ABSTRACT
Dopamine and adenosine both regulate transport of sodium chloride in the renal tubules in mammals. We have studied the effect of dopamine and adenosine on spontaneous activity of contractile vacuole of Amoeba proteous. Both substances stimulated contractile vacuole. The effect of dopamine was suppressed by D2 receptor antagonist, haloperidol, but not by D1 antagonist, SCH 39166. Adenylate cyclase inhibitor, 2.5-dideoxyadenosine, suppressed the effect of dopamine, but not of adenosine. Inhibitor of protein kinase C, staurosporine, in contrast, blocked the effect of adenosine, but not dopamine. Notably, dopamine opposed effect of adenosine and vice versa. These results suggest that similar effects of dopamine and adenosine could be mediated by different intracellulare mechanisms.
Subject(s)
Adenosine/pharmacology , Amoeba/drug effects , Dopamine/pharmacology , Vacuoles/drug effects , Water-Electrolyte Balance/drug effects , Adenylyl Cyclases/metabolism , Amoeba/metabolism , Benzazepines/pharmacology , Biological Transport , Dideoxyadenosine/pharmacology , Dopamine D2 Receptor Antagonists/pharmacology , Haloperidol/pharmacology , Protein Kinase C/metabolism , Protein Kinase Inhibitors/pharmacology , Receptors, Dopamine D2/metabolism , Staurosporine/pharmacology , Vacuoles/metabolism , Water-Electrolyte Balance/physiologyABSTRACT
In the process of evolution, such compensatory reactions as enhanced reabsorption of sodium chloride and an increase of arterial pressure could be formed only for compensation of acute pathological states (blood loss, dehydration). At present they remain similarly adequate in acute disturbances of blood circulation and of water-electrolyte balance. However, in severe chronic pathology of heart and kidney they often lose their compensatory function and even become dangerous. Evolution of human and of human society has created novel social conditions of adaptation. They are of humanitarian and technogenic character by promoting prevention and treatment of diseases.
Subject(s)
Biological Evolution , Disease , Kidney , Sodium Chloride/metabolism , Adaptation, Physiological , Blood Circulation/physiology , Blood Pressure/physiology , Glomerular Filtration Rate , Humans , Kidney/blood supply , Kidney/physiopathology , Kidney Tubules/blood supply , Kidney Tubules/physiology , Water-Electrolyte Balance/physiologyABSTRACT
Acetylcholine (ACh, 1 microM) stimulates activity of the contractile vacuole of proteus. The effect of ACh is not mimicked by its analogs which are not hydrolyzed by acetylcholinesterase (AChE), i. e., carbacholine and 5-methylfurmethide. The effect of ACh is not sensitive to the blocking action of M-cholinolytics, atropine and mytolone, but is suppressed by N-cholinolytic, tubocurarine. The inhibitors of AChE, eserine (0.01 microM) and armine (0.1 microM), suppress the effect of ACh on amoeba contractile vacuole. ACh does not affect activation of contractile vacuole induced by arginine-vasopressin (1 microM), but it blocks such effect of opiate receptors agonist, dynorphin A1-13 (0.01 microM). This effect of ACh is also suppressed by the inhibitors of AChE. These results suggest that, in the above-described effects of ACh, AChE acts not as an antagonist, but rather as a synergist.
Subject(s)
Acetylcholine/pharmacology , Acetylcholinesterase/pharmacology , Amoeba , Cholinergic Antagonists/pharmacology , Cholinesterase Inhibitors/pharmacology , Narcotic Antagonists , Nicotinic Antagonists/pharmacology , Vacuoles , Acetylcholinesterase/metabolism , Amoeba/drug effects , Amoeba/physiology , Armin/pharmacology , Atropine/pharmacology , Carbachol/pharmacology , Dynorphins/pharmacology , Motor Activity/drug effects , Muscarine/analogs & derivatives , Muscarine/pharmacology , Physostigmine/pharmacology , Tubocurarine/pharmacology , Vacuoles/drug effects , Vacuoles/physiologySubject(s)
Amoeba/physiology , Rana temporaria/physiology , Receptors, Vasopressin/physiology , Water/metabolism , Animals , Arginine/pharmacology , Biological Transport/drug effects , Cell Membrane/chemistry , Cell Membrane/drug effects , Cell Membrane/metabolism , Epithelium/chemistry , Epithelium/drug effects , Epithelium/metabolism , Receptors, Vasopressin/analysis , Receptors, Vasopressin/drug effects , Signal Transduction , Urinary Bladder/cytology , Urinary Bladder/drug effects , Urinary Bladder/metabolism , Vasopressins/pharmacologyABSTRACT
Intraperitoneal administration of marinobufagenin resulted in a reliable and dose-dependent suppression of ethanol self-administration in drug- and experimentally naive DBA/2 mice. The findings suggest that Na/K-ATPase contributes to both mediation of the ethanol reinforcing properties and the mood regulation.
Subject(s)
Alcohol Drinking , Bufanolides/pharmacology , Conditioning, Operant/drug effects , Enzyme Inhibitors/pharmacology , Reinforcement, Psychology , Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors , Alcohol Drinking/psychology , Animals , Male , Mice , Mice, Inbred DBASubject(s)
Arginine Vasopressin/pharmacology , Urinary Bladder/metabolism , Urothelium/metabolism , Water/physiology , Animals , Antidiuretic Hormone Receptor Antagonists , Arginine Vasopressin/physiology , Culture Media , Deamino Arginine Vasopressin/pharmacology , Hydrogen-Ion Concentration , In Vitro Techniques , Osmosis , Rana temporariaABSTRACT
Genistein was shown to potentiate the effects of all the activators of the water flow except the cAMP action. The thyrosine kinase (TK) seems to suppress the hydrosmotic action of arginine vasopressin at the period preceding the cAMP formation and to potentiate this effect afterwards.
Subject(s)
Enzyme Inhibitors/pharmacology , Isoflavones/pharmacology , Protein-Tyrosine Kinases/antagonists & inhibitors , Renal Agents/pharmacology , Vasopressins/pharmacology , Animals , Arginine Vasopressin/pharmacology , Biological Transport/drug effects , Drug Synergism , Genistein , In Vitro Techniques , Protein Kinase C/antagonists & inhibitors , Rana temporaria , Staurosporine/pharmacology , Urinary Bladder/drug effects , Urinary Bladder/metabolism , Water/metabolismSubject(s)
Muscarinic Agonists/pharmacology , Muscarinic Antagonists/pharmacology , Urinary Bladder/drug effects , Vasopressins/pharmacology , Water/metabolism , Adenylyl Cyclase Inhibitors , Animals , Biological Transport/drug effects , Calmodulin/antagonists & inhibitors , Epithelium/drug effects , Neomycin/pharmacology , Rana temporaria , Sulfonamides/pharmacology , Type C Phospholipases/antagonists & inhibitors , Urinary Bladder/enzymology , Urinary Bladder/metabolism , Vasodilator Agents/pharmacologyABSTRACT
The role of protein kinase C (PKC) in the control of vasopressin-stimulated water transport in the frog urinary bladder and its modulation by M2-agonist oxotremorine has been studied. Using the PKC inhibitor, staurosporine we showed that PKC in the region pf the basal membrane suppressed vasopressin-stimulated water transport, whereas PKC in the apical region potentiated this transport. It was also found that from the two types of oxotremorine action on stimulated water transport determined by its concentration only inhibition is mediated through PKC.