Prior receptor occupancy as a determinant of the pressor activity of infused angiotensin II in the rat.
The pressor responsiveness to angiotensin II and norepinephrine was examined in rats before and during blockade of coverting enzyme activity with the nonapeptide SQ 20881. Responses to angiotensin II were impaired by sodium deprivation but enhanced by sodium loading or bilateral nephrectomy. During the period of converting enzyme blockade, a twofold increase in the angiotensin II pressor response was observed in the salt-restricted rats, whereas only a small change occurred in the salt-loaded rats. Infusion of the inhibitor produced a profound fall in the blood pressure of the salt-depleted rats with a relatively minor fall in the sodium-loaded rats. Norepinephrine pressor responses were slightly potentiated in the salt-restricted rats after administration of SQ 20881, but no change occurred in the salt-loaded or the nephrectomized rats. These observations support the view that the decreased angiotensin II pressor activity during salt deprivation is the result of a prior occupancy of receptor sites by endogenous hormone. Therefore, a change in the number or the affinity of receptors consequent to changes in sodium balance need not be postulated to explain the phenomenon.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001667:Binding, Competitive; D001794:Blood Pressure / Q000187:drug effects*; D009392:Nephrectomy; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011955:Receptors, Drug; D012964:Sodium / Q000172:deficiency; D000092502:Renin Inhibitors
D000804:Angiotensin II; D009638:Norepinephrine; D011955:Receptors, Drug; D012964:Sodium; D000092502:Renin Inhibitors