234)A person is confronted by a dangerous dog. His heart begins to race and beat strongly, his pupilsdilate, and his hairs stand up. These signs are the result of234)A)increased activity of autonomic centers in the hypothalamus.B)sympathetic activation.C)increased levels of epinephrine in the blood.D)A, B, and CE)B and C only Show 235)Mary accidentally ate poison mushrooms that contain muscarine. What symptoms would youexpect to observe?235) Get answer to your question and much more 236)[The actual neurotransmitters involved in Huntington's chorea]The inherited brain disorderHuntington disease is caused by the destruction of basal nuclei that use different neurotransmitters.One neurotransmitter is ________ and the other is ________.236) Get answer to your question and much more 237)Drugs known as beta-blockers may be useful for treating237) Get answer to your question and much more SHORT ANSWER.Write the word or phrase that best completes each statement or answers the question.238)The level of tonic activity of autonomic neurons determines the ________ of an individual.238)239)During ________ sleep, the entire body relaxes and the activity of the cerebral cortex is at aminimum.239)240)During ________ sleep, dreaming occurs.240)241)The integrative centers for autonomic activity are located in the ________.241)242)Neurons that use norepinephrine as a transmitter are called ________.242)243)Most vital organs receive ________ innervation. That is, they receive input from bothsympathetic and parasympathetic divisions.243)244)The ________ nervous system stimulates the arrector pili muscles and gives you"goosebumps."244)32  The rate of SA nodal firing can be altered by: 1. Changes in autonomic nerve activity (sympathetic and vagal)To increase heart rate, the autonomic nervous system increases sympathetic outflow to the SA node, with concurrent inhibition of vagal tone. Inhibition of vagal tone is necessary for the sympathetic nerves to increase heart rate because vagal influences inhibit the action of sympathetic nerve activity at the SA node. Norepinephrine released by sympathetic activation of the SA node binds to beta-adrenoceptors. This increases the rate of pacemaker firing primarily by increasing the slope of phase 4, which decreases the time to reach threshold. This occurs by increasing If ("funny" pacemaker currents) and increasing slow inward Ca++ currents. Sympathetic activation also lowers the threshold for initiating phase 0 of the action potential. Parasympathetic (vagal) activation, which releases acetylcholine onto the SA node that binds to muscarinic receptors, decreases pacemaker rate (phase 4 slope) by increasing gK+ and decreasing the pacemaker currents (If) and slow inward Ca++ currents. These changes in ion currents decrease the slope of phase 4 of the action potential, thereby increasing the time required to reach threshold. Vagal activity also hyperpolarizes the pacemaker cell during Phase 4, which contributes to the longer time to reach threshold voltage. 2. Circulating hormones Pacemaker activity is also altered by hormones. For example, hyperthyroidism induces tachycardia and hypothyroidism induces bradycardia. Circulating epinephrine causes tachycardia by a mechanism similar to norepinephrine released by sympathetic nerves. 3. Serum ion concentrationsChanges in the serum concentration of ions, particularly potassium, can cause changes in SA nodal firing rate. Hyperkalemia induces bradycardia or can even stop SA nodal firing. Hyperkalemia causes membrane depolarization, which diminishes the degree of hyperpolarization that occurs at the end of phase 3. This, in turn, prevents full reactivation of pacemaker channels for Na+ and Ca++ so that the slope of phase 4 is decreased. Hypokalemia increases the rate of phase 4 depolarization and causes tachycardia by enhancing phase 3 repolarization, which causes greater activation of channels responsible for the inward pacemaker currents. Note, however, that the effects of changes in serum potassium are complex with multiple channels and ion pumps being affected by potassium concentration. 4. Cellular hypoxiaCellular hypoxia (usually due to ischemia) depolarizes the membrane potential causing bradycardia. Without adequate oxygen, ATP dependent ion pumps in the cell membrane cannot operate. This leads to cellular depolarization because of a loss of normal ion gradients (particularly K+) across the membrane. Because a hyperpolarized state at the end of phase 3 is necessary for pacemaker channels to become reactivated, pacemaker channels remain inactivated in depolarized cells. This suppresses pacemaker currents and decreases the slope of phase 4. This is one reason why cellular hypoxia, which depolarizes the cell and alters phase 3 hyperpolarization, leads to a reduction in pacemaker rate (i.e., produces bradycardia). Severe hypoxia completely stops pacemaker activity. 5. DrugsVarious drugs used as antiarrhythmics also affect SA nodal rhythm. Calcium-channel blockers, for example, cause bradycardia by inhibiting the slow inward Ca++ currents during phase 4 and phase 0. Drugs affecting autonomic control or autonomic receptors (e.g., beta-blockers, muscarinic antagonists) directly or indirectly alter pacemaker activity. Digitalis causes bradycardia by increasing parasympathetic (vagal) activity on the SA node; however, at toxic concentrations, digitalis increases automaticity and therefore can cause tachyarrhythmias. This toxic effect is related to the inhibitory effects of digitalis on the membrane Na+/K+-ATPase, which leads to cellular depolarization, increased intracellular calcium, and changes in ion conductances. 6. AgePacemaker activity is influenced dramatically by age. Many different formulas have been developed to estimate the effects of age on maximal HR (HRmax); however, the following simple formula is commonly used and serves to illustrate how age generally affects HRmax: HRmax = 220 — age in years Using this formula, a 20-year-old person will have a HRmax of about 200 beats/min, and this will decrease to about 170 beats/min when the person is 50 years of age. HRmax cannot be modified appreciably by exercise training; therefore, even highly conditioned older athletes will have a reduced HRmax. Please note that for any given individual, their HRmax will be strongly influenced by genetic factors as well as by other factors previously mentioned. Revised 10/15/19 DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice. Which receptors would you block to decrease heart rate?Or we can use a beta-1 antagonist medication more commonly called a beta-blocker such as metoprolol (or other drugs ending in 'olol') which blocks beta-1 receptors thus decreasing heart rate and contractility which decreases blood pressure for the hypertensive patient and decreases the chance of a dysrhythmia after a ...
What chemicals decrease the heart rate?The parasympathetic nervous system (PNS) releases the hormone acetylcholine to slow the heart rate.
What receptors regulate heart rate?Atrial type B receptors located in the two atria and veno-atrial junctions, which are stimulated by atrial filling are believed to play an important role in the regulation of body fluid volume and heart rate.
What drugs block the parasympathetic nervous system?Anticholinergic drugs act as antagonists at muscarinic receptors, thereby inhibiting parasympathetic influences.
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A certain drug decreases heart rate by blocking a receptor on cardiac pacemaker cells
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