| Cardiac Output
| The amount of blood the heart pumps in mL/min
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| Intrinsic regulation of heart function
| The things that happen in the heart itself to regulate its function
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| Preload
| The amount of blood entering the ventricles when they are relaxed
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| Afterload
| The pressure of blood already in the arteries, which the ventricles must push against when they try to force new blood out during systole. Called afterload because it is located after the ventricles in the path of blood flow.
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| Ejection fraction
| the percent of the blood in the ventricles that is pushed out into the arteries when the ventricles contract
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| Starling principle or Frank-Starling principle
| When ventricle muscles are stretched by a larger preload, they are able to contract more strongly (unless they are stretched way too far)
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| Atrial natriuretic hormone/factor/peptide
| A hormone secreted by the atria when they are stretched too far; it causes the body to release Na+ and water in the urine, decreasing blood volume and reducing the workload on the atria.
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| B-type natriuretic hormone/factor/peptide
| Similar to ANH, but released from the ventricles when they are stretched.
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| Extrinsic regulation of heart function
| The ways the rest of the body influences the heart, to keep it supplying the body with enough blood
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| Baroreceptors
| Blood pressure-sensing cells in the carotids and the aorta
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| Baroreceptor reflex
| The negative feedback loop in which the baroreceptors detect a change in blood pressure and the heart rate and blood vessels adjust to bring it back to normal
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| Cardiac control center
| The part of the medulla oblongata that is the integrative center controlling heart rate
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| Peripheral Resistance or Systemic Vascular Resistance
| The resistance to pushing blood through blood vessels. The higher the PR is, the higher the blood pressure will be and the higher the afterload will be.
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| Precapillary or arteriolar sphincters
| The rings of smooth muscle that can close off the blood from entering a capillary bed. These sphincters adjust the peripheral resistance by making it easier or harder for the blood to flow through the vessels.
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| Vasodilation
| When the precapillary sphincters open, letting blood flow freely into the capillaries. Lowers PR and BP
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| Vasoconstriction
| When the precapillary sphincters close. Raises PR and BP
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| Local control of blood flow
| When conditions in a specific tissue cause the precapillary sphincters to open or close.
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| NO
| Nitric oxide, a vasodilating compound formed in blood vessels and tissues
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| Endothelin
| A vasoconstricting compound formed in the lining of blood vessels
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| Vasomotor center
| The part of the medulla oblongata that is the integrative center controlling whether blood vessels constrict or dilate
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Renin-angiotensin-aldosterone system or RAAS
| A pathway by which the kidneys can raise BP if they detect low blood flow.
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| Renin
| The compound secreted by the kidneys when they don't get enough blood
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| Angiotensinogen
| Means angiotensin maker - a compound already in the bloodstream, which reacts with renin to form angiotensin I
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| Angiotensin I
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Means blood vessel tightener. A weak vasoconstrictor.
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| Angiotensin converting enzyme or ACE
| An enzyme found in the lungs. Converts angiotensin I to angiotensin II.
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| Angiotensin II
| A stronger vasoconstrictor. It also stimulates the production of Aldosterone by the adrenal cortex
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| Adrenal cortex
| The outer layer of the adrenal gland
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| Aldosterone
| A hormone produced by the adrenal cortex when it detects angiotensin II in the blood. This hormone causes the kidneys to turn on their Na+/K+ ATPase, and they then pump 3 Na+ from the urine into the blood and 2K+ from the blood into the urine. Water follows the majority of ions, so water also enters the blood, raising the blood volume.
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