**9. Cholinergic pathway**

8 Neuroendocrinology and Behavior

**7. Vasopressin system** 

preserve vital organ blood flow.

**8. Thyroid hormones** 

retention and prolonged pleural effusions (6).

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.

Vasopressin (ADH) is released by the hypothalamus as a result of baroreceptor, osmotic, and neurohormonal stimuli. It normally maintains body fluid balance, vascular tone, and regulates contractility. Heart failure causes a paradoxical increase in AVP. The increased blood volume and atrial pressure in heart failure suggest inhibition of vasopressin secretion, but it does not occur. This phenomenon is related to SNS and RAAS activation overriding the volume and low-pressure cardiovascular receptors and osmotic vasopressin regulation causing increase in AVP secretion. It contributes to the increased systemic vascular resistance (V1 receptors) and to renal retention of fluid (V2 receptors). Stimulation of V1 receptors can also case vasoconstriction of the peripheral vessels, platelet aggregation, and adrenocorticotrophic hormone stimulation. Low-dose arginine infusion initiated in the operating room after complex neonatal cardiac surgery was associated with decreased fluid resuscitation and catecholamine. The vasopressin levels are usually high in the early phase

The important mechanism of vasopressin action in stress states is its potentiating effect on ACTH secretion leading to cortisol release. Although vasopressin is a powerful vasoconstrictor it dilates the pulmonary, cerebral, and myocardial circulations helping to

In our group of patients with single ventricle, there was a significant correlation between vasopressin concentration and disturbances of water – electrolyte balance in single ventricle patients. Higher vasopressin plasma levels were connected with greater propensity for fluid

Thyroid hormones are stimulated by TSH anterior pituitary secretion. There is many actions of thyroid hormones on cardiovascular system exerted mainly by triiodothyronine (T3). These effects can be divided into genomic and extragenomic actions. T3 bounds to the nuclear receptors and activates many gens corresponding to key myocardial functions: myosin heavy chain (MHC), sarcoplasmic reticulum Caţţ-ATPase (SERCA2) and its inhibitor phospholamban (affecting cardiac contractile function and diastolic relaxation), voltage-gated Kţ channels, b1-adrenergic receptor, guanine nucleotide regulatory proteins, adenylate cyclase, NAţ/Kţ-ATPase, and Na/Ca exchanger. The main cardiovascular effects

And its major role is to maintain the circulating volume status*.*

of septic shock, but it's deficiency was noted in vasodilatory shock.

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 exaggerated responses to bacterial products and injury.
