Peptideinduced Emesis in Dogs: Possible Relevance to Radiation-Induced Emesis.

Carpenter, David O.

doi:10.21236/ada120667

Cited by 3 publications

(2 citation statements)

References 7 publications

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“…Morphine (39), enkephalin (2), and histamine (3) all are emetic and their actions are dependent upon integrity of the area postrema. We have found that angiotensin II, neurotensin, leu-enkephalin, TRH, VIP, gastrin, substance P and vasopressin are emetic on IV administration while CCK and somatostatin are not (11,12). Together these observations provide strong support for the proposed function of the area postrema as being the chemosensory trigger zone for emesis.…”

Section: A_supporting

confidence: 57%

Responses of neurons of canine area postrema to neurotransmitters and peptides

1983

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Captain "'Lomas E. Dayton (USAFSAM/RZV) was the Laboratory Project ScienZis-n-Cnarge.-When Government drawing: , pejecifications, or other data are used for any purpose other than in connection with a definitely Government-related procurement, tie United States Government incurs no responsibility or any obligation whatsoever. The fact that the Government may have formulated or in any way supplied the said drawings, specifications, or other data, is not to be regarded by implication, or otherwise in any manner construed, as lIcensing the holder, or any other person or corporation; or as conveying any rights o," permission to manufacture, use, or sell any patented invention that may in at. way be related the-'reto. The animals involved in this study were procured, maintaired, and used in accordance with the Animal Welfare Act and the "Guide for the Care and

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Section: A_supporting

confidence: 57%

Responses of neurons of canine area postrema to neurotransmitters and peptides

1983

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“…Few electrophysiological in vivo studies have looked at the AVP effects on AP neurons in animal species that vomit. In dogs, AVP which induced emesis when administered intravenously [45], induced an increase in the firing rate of 5 of 10 quiescent AP neurons when applied iontophoretically [46]. Such an excitation of AP neurons likely resulted from the activation of V 1a receptors, known to mediate the effects of AVP on the CNS.…”

Section: Discussionmentioning

confidence: 99%

A nonpeptide vasopressin V_1a receptor antagonist, SR 49059, does not prevent cisplatin‐induced emesis in piglets

Grélot

Girod²,

Dapzol³

et al. 2001

Fundamemntal Clinical Pharma

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We determined the pharmacological and the antiemetic properties of SR 49059, a selective nonpeptide V(1a) receptor antagonist, on cisplatin-induced emesis in the piglet. Firstly, we clearly demonstrate that SR 49059 is a potent V(1a) receptor antagonist in vitro and in vivo in the piglet. In binding studies, [3H]-SR 49059 exhibited high affinity for V(1a) receptors in piglet liver membranes (K(d) of 0.76 +/- 0.12 nM and B(max) of 138 +/- 22 fmol/mg prot.). In vivo, in decerebrate piglets, SR 49059 (1 mg/kg iv) antagonized AVP (500 ng/kg iv)-induced hypertension for at least 150 min and also blocked, for at least 270 min at 3 mg/kg iv, the pressor responses to exogenous LVP. After single and repeated iv or icv administration, we studied the antiemetic properties of SR 49059 on cisplatin-induced emesis in piglets. Animals receiving an emetic dose of cisplatin (5.5 mg/kg, iv) were observed continuously for 60 h. Piglets acting as controls were iv administered with vehicle 15 min prior to cisplatin infusion (T0(-15min)), while experimental animals received a single iv administration of SR 49059 at the dose of 1 or 3 mg/kg. In additional piglets, we administered SR 49059 (3 mg/kg) every 12 h from T0(-15min) to T48(-15min) (cumulative dose, 15 mg/kg). Another set of animals - observed only during the acute phase - was administered with SR 49059 (10 mg/kg) every 3 h from T0(-15min) to T15(-15min) (cumulative dose, 60 mg/kg). Lastly, 10 piglets were given a bilateral icv injection of SR 49059 (500 microg and 1500 microg/side) 1 h prior to cisplatin infusion. In all groups treated with SR 49059, the latency of the first emetic episode and the incidence of vomiting during the acute, the delayed and the cumulative phases remained statistically similar to that observed in controls, suggesting that V(1a) receptors are not involved in the onset and completion of nausea and vomiting.

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