Term
| What are the cardiovascular effects of exercise on the heart? |
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Definition
- Heart will pump more blood per beat (stroke volume)
- Heart will recover quicker.
- Heart will beat slower at rest (reduced resting pulse rate)
- Number of capillaries will increase. |
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Term
| What bind to β-adrenoceptors and what are the effects? |
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Definition
catecholamines: epinephrine and norepinephrine, released from autonomic fibers
increasing heart rate and contractile force and vasodilation |
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Term
| Describe the classic pathway for the vasodilator response to β-adrenergic stimulation |
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Definition
1. epinephrine stimulates Gs protein
2. cAMP formation
3. cAMP normally inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating smooth muscle myosin and causing contraction.
4. MLCK is further inhibited when cAMP levels increase
5. cAMP also activate protein kinase A that will promote reduction in intracellular Ca2+ concentration in vascular smooth muscle cells, with consequent vasodilation. |
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Term
| What are the effects or propranolol? |
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Definition
| Propranolol is a non-selective β-blocker; it blocks the actions of adrenaline and noradrenaline on both β1- and β2-adrenoceptors, meaning that the ‘stress response’ is reduced and sympathetic activity causing vasoconstriction is also blocked. |
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Term
| What are the effects or beta blockers? |
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Definition
β-blockers reduce the effects of sympathetic stimulation of the heart. The cardiac output is decreased and so there is a decrease in the cardiac O2 demand; a reduction in ‘cardiac work’ (one of the premises for treating angina).
β-blockers will obviously work in the same way, whether they are treating dysrhythmias, heart failure or angina. |
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Term
| Adverse effects of beta blockers? |
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Definition
| exacerbate heart failure, fatigue and nightmares. |
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Term
| What are the effects of β-adrenoceptor agonists? |
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Definition
| relax muscles of the airways, which widens the airways and results in easier breathing. The activation of β1, β2 and β3 activates the enzyme, adenylate cyclase. This in turn leads to the activation of the secondary messenger cyclic adenosine monophosphate (cAMP), cAMP then activates Protein Kinase A (PKA) which phosphorylates target proteins ultimately inducing smooth muscle relaxation and contraction of the cardiac tissue. |
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Term
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Definition
| Pulse pressure is the difference between the systolic and diastolic pressure readings. |
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Term
| How do you calculate MAP? |
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Definition
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Term
| What are the effects of GTN? |
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Definition
GTN works as an NO donor, and therefore as a vasodilator.
1. NO stimulates soluble granulate cyclase which forms cGMP
2. cGMP activates protein kinase G, which causes reuptake of Ca2+ and the opening of Ca2+-activated K+ channels.
3. The fall in concentration of Ca2+ ensures that the myosin light-chain kinase can no longer phosphorylate the myosin molecule, thereby stopping the cross-bridge cycle and leading to relaxation of the smooth muscle cell. |
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Term
| Why could propranolol not be administered to a subject who had a resting heart rate below 70bpm? |
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Definition
| This would dangerously drop the subjects HR as propranolol. Gs-protein activation increases heart rate so by blocking beta-adrenoceptors, less contraction occurs. |
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