledge of circadian rhythms in order to reduce these events. Therefore, targeting brain RAS with drugs such as renin or ACE inhibitors or receptor blockers having increased brain penetrability could be of benefit.

These RAS-targeting drugs are first-line therapy for all heart failure patients. Since the RAS has both endocrine and local tissue components, RAS drugs are being developed to attain increased tissue penetrability and volume of distribution and consequently an efficient inhibition of both RAS components.

Figure 2. Brain RAS in pathophysiological states interacts synergistically with the chronically overactive RAS through a positive biofeedback in order to maintain a state of alert diseased conditions, such as cardiac hypertrophy and failure. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


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Bader, M. Tissue renin-angiotensin systems: new insights from experimental animal models in hypertension research. Baltatu, O. Locally synthesized angiotensin modulates pineal melatonin generation. Genetic targeting of the brain renin-angiotensin system in transgenic rats: impact on stress-induced renin release. Acta Physiol. Alterations in blood pressure and heart rate variability in transgenic rats with low brain angiotensinogen. Hypertension 37, — Pubmed Abstract Pubmed Full Text. The brain renin-angiotensin system modulates angiotensin II-induced hypertension and cardiac hypertrophy.

Hypertension 35, — Local renin-angiotensin system and the brain — a continuous quest for knowledge.

Role of the renin-angiotensin system in cardiovascular disease.

Peptides 32, — Campos, L. Altered circadian rhythm reentrainment and pineal indoles in rats with low brain angiotensinogen. Differential regulation of central vasopressin receptors in transgenic rats with low brain angiotensinogen. Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen.


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  • Heart Circ. CrossRef Full Text. Altered circadian rhythm reentrainment to light phase shifts in rats with low levels of brain angiotensinogen. Campos-Santos, L. Beneficial effect of melatonin on baroreceptor reflex control of heart rate is blocked in spontaneously hypertensive rats. Carlson, S.

    Neurohormonal regulation of the sympathetic nervous system: new insights into central mechanisms of action. Chobanian, A. Hypertension 42, — The renin angiotensin system RAS is a coordinated hormonal cascade mediating cardiovascular, renal and adrenal function, with pleiotrophic actions including stimulation of oxidative stress, inflammation and growth. The RAS is key to the development of cardiovascular diseases, including hypertension, cardiac remodelling and atherosclerosis and pharmacological RAS antagonists are some of the most successful therapies in hypertension and heart failure.

    Our understanding of the function of the RAS in individual tissues in vivo is incomplete and discoveries, including the angiotensin converting enzyme ACE homologue ACE2 and angiotensin [Ang- ] have highlighted additional key mediators of the RAS which may be therapeutic targets in cardiovascular disease. As well as mediating effects systemically, local tissue-specific generation in organs, including heart, are critical in RAS-mediated effects. Previously thought to be an inactive substrate for Ang- generation we have demonstrated that Ang- is able to antagonise the pathophysiological effects of AngII in cardiomyocytes via the angiotensin type 2 receptor and produces anti fibriotic effects in a model of essential hypertension, the stroke prone spontaneously hypertensive rat SHRSP.

    We are now extending these investigations into the effects of Ang- and Ang- in an angiotensin II-infusion model of hypertension in mice and in vasculare remodelling in acute vascular injury. Furthermore, we are exploring opportunities for the peptides as therapeutics in a mouse model of myocardial infarction and in hypertensive cardiac remodelling using gene therapy approaches via efficient and specific viral vector -mediated gene transfer and direct peptide infusion.

    We are also investigating the underlying cell signalling mechanisms for each peptide at the protein, gene and microRNA level. Ultimately, we aim to identify therapeutic applications which can be developed in cardiovascular disease. Search icon. Close menu icon. Menu icon bar 1 Menu icon bar 2 Menu icon bar 3. Research Vascular Research Counter-regulatory renin angiotensin system. Investigation of the counter-regulatory renin angiotensin system in cardiovascular disease In the body hormones travel via the bloodstream and engage receptors which contribute to the normal function of blood vessels, heart and kidney.

    Regulation of cardiovascular remodelling by the by the counter-regulatory axis of the renin angiotensin system. Adenoviral gene transfer of angiotensin- or angiotensin- inhibits cardiomyocyte hypertrophy via the mas receptor or angiotensin type 2 receptor respectively. Hypertension ;

    Renin Angiotensin System and Cardiovascular Disease Renin Angiotensin System and Cardiovascular Disease
    Renin Angiotensin System and Cardiovascular Disease Renin Angiotensin System and Cardiovascular Disease
    Renin Angiotensin System and Cardiovascular Disease Renin Angiotensin System and Cardiovascular Disease
    Renin Angiotensin System and Cardiovascular Disease Renin Angiotensin System and Cardiovascular Disease
    Renin Angiotensin System and Cardiovascular Disease Renin Angiotensin System and Cardiovascular Disease
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