Subject(s)
Kidney Tubules, Proximal/physiology , Kidney/physiology , Prostaglandins/pharmacology , Sodium/metabolism , Animals , Blood Proteins/analysis , Cyclic AMP/biosynthesis , Depression, Chemical , Diuresis/drug effects , Dogs , Glomerular Filtration Rate/drug effects , Hydrostatic Pressure , In Vitro Techniques , Kidney Cortex/metabolism , Kidney Medulla/metabolism , Lymph , Natriuresis/drug effectsABSTRACT
Parathyroid hormone increased basal adenyl cyclase activity and that increase was inhibited by prostaglandin E(1) (PGE(1)). Tissue cyclic 3',5'-adenosine monophosphate (cyclic AMP) concentrations were increased by parathyroid hormone and that increase was likewise inhibited by PGE(1). Both parathyroid hormone and dibutyryl cyclic AMP increased (32)P incorporation into renal cortical phospholipids. PGE(1) diminished the effect of parathyroid hormone but not dibutyryl cyclic AMP to influence that parameter. PGE(1) likewise modulated the effect of parathyroid hormone but not dibutyryl cyclic AMP to decrease fractional phosphate reabsorption by the renal tubule. It is suggested that PGE(1) inhibits the effect of parathyroid hormone by decreasing its effect on adenyl cyclase. Such interaction may be important in modulating the intracellular action of parathyroid hormone on kidney cortex.
Subject(s)
Kidney/drug effects , Parathyroid Hormone/antagonists & inhibitors , Prostaglandins/pharmacology , Adenylyl Cyclases/metabolism , Animals , Carbon Isotopes , Cyclic AMP/metabolism , Cyclic AMP/pharmacology , Dogs , Dose-Response Relationship, Drug , Injections, Intra-Arterial , Injections, Intravenous , Kidney Cortex/drug effects , Kidney Cortex/physiology , Kidney Tubules/physiology , Male , Methods , Parathyroid Hormone/administration & dosage , Parathyroid Hormone/pharmacology , Phosphates/metabolism , Phospholipids/biosynthesis , Phosphorus Isotopes , Prostaglandins/administration & dosage , Rats , Stimulation, ChemicalABSTRACT
Catecholamines have several physiological effects on the kidney. These include: (a) stimulation of renin synthesis in the cortex: (b) antidiuresis by beta adrenergic agents; and (c) diuresis by alpha adrenergic stimulation. The role of cyclic 3',5'-adenosine monophosphate (cyclic AMP) in the renal actions of catecholamines was evaluated by measuring the effects of several adrenergic agents on cyclic AMP concentration in the dog kidney. Beta adrenergic activity increased cyclic AMP concentration in the renal cortex, a finding consistent with the hypothesis that beta-adrenergic stimulation augments renin synthesis by increasing cyclic AMP generation. Beta adrenergic stimulation, like vasopressin, increased cyclic AMP concentration in the renal medulla. This suggests that beta adrenergic stimulation causes antidiuresis by augmenting cyclic AMP generation in the renal medulla. Alpha adrenergic activity inhibited the effect of vasopressin to stimulate cyclic AMP generation. These results support the hypothesis that the diuretic effect of alpha adrenergic stimulation is mediated by inhibition of the effect of vasopressin to increase cyclic AMP generation.
Subject(s)
Cyclic AMP/biosynthesis , Drug Antagonism , Epinephrine/pharmacology , Kidney/metabolism , Phentolamine/pharmacology , Propranolol/pharmacology , Theophylline/pharmacology , Vasopressins/antagonists & inhibitors , Animals , Dogs , Kidney/enzymology , Norepinephrine/pharmacology , Parathyroid Hormone/pharmacology , Phosphodiesterase Inhibitors , Prostaglandins/pharmacology , Receptors, Adrenergic , Stimulation, ChemicalABSTRACT
Vasopressin increased adenyl cyclase activity in homogenates of both inner and outer renal medulla of the rat. It also increased the concentration of cyclic 3',5'-adenosine monophosphate (AMP) in slices of both inner and outer medulla but not in renal cortex. In the inner medulla, a concentration of prostaglandin E(1) (PGE(1)), which was ineffective by itself significantly reduced the stimulation of adenyl cyclase activity and cyclic AMP concentration induced by vasopressin. These results are consistent with the hypothesis that PGE(1) can compete with vasopressin for adenyl cyclase-binding sites. However, the findings in the outer medulla suggest the situation is more complex. Although 10(-8) M PGE(1) had no effect by itself and inhibited the vasopressin-induced elevation of cyclic AMP, larger amounts of PGE(1) increased both adenyl cyclase activity and cyclic AMP levels. The maximum effect on the latter parameter was at least 6 times as great as that of maximum amounts of vasopressin.
