Receptor a-adrenergic, stimulation

The role of a-adrenergic receptor stimulation in asthma remains controversial. Inhalation of phentolamlne, the a-adrenerglc antagonist, produced both bronchodilatation and bronchoconstrlctlon in extrinsic asthmatics. However, oral phentolamlne partially blocked exercise and cold-induced bronchospasm in asthma without affecting reactivity to histamine, suggesting a-adrenerglc mechanisms may be involved in airway cooling. °... 

O The lower urinary tract symptoms and signs of benign prostatic hyperplasia are due to static, dynamic, or detrusor factors. The static factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate gland. The dynamic factor refers to excessive stimulation of a-adrenergic receptors in the smooth muscle of the prostate, urethra, and bladder neck. The detrusor factor refers to irritability of hypertrophied detrusor muscle as a result of long-standing bladder outlet obstruction. 

The major circulating hormones that influence vascular smooth muscle tone are the catecholamines epinephrine and norepinephrine. These hormones are released from the adrenal medulla in response to sympathetic nervous stimulation. In humans, 80% of catecholamine secretion is epinephrine and 20% is norepinephrine. Stimulation of cy-adrenergic receptors causes vasoconstriction. The selective a,-adrenergic receptor antagonist, prazosin, is effective in management of hypertension because it causes arterial and venous smooth muscle to relax. 

Sympathetic nerves. The afferent and efferent arterioles are densely innervated with sympathetic nerves. Norepinephrine released directly from the nerves or circulating epinephrine released from the adrenal medulla stimulates a, adrenergic receptors to cause vasoconstriction. The predominant site of regulation is the afferent arteriole. Under normal resting conditions, there is little sympathetic tone to these vessels so that RBF is comparatively high. As discussed previously, this facilitates glomerular filtration. 

The answer is e. (Hardman, p 215 J Ritodrine hydrochloride is a selective [ -adrenergic agonist that relaxes uterine smooth muscle. It also has the other effects attributable to J3-adrenergic receptor stimulants, such as b rone hod il at ion, cardiac stimulation, enhanced renin secretion, and hyperglycemia. 

The goal of treatment of SUI is to improve urethral closure by stimulating a-adrenergic receptors in the smooth muscle of the bladder neck and proximal urethra, enhancing supportive structures underlying the urethral epithelium, or enhancing serotonin and norepinephrine effects in the micturition reflex pathways. 

It is believed that trazodone, in therapeutic doses, inhibits the neuronal reuptake of serotonin. It is not a MAO inhibitor or a CNS stimulator. It has a minor influence on the reuptake of norepinephrine and dopamine. In addition, it does not bind with cholinergic or a-adrenergic receptors. Synonyms of this drag are thrombran, pragmarel, desyrel, and others. 

The stimulation of a-adrenergic receptors in specific regions of the CNS leads to hypotension. 

Methyldopa is an a-methoxylated derivative of levodopa that exhibits hypotensive action by reducing overall peripheral vascular resistance and reducing heart work. Antihypertensive action of methyldopa consists of the biotransformation of methyldopa into methylnoradrenaline (methylnorepinephrine), which acts as a pseudo neurotransmitter. The current, universally accepted point of view is that the action of methyldopa is carried out through the CNS, where methylnorepinephrine, a powerful stimulant of a-adrenergic receptors of the medulla, inhibits the vasomotor center. 

Inositol-1,4,5-trisphosphate and related compounds Stimulation of a adrenergic receptors, various other stimuli Opens Ca2+ channels in ER Section E... 

Dopamine stimulates dopamine, a-, and [3-adrenergic receptors. The use of dopamine in congestive heart failure is limited because it causes nausea and vomiting, becomes inactive when given orally, increases afterload (a-adrenergic receptor-mediated peripheral vasoconstriction), and enhances oxygen demand on the left ventricle. 

The a-blockers act as antagonists for the aradrenergic receptor. The a -adrenergic receptor, when stimulated, triggers vasoconstriction. Blocking this receptor prevents vasoconstriction and reduces blood pressure. Doxazosin (Cardura, A.131) is structurally... 

Bogoyevitch MA, Andersson MB, Gillespie BJ, Clerk A, Glennon PE, Fuller SJ, Sugden PH. 1996. Adrenergic receptor stimulation of the mitogen-activated protein kinase cascade and cardiac hypertrophy. Biochem J 314 115-121. 

There are two kinds of catecholamine receptors, the a and fi receptors. The former respond best to norepinephrine, whereas the latter prefer epinephrine. Norepinephrine is normally associated with neurotransmission, and a-adrenergic receptors are indeed found in tissues serviced by the sympathetic nervous system. An example is the smooth muscle, which contracts in response to stimulation by... 

Since norepinephrine [nor ep ee NEF rin] is the neuromediator of adrenergic nerves, it should theoretically stimulate all types of adrenergic receptors. In practice, when the drug is given in therapeutic doses to humans, the a-adrenergic receptor is most affected. 

Correct answer = C. Clonidine reduces sympathetic outflow by stimulating a-adrenergic receptors. Minoxidil is a direct-acting vasodilator. Verapamil causes vasodilation by inhibiting calcium ion flow into smooth muscle. Enalapril blocks the enzyme that converts angiotensin I to angiotensin II. Hydrochlorothiazide acts by decreasing blood volume. 

The response of mast cells includes release of arachidonic acid due to membrane PhL A2 activation following a ligand-induced increase in cellular Ca2+. PTX reduces the Ca2+-mediated GTP S-dependent release of this fatty acid in permeabil-ized cells [102,103]. This raised the possibility of a direct link, not only between receptors and PhL C, but also between receptors and PhL A2. Existence of a G protein-mediated. PTX-sensitive, activation of PhL A2 independent of G protein-mediated activation of PhL C was confirmed in studies first with fibroblasts [104] and then with FRTL thyroid cells [105]. Studies with the latter cells show that a,-adrenergic receptors promote arachidonic acid release [105] and that this effect is mimicked in permeabilized cells by GTP and is not blocked by inhibition of PhL C with neomycin. Thus, at least two Gp proteins need to be defined a Gp-stimu-lating PhL C (Gp(c) and a Gp-stimulating PhL A2 (Gp,a). It is possible that rat brain G is PTX-sensitive Gplc. 

Figure 6.10. Calcium-dependent signalling by adrenergic receptors. a p-Adrenergic receptors activate adenylate cyclase. cAMP activates protein kinase A (PKA). In heart muscle, PKA phospho-rylates several Ca transporters and charmels, so that the amount of Ca available for contraction is increased. PL Phospholam-ban SERCA SR/ER Ca transporter, b In smooth muscle, myosin activation in works by way of phosphorylation, which is performed by myosin light chain kinase (MLCK). Inactivation is accomplished by myosin light chain phosphatase (MLCP). c aj-Adrenergic receptors stimulate phospholipase C, which releases inositoltriphosphate (IP3). IP3 binds to a cognate ligand-gated Ca chaimel in the ER and releases Ca, which with calmodulin activates MLCK.

Phenylephrine, the oldest of the currently available agents, is a synthetic adrenergic agonist. It differs chemically from epinephrine by the absence of the hydroxyl group on position 4 of the benzene ring. At the concentrations used for ocular decongestion, phenylephrine causes vasoconstriction by direct stimulation of a-adrenergic receptors on the conjimctival vasculature. The resultant clinical effect is usually a decrease in conjunctival hyperemia and edema. 

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