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11 Cards in this Set
- Front
- Back
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Renal Control of MAP
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Long term regulation of MAP has traditionally been thought to be due to the renal system (hours/yrs)
The kidneys can regulate salt & water, altering these can influence MAP by altering plasma volume Several lines of evidence support the renocentric view of MAP regulation |
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Stimulation of Renin Release
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Intrarenal baoreceptors
monitor pressure or vascular volume within afferent arterioles renin release inverse to pressure & vascular volume Macula Densa responds to changes in Na+ & Cl- concentrations when MAP changes glomrular filtraion rate, macula densa & intrarenal baroreceptors cooperate RSNA direct stimulatory effect on renin secretion B1 adrenergic receptors on granular cells |
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Physiological Effects of Angiotensin II
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Potent vasoconstrictor
Increases HR & myocardial contractility Stimulates aldosterone synthesis & secretion by adrenal cortex Stimulates secretion of vasopressin Induces thirst |
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Physiological Effects of Aldosterone
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Released from adrenal cortex by Ang II
Increases reabsorption of Na+ by collecting duct in Henley's loop & reduces Na+ excretion Retains water, expanding plasma volume Increased preload, increases CO |
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Physiological Effects of Vasopressin
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Released from posterior pituitary
Release stimulated by Ang II & osmoreceptors in hypothalamus in response to increased plasma osmolality Decreases free water clearance by kidney, maintaining plasma colume increased preload, increased CO |
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Renal Control of MAP
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Regulation of MAP, CO & TPR in dogs with baro-denervation
MAP unchanged but more variable CO & TPR unchanged with no change in variability Transpant kidneys from 1 group to the other group hypertension follows kidney transplant MAP increases with age in humans Linearly related to Na+ intake & renal Na+ excretion Low Na+ diets- minimal age related increase in MAP High Na+ diets- increased MAP 1 mmHg per year after 30 Chronic stimulation of carotid sinus normally induces reflex mediated decreases in SNA minimal effects on chronic MAP regulation in angiotensin model normotensive animals sustain decrease in MAP Chronic increase in MAP is the result of activating renal mechanisms that conserve Na+ & expand plasma volume despite normal MAP |
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SNS Regulation of MAP
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High Na= intake (4-8% saline) has minimal affect on MAP
large affect of MAP with baroreceptor denervation Renal denervation does not effect MAP loweing effect of chronic baroreflex activation Young normotensive subjects exposed to stressors increase in MAP is variable acute increase in MAP is due to increase SNA normotensive subjects with largest increase in MAP are at increased risk for future development of hypertension |
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Role of Baseline SNA & MAP
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Baseline MSNA can vary in normotensive humans
5-10 fold variation (5-10 to 40-50 bursts/ min) Baseline MSNA correlated with whole body NE, renal NE, & cardiac NE Hypertensives show modest increase in baseline MSNA compared to normotensives Lack of relationship between MSNA & MAP may be due to reciprocal relationship between SNA & vasodilators high levels of NO counterbalance effect of high SNA, offset resistance High levels of baseline MSNA do not always result in increased MAP in normotensive humans Appear to be a compensatory mechanisms to limit the increase in MAP in those with high MSNA increased circulating vasodilators (NO) reduced CO reduced adrenergic vasoconstrictor responsiveness |
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Baseline MSNA, CO & TPR
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Wide range of CO in normotensive subjects
Inverse relationship baseline MSNA & CO |
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Importance of SNS Regulation of MAP
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SNA & MSNA increase with age & obesity
also associated with increased MAP MSNA decreases with weight loss Sympathetic support of MAP greater with age & obesity ganglionic blockage- eliminates autonomic outflow significant decreases in MAP in obese subjects |
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SNA Increase ith Age & Obesity
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Most likely due to altrations in several variables
central autonomic regulation stiffening of arterial baroreflex oxidative stress - reduce NO increased production of vasoconstrictors from endothelium |
