Neurohormone

N euro transmitters are chemical substances called neurohormones. These are released at Hie nerve ending that facilitate the transmission of nerve impulses. The two neurohormones (neurotransmitters) of the sympathetic nervous system are epinephrine and norepinephrine Epinephrine is secreted by the adrenal medulla Norepinephrine is secreted mainly at nerve ending of sympathetic (also called adrenergic) nerve fibers (Pig. 22-2). 

Adrenergic dru mimic the activity of the sympathetic nervous system. These dragp also are called sympathomimetic druc s. Epinephrine and norepinephrine are neurohormones produced naturally by the body. Synthetic preparations of these two neurohormones,... 

One group of antiadreneigic drugs inhibits the release of norepinephrine (a neurohormone of the sympathetic nervous system, see Chap. 22) from certain adrenergic... 

Electron microscopic study reveals an incalculably small space between nerve endings and the effector organ (eg, tlie muscle, cell, or gland) diat is innervated (or controlled) by a nerve fiber. Fbr a nerve impulse to be transmitted from die nerve ending (motor end plate) across die space to die effector organ, a neurohormone is needed. 

The PNS has two neurohormones (neurotransmitters) acetylcholine (ACh) and acetylcholinesterase (ACliE). ACh is a neurotransmitter responsible for die transmission of nerve impulses to effector cells of die parasympathetic nervous system. ACh plays an important role in die transmission of nerve impulses at synapses and myoneural junctions. ACh is quickly... 

Drugp with anticholinergic activity inhibit acetylcholine (a neurohormone produced in excess in Fhrkinson s disease) in the CNS. Dru with anticholinergic activity are generally less effective than levodopa... 

The TCAs, such as amitriptyline (Elavil) and dox-epin (Sinequan), inhibit reuptake of norepinephrine or serotonin at the presynaptic neuron. Drug classified as MAOIs inhibit the activity of monoamine oxidase a complex enzyme system that is responsible for breaking down amines. This results in an increase in endogenous epinephrine, norepinephrine and serotonin in the nervous system. An increase in these neurohormones results in stimulation of the CNS. The action of the SSRIs is linked to their inhibition of CNS neuronal uptake of serotonin (a CNS neurotransmitter). The increase in serotonin levels is thought to act as a stimulant to reverse depression. 

Discuss heart failure in relationship to left ventricular failure, right ventricular failure, neurohormonal activity, and treatment options. 

DISPLAY 39-1 Neurohormonal Responses Affecting Heart Failure... 

The body activates the neurohormonal compensatory mechanisms, which result in ... 

Increased secretion of the neurohormones by the sympathetic nervous system... 

Class II antiarrhythmic drugs include beta (( -adrenergic blocking drugs, such as acebutolol (Sectral), esmolol (Brevibloc), and propranolol (Inderal). These drugp also decrease myocardial response to epinephrine and norepinephrine (adrenergic neurohormones) because of their ability to block stimulation of p receptors of the... 

The question is obviously an important one. Substances released from neurons are not always called neurotransmitters. Some of them are referred to as neuromodulators, neurohormones, neurotrophic factors or neurotoxins but since they all produce some effect on a neuron they could be said to have a transmitter role and justify the term... 

Describe the pathophysiology of heart failure as it relates to neurohormonal activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system. 

Development and progression of heart failure involves activation of neurohormonal pathways, including the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). 

Activation of both the RAAS and the SNS also contribute to vasoconstriction in an attempt to redistribute blood flow from peripheral organs such as the kidneys to coronary and cerebral circulation.7 However, arterial vasoconstriction leads to impaired forward ejection of blood from the heart due to an increase in afterload. This results in a decrease in CO and continued stimulation of compensatory responses, creating a vicious cycle of neurohormonal activation. 

Bradykinin is part of the kallikrein-kinin system, which shares a link to the RAAS through angiotensin-converting enzyme. Bradykinin is a vasodilatory peptide that is released in response to a variety of stimuli, including neurohormonal and inflammatory mediators known to be activated in HF.9 As a... 

Nitric oxide, a vasodilatory hormone released by the endothelium, is found in higher concentrations in HF patients and provides two main benefits in HF vasodilation and neurohormonal antagonism of endothelin.9 Nitric oxide s production is affected by the enzyme inducible nitric oxide synthetase (iNOS), which is up-regulated in the setting of HF, likely due to increased levels of angiotensin II, norepinephrine, and multiple cytokines. In HF, the physiologic response to nitric oxide appears to be blunted, which contributes to the imbalance between vasoconstriction and vasodilation. 

There is growing evidence of a link between renal disease and HF.8 Renal insufficiency is present in one-third of HF patients and is associated with a worse prognosis. In hospitalized HF patients, the presence of renal insufficiency is associated with longer lengths of stay, increased in-hospital morbidity and mortality, and detrimental neurohormonal alterations. Conversely, renal dysfunction is a common complication of HF or results from its treatment. Renal failure is also a common cause for HF decompensation. 

TABLE 3-7. Dosing and Monitoring for Neurohormonal Blocking Agents... 

It was hoped that the more complete blockade of angiotensin II s AT effects would confer greater long-term efficacy with ARBs compared to ACE inhibitors. However, prospective, randomized trials suggest that the clinical efficacy of ARBs is similar to that of ACE inhibitors for reduction of hospitalizations for HF, sudden cardiac death, and all cause mortality.23-25 Despite poorer suppression of AT2, comparable efficacy of ACE inhibitors may be due to the additional effects on the kallikrein-kinin system. Although ARBs produce hemodynamic and neurohormonal effects similar to those of ACE inhibitors, they are considered second-line therapy due to the overwhelming clinical trial experience with ACE inhibitors. 

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