Enhanced pressor responses to angiotensin II caused by excessive sodium loading in the pithed rat.

The influence of changes in the sodium balance on angiotensin II-induced pressor responses were studied in the pithed rat preparation, which is characterized by a highly activated renin-angiotensin-aldosterone system (RAAS) with high plasma renin and angiotensin II concentrations. The pressor response to angiotensin II was enhanced by excessive sodium loading only, as induced by a high sodium diet combined with a mineralocorticoid, but not by a high salt diet as such. The stimulating effect of salt loading directly influences angiotensin II vasoconstriction without indirectly involving a facilitation of sympathetic neurotransmission. Salt depletion by a low salt diet combined with furosemide treatment did not alter the vasopressor response to angiotensin II. Changes in endogenous angiotensin II production secondary to alterations in serum sodium are of minor relevance in the pithed rat because of the strongly stimulated RAAS. Our finding that in this preparation excessive sodium loading still appears to enhance pressor responses to angiotensin II supports the conclusion that increased sodium load directly sensitizes vascular angiotensin II receptors.