Abstract. Experiments were performed in conscious dogs, in order to study the possibility of dopaminergic or opioid modulation of the osmolality-regulated release of AVP. Hypertonic saline (20%), infused during a period of 2 h at a rate of 0.03 ml· kg−1 · min−1, induced a significant AVP response, which was not influenced by prior administration of bromocriptine or naloxone. Data presented in this report, therefore, are not in support of a dopaminergic or opioid modulation of the osmolality-regulated AVP release in dogs. The results demonstrate a great consistency in individual plasma osmolality-plasma AVP relationships, next to a large inter-individual variation.
L. J. Hellebrekers, E. Lagerweij, H. W. de Vries and Tj. B. Van Wimersma Greidanus
L.J. Hellebrekers, E. Lagerweij, H W. de Vries and Tj. B. van Wimersma Greidanus
Abstract. The possibility of a dopaminergic and/or opioid modulation of the volume-regulated release of AVP was investigated in conscious dogs. Either bromocriptine, 10 μg/kg body weight po, or naloxone, 0.1 mg/kg body weight iv, was administered prior to induction of nonhypotensive hypovolemia. Volume contraction of 15 ml/kg body weight was induced gradually, over a period of 30 min. Basal plasma AVP levels in the bromocriptine group were not significantly different from control group values. Bromocriptine administration significantly augmented AVP release following volume contraction. Mean arterial pressure in the bromocriptine group decreased to a slightly, but significantly, lower level than that in the control group. Mean arterial pressures, however, did not adequately explain the magnitude of the AVP response in the bromocriptine group. In the naloxone group, neither baseline levels, nor AVP values following volume contraction, differed significantly from respective control group values. In conclusion, the results suggest the possibility of a stimulatory role for endogenous dopamine in the volume-regulated, but not the basal, release of AVP in conscious dogs.