Endothelin antiserum decreases volume- stimulated and basal plasma concentration of atrial natriuretic peptide.
BACKGROUND. Endothelin-1 (ET-1) is the most powerful factor known to release atrial natriuretic peptide ( ANP) in vivo and in cultured cardiac myocytes or preparations of atrium. We tested the role of endogenous ET-1 in the regulation of ANP release by passive immunization in anesthetized rats. METHODS AND RESULTS. Intravenous injection of antiserum against ET-1 was shown to decrease basal and volume- stimulated plasma concentrations of ANP, whereas control serum was without effect. Antiserum generated in rabbits cross-reacted 100% with endothelin-2 and -3. In pentobarbital-anesthetized Wistar rats treated with ET-1 antiserum, plasma ANP concentration measured by radioimmunoassay was reduced by 37% from starting level after 10 minutes and by 30% after 60 minutes. Control rat serum had no effect on plasma ANP. Rapid intravenous infusion of 8 mL of 0.9% NaCl caused a sixfold increase of plasma ANP concentration in control rats but only twofold in rats pretreated with ET-1 antiserum (P < .01). This effect of ET-1 antiserum was dose dependent. ET-1 antiserum changed neither blood pressure nor heart rate significantly in anesthetized rats. Pretreatment with ET-1 antiserum did not affect the initial hypotensive response to intravenous ET-1 0.5 nmol/kg but significantly attenuated the subsequent hypertensive response to endothelin. CONCLUSIONS. Endothelin may be a physiological modulator of both basal and stimulated ANP release.[1]References
- Endothelin antiserum decreases volume-stimulated and basal plasma concentration of atrial natriuretic peptide. Fyhrquist, F., Sirviö, M.L., Helin, K., Saijonmaa, O., Metsärinne, K., Paakkari, I., Järvinen, A., Tikkanen, I. Circulation (1993) [Pubmed]
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