**6. Renin angiotensin aldosterone axis**

Renin angiotensin aldosterone axis exerts many effects in cardiovascular system. Neural connexion of the brain and kidneys is stimulated by low sodium, decreased perfusion,

increased alpha – adrenergic activity. It can effect juxtaglomerular apparatus increasing renien - protease transforming angiotensinogen to angiotensin I which is converted within the endothelial cells (particularly concentrated in the lungs) to angiotensin II by angiotensinconverting enzyme (ACE). Angiotensin II is the most potent vasoconstrictor increasing vascular resistance in stress situations (especially in hypovolemia) and effecting adrenal cortex increasing aldosterone production which increases reclaiming of sodium and water. And its major role is to maintain the circulating volume status*.*

Neuroendocrine Regulation of Stress Response in Clinical Models 9

of T3 are: increased cardiac contractility, reduction of afterload, reduction of vascular resistance, chronotropic effect (increased heart rate), increases sodium reabsorption and

T3 has genomic effects that maintain endothelial integrity, such as angiotensin receptors in vascular smooth muscle cells (VSMC). This supports the hypothesis that the vasculature is a principal target for T3 action. T3 decreases resistance in peripheral arterioles. Extragenomic actions include: modulation of cellular metabolic activities, such as glucose and amino acid transport, ion fluxes at the level of the plasma membrane, and mitochondrial gene

Together with the stimulation of the adrenergic system the feedback is also started as antiinflammatory cholinergic pathway. It is comprised of vagus nerve signals leading to acetylcholine interaction with receptors on monocytes and macrophages, resulting in reduced cytokine production. It can prevent tissue injury and improve survival by external stimulation. The cholinergic anti-inflammatory pathway exerts a tonic, inhibitory influence on immune responses to infection and tissue injury. Interrupting this pathway, produces

Natruretic peptide system counteracts of some of the effects of neurohormonal activation causing vasodilatation, reduction of aldosterone production (by direct influence on the adrenal gland), increased diuresis and natriuresis, reduction of renin production, decreased vasopressin realize, decreased activation of the sympathethic nervous system. Direct influence of the naturetic peptydes on the myocardium includes prevention of hypertrophy and reduction of fibroblast proliferation. BNP is a natriuretic peptide released in response to

Cardiopulmonary by-pass in children induces renal and neurohormonal changes similar to those observed in congestive heart failure: upregulation of the RAA axis, increase of renin concentration, release of vasopressin. The endogenous biological activity of natriuretic hormone system is decreased after the bypass. This is caused by deficiency of biologically active neurohormons, presence of inactive neurohormons, resistance to natriuretic hormone activity, receptor down-regulation, abnormal signal transduction, increased

It has been also shown that neurohormons can decrease ischemia-reperfusion injury in multiple tissue including heart by inhibition of angiotensin II and aldosterone, limitation of intracellular Ca++ overload, maintainance of ATP stores, preservation of myofibril,

In the natural history of diseased cardiovascular system complex interactions between local, humoral, and neural factors lead to abnormalities in the circulatory control. These adaptive

water improves atrial filing pressure. All of this increase cardiac output.

expression and function.

**9. Cholinergic pathway** 

**10. Natruretic peptydes** 

phosphodiesterase activity.

exaggerated responses to bacterial products and injury.

ventricular volume expansion and pressure overload.

mitochondrial and nuclear structure of cardiomyocytes.
