Figure 137

Predominance of the renin-angiotensin-aldosterone mechanisms. Collectively, the various mechanisms discussed provide overlapping influences responsible for the highly efficient regulation of sodium balance, extracellular fluid (ECF) volume, blood volume, and arterial pressure. Nevertheless, the synergistic actions of the renin-angiotensin-aldosterone system on both vasoconstrictor as well as sodium-retaining mechanisms exert a particularly powerful influence that is not easily counteracted. In a recent study by Seeliger and coworkers [56], renal perfusion pressure was lowered to 90 to 95 mm Hg. The angiotensin II and aldosterone levels were not allowed to decrease and were fixed at normal levels by continuous infusions. The results demonstrated that all compensatory mechanisms (such as increased release of atrial natriuretic peptide and reduced activity of the sympathetic system) could not overcome the hypertensinogenic influence of maintained aldosterone or aldosterone plus angiotensin II as long as renal perfusion pressure was not allowed to increase. Thus, under conditions of increased activity of the renin-angiotensin system, an increased renal arterial pressure seems essential to reestablish sodium balance. In conclusion, regardless of the specific intrarenal mechanism involved, the net effect of a long-term hypertensinogenic derangement is a reduced capability for sodium excretion at normotensive arterial pressures that cannot be completely compensated by other neural, humoral, or paracrine mechanisms, leaving only the option to increase arterial pressure and elicit a pressure natriuresis. (Adapted from Seeliger et al. [56].)

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