We found that neither the endogenous release of ANP in response to acute volume expansion nor its elimination following a volume load or an intravenous bolus injection of synthetic ANP is markedly altered by inhibition of ACE or kallikrein. We therefore conclude that neither ACE nor kallikrein are key enzymes in the activation or elimination of ANP. Plasma levels of ANP in the basal state and following acute blood volume expansion are reduced during hypothyroidism but the responsiveness, i.e. the magnitude of increase following acute volume expansion, is unchanged. Hyperthyroidism does not alter basal or stimulated plasma levels of ANP. Acute TRH administration increases ANP levels in parallel with the increase in blood pressure, but does not alter responsiveness to acute volume expansion. Thus the metabolic state induced by thyroid hormone may modulate the basal levels of ANP, but does not alter its release. TRH does not appear to modulate the release of ANP apart from its effect on the sympathetic nervous system.
