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Published on : Dec 06, 2013
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Pathophysiology of hypertension Presentation Transcript

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Pathophysiology of Hypertension Tatár M. Dept. of Pathophysiology Jessenius Med. School

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- venous return - extracellular fluid volume - myocardial contractility - vasoactive substances thickening of arteriolar wall

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Essential Hypertension Hemodynamic effect of hormonal, neural and renal dysregulation of blood pressure Pathogenesis is probably a slow and gradual process No single or specific cause Initiating factors may no longer be apparent when hypertension is developed, since they have been „normalised“ by the compensatory interactions Initial phase:  cardiac output Late phase:  peripheral arteriolar resistance, cardiac output is normalised

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INCREASED EXTRACELLULAR FLUID VOLUME INCREASED BLOOD VOLUME INCREASED VENOUS RETURN INCREASED CARDIAC OUTPUT AUTOREGULATION INCREASED TOTAL PERIPHERAL RESISTANCE INCREASED BLOOD PRESSURE

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Mechanisms of EH  activity of renin-angiotensin-aldosteron Hyperfunction of sympathetic system Vasoactive substances - endothelial dysfunction Insulin resistance  obesity Arteriolar hypertrophy Renal defect to excrete sodium

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Increased R-A-A activity J-G RENIN ANGIOTENSINOGENE ANGIOTENSIN I ANGIOTENSIN II ALDOSTERON Na+ RETENTION BLOOD PRESSURE VASOCONSTRICTION negative feed back ACE

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Tissue R-A system - catecholamine and endothelin release induction of hypertrophy of smooth muscle cells, cardiomyocytes (Beevers et al., 2001)

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Hyperfunction of sympathetic system Primary  activity of vasomotor neurons Angiotensin II and endothelin increases activity of vasomotor neurons Norepinephrine potentiates renin releasing

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Vacoactive substances Endothelin Digitalis (ouabain) – like substance Natriuretic peptides Influence on vascular tone and sodium transport

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Sodium transport across vascular smooth muscle cell membrane Sodium retention  activation of natriuretic mechanisms Digitalis - like inhibitor of Na+,K+,ATP-ase

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SYNDROME X INSULIN RESISTANCE  HDL  VLDL GLUCOSE INTOLERANCE HYPERINSULINEMIA HYPERTENSION OBESITY

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INSULIN RESISTANCE HYPERINSULINEMIA ARTERIOLAR HYPERTROPHY SODIUM RETENTION SYMPATHETIC ACTIVITY HYPERTENSION

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(Reaven et al., 1996) Regulatory cells (tonic activity)

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Hypertrophy of Arteriolar Wall OBESITY STRESS Na+ RETENTION RENAL HYPOPERFUSION INSULIN CATECHOLAMINES NATRIURETIC HORMON ANGIOTENSIN PRESSURE-GROWTH EFFECTS  INTRACELLULAR Ca2+  Na+/H+ EXCHANGE SMOOTH MUSCLE CONTRACTION VASCULAR WALL HYPERTROPHY PERIPHERAL VASCULAR RESISTANCE

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(Brown, 1997)

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Role of Kidneys (Johnson et al., 2002)

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Renal Lesions 1st phase - normal kydneys and sodium excretion - sympathetic hyperactivity, R-A stimulation  2nd phase - tubular ischemia - interstitial inflammation -  ultrafiltration and  Na+ reabsorbtion  3rd phase - elimination of tubular ischemia; sodium excretion is normal renal vasoconstriction increased blood pressure BP is more increased after enhanced salt intake

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Right shift of „pressure-natriuretic“ line (Cowley and Roman, 1996)

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Conclusions Interaction between increased activity of sympatihetic and R-A systems and dysregulation of sodium balance and intravascular volume Endothelial dysfunction – dysbalance between vasoconstrictor and vasodilator agents Hyperinsulinemia – a) direct effect on sodium retention, b) sympathetic activation through the suppression of regulatory neurons in hypothalamus Hypertrophy of arteriolar wall – increased vasoconstrictor reactivity Genetic factors: dysfunction of membrane mechanisms of vascular smooth muscle cells; disorder of sodium exchange in nephron epithelial cells Acquired renal injury: sodium intake is excreted only with increased blood pressure

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