A Model of the Human Circulation: REGULATION BY AUTONOMIC NERVOUS SYSTEM AND RENIN-ANGIOTENSIN SYSTEM, AND INFLUENCE OF BLOOD VOLUME ON CARDIAC OUTPUT AND BLOOD PRESSURE

In our model of the human circulation, the normal distribution and flow of blood to the systemic compartments and the central blood volume are regulated by the autonomic nervous system. Central blood volume (CBV), cardiac output (CO), and arterial pressure (AP) are stabilized during postural change...

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Veröffentlicht in:Circulation research 1973-05, Vol.32 (5 Suppl No I), p.I-84-I-98
Hauptverfasser: LUETSCHER, JOHN A, BOYERS, DAVID G, CUTHBERTSON, JAMES G, MCMAHON, DAVID F
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Sprache:eng
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Zusammenfassung:In our model of the human circulation, the normal distribution and flow of blood to the systemic compartments and the central blood volume are regulated by the autonomic nervous system. Central blood volume (CBV), cardiac output (CO), and arterial pressure (AP) are stabilized during postural change and after loss or transfusion of blood, so long as autonomic control is normal; but autonomic blockade results in increased sensitivity of CBV, CO, and AP to changes in total blood volume. The autoregulated renal circulation, the release of renin, and the generation of angiotensin are simulated by the model under physiological conditions. The vasoconstrictor effects of angiotensin II are dependent on sodium balance and other factors affecting the concentration of circulating angiotensin and its interaction with receptors in arterioles.Wide variations in plasma renin activity (PRA), autonomic responses, plasma volume, peripheral resistance, and cardiac output have been found in different groups of hypertensive patients. The different constellations of pathological physiological data suggest at least two general classes of hypertensionone group associated with increased autonomic activity or circulating catecholamines, high PRA, low to normal plasma volume, and high to normal cardiac output; and a second group having increased exchangeable sodium, high-normal plasma volume, subnormal PRA, and often evidences of impaired autonomic function. Possible models of each type are proposed, relating the differences in pathogenesis and pathophysiology.
ISSN:0009-7330
1524-4571