HTN Pathophysiology Lecture Fall (4) (1)

Increases heart rate contractility peripheral

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Increases heart rate, contractility, peripheral vascular resistance (PVR) Parasympathetic signals are transmitted to the heart via the vagus nerve Decreases heart rate ANS control is mediated via intrinsic and extrinsic reflexes
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Neural Mechanisms Pre-synaptic in the CNS Stimulation of α 2 receptors Inhibits norepinephrine release Positive feedback mechanism Stimulation of β receptors Causes norepinephrine release Post-synaptic Stimulation of β 1 receptors in heart HR Stimulation of β 2 receptors in arterioles & venules Vasodilation Stimulation of α 1 receptors in arterioles & venules Vasoconstriction
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Neural Mechanisms Intrinsic control of ANS 1. Baroreceptors Pressure sensitive receptors located in the walls of blood vessels and the heart Respond to changes in the stretch of the vessel wall Example: juxtoglomerular cells of the kidney 1. Chemoreceptors Monitor oxygen, carbon dioxide and hydrogen contents of blood Hypoxemia due to a chronic lung disease could trigger HTN
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Neural Mechanisms Extrinsic control of the ANS Found outside circulation Very diffuse Responses are inconsistent Associated with factors like pain, cold, and emotion
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Humoral Mechanisms: RAAS System Most influential in the control of homeostatic BP Regulates Sodium, potassium, and fluid balance Vascular tone and sympathetic activity Influenced by Intrarenal factors: renal perfusion, catecholamines, angiotensin II Extra renal factors: sodium, chloride, potassium Juxtoglomerular cells sense decreased renal artery pressure and kidney blood flow Release renin Macula densa and/or juxtoglomerular cells sense a decrease in sodium and chloride Releases renin
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Humoral Mechanisms Renin-angiotensin-aldosterone system (RAAS)
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Extracellular Fluid Volume Elevates BP directly and indirectly Direct Higher volumes directly increase CO SV x HR x PVR Indirect Higher blood flow to organs causes vasoconstriction (increase in PVR) Stimulates a tissue-regulation response
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Tissue Auto-regulation Purpose is to maintain adequate tissue perfusion and oxygenation Kidney’s volume-pressure balance/adaptation Tissues have auto-regulatory mechanisms Normal With low-normal metabolism vasocontriction High metabolism vasodilation Defects in renal volume & blood flow to tissues Vasoconstriction PVR
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Different types of HTN
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Primary Vs. Secondary Hypertension Primary 90% of HTN cases Chronic elevations in blood pressure No evidence of other disease Secondary Minority of cases HTN that results from another disorder
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Mechanisms of Pathogenesis: Primary Hypertension Increased cardiac output Increased fluid volume from excess sodium intake or renal sodium retention Excess stimulation of the RAAS Sympathetic over activity Increased peripheral resistance
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