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It is known that iv antidiuretic hormone (ADH) infusions produce potentiated pressor responses in animals which have been made areflexic or in which the sympathetic nervous system has been blocked. However, other researchers have reported that ADH will potentiate the vasoconstrictor activity of norepinephrine or sympathetic nerve activity. To determine regional vascular resistance changes to ADH infusions in control vs. sympathetic blocked animals, regional blood flow changes were observed in these experiments in response to iv ADH infusions in normal and hexamethonium- and phenoxybenzamine- treated rats. Tissue blood flow was measured in unanesthetized rats with the use of radioactive microspheres. Preliminary experiments were performed which confirmed the suitability of sampling methods and the mixing of microspheres under test conditions. Experiments showed that ADH treatment produces the greatest increase in vascular resistance of muscle and skin tissues of both normal and sympathetic blocked rats. Results confirm previous reports that ganglionic or sympathetic blockade will potentiate pressor effects of ADH infusions. Regional blood flow and vascular resistance changes in normal and sympathetic blocked rats were similar, except in renal and intestinal tissues where normal rats had increased vascular responsiveness to ADH compared to both hexamethonium- and phenoxybenzamine- treated animals. These results support previous indications of a positive interaction between ADH and sympathetic mechanisms in the normal rat which may redistribute blood flow away from muscle, skin, intestinal, and renal tissues and maintain blood flow in brain and heart tissues. Attenuated pressor effects in response to ADH infusions in normal rats are probably due to reflex inhibition of the central cardiovascular system.
William E. Hoffman (1980) studied this question.