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)

Clonidine s.c. (0.01-0.3 mg/kg), in unanesthetized rats, caused an initial rise (+20 mm Hg), followed by a continuous fall of BP and a dose-dependent natriuresis and diuresis for up to 2 h. Glomerular filtration rate (GFR) (CIn) increased during the first 20 min, while effective renal plasma flow (ERPF) (CPAH) remained normal. Subsequently, between 20 and 60 min after injection, ERPF (CPAH) decreased considerably while GFR had reverted to its normal value. In saline-infused rats clonidine diuresis was accompanied by an "inappropriate" positive free water clearance. Pentobarbital anesthesia suppressed the initial BP peak and the diuresis. Phenoxybenzamine (1 mg/kg i.v.) was antinatriuretic in saline diuresis; the effect of phenoxybenzamine + clonidine on diuresis and salt excretion represented the sum of the effects of both drugs, but phenoxybenzamine enhanced the clonidine-induced increase of GFR. Neither haloperidol (1 mg/kg i.v.) nor bulbocapnine (3 mg/kg i.v.) interfered with the renal effects of clonidine. Clonidine s.c. caused hyperglycemia and glucosuria which did not account for the natriuresis. Clonidine thus appears to increase the GFR and "filtration fraction" (FF) by a phenoxybenzamine-insensitive rise of glomerular ultrafiltration, to depress ERPF by alpha-adrenergic afferent vasoconstriction, to induce natriuresis by a tubular action not blocked by phenoxybenzamine and to exert an antivasopressin effect, either by depressing pituitary vasopressin secretion or the renal response to vasopressin.
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PMID:The renal effects of clonidine in unanesthetized rats. 4 24

(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

The i.v. bolus of 50 ng kg-1 Arginine-vasopressin administered to adult male rats anaesthetized with Pentobarbital (50 mg kg-1 i.p.) increases the activity of liver glycogen phosphorylase in fed and 24 h fasted rats to the same extent; after 25 ng kg-1 of the drug the enzyme response after fasting is barely detectable, whereas in the fed animals a response similar to that after 50 ng kg-1 persists.
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PMID:Inhibitory effect of fasting on the activation of liver glycogen phosphorylase of rats by arginine-vasopressin. 631 93

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.
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PMID:Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs. 823 67