Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(1) The effects of 5 anesthetics (chloralose, chloroform, ethanol, pentobarbital and urethane) and one anticonvulsant (diphenylhydantoin) were studied on the membrane properties and post-synaptic responses of crustacean neuromuscular junction preparations and molluscan neurons to putative transmitters and peptides. (2) In crustacean preparations pentobarbital selectively depressed, in a dose-dependent, reversible manner, post-synaptic, Na+-dependent, depolarizing responses to the putative transmitter glutamate without altering post-synaptic, Cl(-)-dependent inhibitory responses to the putative transmitter gamma-aminobutyric acid. (3) The effects of all the agents on post-synaptic pharmacology of a molluscan neurosecretory cell were studied either by causing the cell to hyperpolarize to about--100mV through repeated application of acetylcholine (ACh) in a K+-free, Ca++-containing solution or by hyperpolarization through injection of intracellular current in a K+-free solution. Effects of these agents on post-synaptic responses on other molluscan neurons were studied using intracellular current injection to manipulate membrane potential. (4) All of the agents tested selectively depressed the depolarizing Na+-K+-dependent post-synaptic responses of the neurosecretory cell to ACh in a dose-dependent reversible manner without appreciably altering the membrane properties of the cell (over the potential range of the ACh responses). (5) Pentobarbital did not alter the inversion potential of the ACh response. (6) Reciprocal plot analysis of all of the agents tested revealed that the antagonism of the ACh response was primarily non-competitive. (7) None of the agents tested altered hyperpolarizing, K+-dependent responses to dopamine and glutamate on the neurosecretory cell, nor did they affect either the induction or enhancement of BPP activity by the vertebrate peptide vasopressin on this cell.
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PMID:CNS depressants: effects on post-synaptic pharmacology. 117 46

1. Long-lasting haemorrhagic hypotension (4.5 hr at 35 mmHg) leading to irreversible haemorrhagic shock, has been studied in normal dogs, in dogs treated with a bradykinin potentiating nonapeptide (BPP(9a)), which blocks the conversion of angiotensin I to angiotensin II, and in dogs with experimental chronic diabetes insipidus (DI dogs). BPP(9a) was given by I.V. injection before the start of bleeding (BPP pre-treated group), 45 min after blood pressure had reached 35 mmHg (BPP early treated group) or 2 hr after blood pressure had reached 35 mmHg (BPP late-treated group). After retransfusion of blood all dogs were allowed to recover and observed for a further period of 3 days.2. Untreated control dogs developed haemorrhagic shock with tachycardia, low cardiac output, low total peripheral conductance and low stroke volume. All died within 24 hr of retransfusion, with pathological lesions typical of irreversible haemorrhagic shock.3. BPP pre-treated dogs developed haemorrhagic shock with bradycardia (during early shock), high cardiac output, high peripheral vascular conductance and high stroke volume when compared with the untreated controls. All pre-treated animals survived the 3 day observation period. They were then killed and on post-mortem showed no signs of irreversible haemorrhagic shock.4. BPP early-treated animals behaved like controls before BPP, but like pre-treated animals after the drug. Only one out of eight died within the 3 day observation period.5. BPP late-treated dogs behaved like controls before BPP. They responded to the drug with a rise in cardiac output, peripheral vascular conductance and stroke volume, and with a fall in heart rate. These responses were, however, short-lived. Four out of these eight animals died within the 3 day observation period, with lesions of irreversible haemorrhagic shock.6. DI dogs developed haemorrhagic shock with tachycardia (like controls), but with high cardiac output and peripheral vascular conductance (like BPP pre-treated dogs). The stroke volume of DI dogs was intermediate between those of controls and pre-treated groups. All six dogs survived the 3 day observation period.7. BPP(9a) had no measurable effect on the course of endotoxic shock.8. It is suggested that the normally severe vasoconstriction of the mesenteric vascular bed, which is thought to be responsible for irreversible haemorrhagic shock, is absent or attenuated in the absence of vasopressin or angiotensin. The consequences of this on the development of irreversibility are discussed.
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PMID:On the role of vasopressin and angiotensin in the development of irreversible haemorrhagic shock. 437 70