Summary
Rats anaesthetised with Inactin, body temp. maintained at 37°C, were infused with mannitol-saline until both urine flow rate and conductivity reached a balanced state. In separate experiments under analogous conditions cardiac output was measured by dye dilution and organ flow rates by86Rb distribution. Doses of oxytocin of 3 ng or less, injected at or just below the carotid bifurcation, caused a highly significant natriuresis with increased tubular rejection, but no measureable haemodynamic changes. The same oxytocin dose given into the internal or external carotid artery above the bifurcation caused neither haemodynamic changes nor natriuresis. Injection of vasopressin, angiotensin and α-MSH at the sensitive site did not result in natriuresis in the same dosage range. Section of the sinus nerve significantly decreased the natriuretic response to oxytocin. It is suggested that the carotid body contains a specific oxytocin receptor capable of eliciting natriuresis in the rat.
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Škopková, J., Albrecht, I. & Cort, J.H. A natriuresis receptor at the carotid bifurcation specifically activated by oxytocin. Pflugers Arch. 343, 123–132 (1973). https://doi.org/10.1007/BF00585707
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DOI: https://doi.org/10.1007/BF00585707