Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.6.1.1 (adenylate cyclase)
19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II can elicit cellular responses by 2 different receptor-dependent mechanisms: increase in intracellular calcium or inhibition of adenylate cyclase activity. The well-known inhibition of renin release from granulated cells of the kidney is thought to be mediated by an increase in intracellular calcium. However, the participation of the other possible pathway, i.e. inhibition of adenylate cyclase, has not been excluded. We studied this question by using the toxin from Bordetella pertussis, which inactivates the inhibitory coupling units Ni and thus permits to identify hormonal actions mediated through inhibition of adenylate cyclase. In isolated perfused kidneys from rats pretreated with pertussis toxin (2 micrograms/100 g i.v., single injection) the inhibition of renin release by angiotensin II (10(-11) to 10(-8) M) was significantly attenuated. In parallel, the vasoconstrictor response to angiotensin II was also diminished in these rat kidneys. The effect of pertussis toxin was apparent 3, 5 and 10 days after treatment, with a maximal effect at the fifth day. These data suggest that angiotensin II may exert the inhibitory effect on renin release in part through inhibition of adenylate cyclase in granulated cells of the kidney.
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PMID:Pertussis toxin attenuates angiotensin II-induced vasoconstriction and inhibition of renin release. 393 13

The effect of drastic sodium chloride changes (performed by using low-Na diet + furanthril and high-Na diet) on renin-angiotensin-aldosterone system, vasopressin and renal prostaglandins was studied in normal subjects after inhibition of prostaglandin synthesis by indomethacin (0.35 mg/kg three times daily for 13 days). The purpose of the investigation was to evaluate the mechanism of prostaglandin-vasopressin interrelationship. Indomethacin inhibition of PG-synthesis was performed, and after high-Na provocation, an increase of vasopressin and cyclic AMP excretion by 15% and 376% more than that without indomethacin was found. Indomethacin by itself caused sodium retention and antidiuretic effect. The results confirmed the assumption that renal prostaglandins are modulators of renin release from the kidney and that they alternate vasopressin effect on urine concentration, most probably through adenylate cyclase-cAMP system.
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PMID:Humoral factors involved in the regulation of sodium-fluid balance in normal man. II. Effect of indomethacin on sodium concentration, renal prostaglandins, vasopressin and renin-angiotensin-aldosterone system. 609 12

A case of pseudohypoparathyroidism (PHP) associated with several hormonal abnormalities in addition to parathyroid hormone (PTH) was reported. Several endocrinological examinations before and after treatment with 1 alpha-OH-D3 revealed abnormal thyroid stimulating hormone and prolactin responses to thyrotropin releasing hormone, abnormal plasma renin activity responses to renin stimulation test, and abnormal calcitonin responses to calcium infusion test. These abnormalities were not corrected when serum calcium levels returned to normal after therapy. From these results, it was suggested that in PHP resistance to multiple hormones that worked by stimulating adenylate cyclase might be the cause of these hormonal abnormalities, irrespective of serum calcium levels.
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PMID:A case of pseudohypoparathyroidism (PHP) associated with multiple hormonal abnormalities. 609 49

Using cell cultures rich in renal juxtaglomerular cells we found that a change of the intracellular c-AMP concentration is not a prerequisite for an alteration of the renin secretion rate. Modulators of renin secretion including activators of the adenylate cyclase, however, altered the calcium permeability of the cellular plasma membrane in a way that stimulators of renin secretion lowered the calcium permeability and vice versa. Our results suggest that renin secretion is controlled by the intracellular calcium concentration and not by c-AMP. We postulate that modulators of renin secretion act by changing the calcium permeability of the cell membrane.
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PMID:Is renin secretion governed by the calcium permeability of the juxtaglomerular cell membrane? 609 95

Forskolin, a novel receptor-independent adenylate cyclase activator, stimulated renin release from the isolated perfused rat kidney twofold at 10(-7) M and threefold at 10(-6) M. This stimulation was blocked by angiotensin II but not by the beta-adrenoceptor antagonist atenolol. These findings strengthen the concept that an intracellular increase of 3',5'-cyclic AMP by adenylate cyclase activation can induce stimulation of renin release.
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PMID:Forskolin stimulates renin release from the isolated perfused rat kidney. 612 35

In the isolated perfused rat kidney renin release is increased by physiological agents which stimulate adenylate cyclase activity, such as beta-adrenoceptor agonists, prostaglandins, histamine (histamine H2-receptor mediated) and adenosine (adenosine RA-receptor mediated). The role of adenylate cyclase and cAMP in the stimulatory pathway for renin release was confirmed by the effect of forskolin, a receptor-independent stimulator of adenylate cyclase, which also stimulated renin release. The intracellular calmodulin-calcium complex was identified as part of an opposing inhibitory pathway. This conclusion is based on the observation that various inhibitors of calmodulin stimulated renin release and that the calcium-dependent inhibition of renin release by angiotensin II was abolished in the presence of these inhibitors. The intracellular control mechanisms for renin release are discussed with respect to the vascular smooth muscle origin of renin-producing cells.
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PMID:Cellular mechanisms of renin release. 613 89

These experiments were designed to elucidate which of two second messengers (cyclic 3',5' adenosine monophosphate [c-AMP]; intracellular calcium [Cai]) was more closely related to the renin secretory process. The rat renal cortical slice preparation was used. Agents which previously were shown to inhibit basal renin secretion by increasing Cai (ouabain, vanadate, angiotensin II, antidiuretic hormone, and 60 mM K) antagonized and/or blocked isoproterenol-stimulated secretion, which is thought to be mediated by adenylate cyclase activation and increased levels of c-AMP. The stimulatory effect of dibutyryl c-AMP was antagonized and/or blocked by the same agents which antagonized and/or blocked isoproterenol-stimulated secretion. Thus, the inhibitory effects of these agents on isoproterenol-stimulated secretion cannot be explained by a Ca-induced decrease in c-AMP production. Secretory rate was stimulated by a potent phosphodiesterase inhibitor (3-isobutyl-1-methylxanthine). A combination of this and dibutyryl c-AMP produced even greater stimulation. Ouabain blocked the stimulatory effect of this combination. These results are not consistent with an invariant direct relationship between c-AMP and renin secretory rate, but are consistent with an inverse relationship between Ca; and renin secretion. Further, they are consistent with the hypothesis that in isoproterenol-stimulated renin secretion. c-AMP is the second and Cai the third or the final messenger.
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PMID:Isoproterenol-stimulated renin secretion in the rat: second messenger roles of Ca and cyclic AMP. 617 94

Prostaglandins have been hypothesized to have several mechanistic functions in sympathetically mediated release of renin. The rabbit renal cortical slice system was chosen to examine the prostaglandin dependency of renin release directly stimulated by either a direct adenylate cyclase activator, forskolin, or a beta-agonist, isoproterenol. In this study, we demonstrate that with forskolin (1 X 10(-5) M) or isoproterenol (1 X 10(-6) M), renin release was elevated 2-3 fold above control, and that this increase was shown to accompany a substantial increase in the tissue levels of cAMP (19.5 fold and 3.5 fold respectively). We also demonstrate that the increase in renin release produced by these compounds was not inhibited by cyclooxygenase inhibitors, indomethacin (25 microM) or eicosatetraynoic acid (30 micrograms/ml), nor was it inhibited by the selective prostacyclin synthesis inhibitor, U-51605 (30 micrograms/ml). Each of these inhibitors was demonstrated to block the synthesis of prostaglandins in the cortical slices at the concentrations used. Thus we propose that prostaglandins do not play a role in the induction of renin release resulting from elevated cyclic nucleotide levels or beta-adrenergic stimulation.
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PMID:The effect of prostaglandin synthesis inhibition on the direct stimulation of renin release from rabbit renal cortical slices. 632 90

The effects of dopamine (DA) on the smooth muscle fibres of the renal vascular bed are complex. They involve the postsynaptic alpha- and beta-adrenoceptors as well as the dopamine ones. On denervated kidney, in presence of alpha- and beta-blockers, intrarenal DA perfusion provokes vasodilation, increases natriuresis and stimulates renin secretion. The vasodilator effect of DA on the renal vascular bed was studied thanks to an isolated perfused rat kidney preparation which, when high concentrations of phenoxybenzamine and sotalol were present, made it possible to measure the effect of dopaminomimetics and dopaminolytics on the renal vascular resistance of a kidney previously vasoconstricted by continuous PGF2 alpha perfusion. (+)--Butaclamol and cis-flupenthixol proved to be invaluable tools to demonstrate the specificity of the dopamino-agonists response, since both shift the dose-response curve according to the criteria for competitive antagonism at doses at which their isomers are not active (fig. 2). Thus, it was possible to calculate the apparent pA2 for the various dopaminolytics and to classify them according to their affinity for the renal vascular dopamine receptors. Table 1 gives the classification. Flupenthixol, which has only a low affinity for the alpha 2-adrenoceptors, already inhibits the vasodilator effect of DA at 10(-8) M. The low stereospecificity of the enantiomers of sulpiride allows a distinction to be drawn between the "postsynaptic" vascular dopamine receptors and the presynaptic ones. The agonists of the renal vascular dopamine receptors provoked dose-dependent renal vasodilation on our preparation when phenoxybenzamine and sotalol were present and this was stereoselectively inhibited by (+)-butaclamol. Table II shows the activity of the dopaminomimetics meeting these criteria. p-Tyramine, di-propyl-m-tyramine and RU 24926 proved to have no dopaminomimetic effect. Their lack of activity seems to be attributable to the suppression of the hydroxyl in position 4. Mesenteric, splenic or cerebral artery preparations were also used to characterize the vascular dopamine receptors : tables III and IV compare the results taken from the literature. The classification obtained tallies quite well which suggests that the dopamine receptors located in the various vascular beds are identical. We compared the characteristics of the renal vascular dopamine receptor established from isolated rat kidney, with three other pharmacological models of dopamine receptor : the activation of dopamine-sensitive adenylate cyclase, the presynaptic modulation of the transmission of the sympathetic influx, and prolactin release (Table V).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pharmacologic characteristics of renal dopaminergic receptors: therapeutic perspectives]. 636 99

In this study we examine the role of membrane-permeable ions in renin secretion from renal juxtaglomerular (JG) cells. To this end, extracellular Cl- (100 mmol/l) in the culture medium of isolated mouse renal JG cells was replaced by the permeable anion NO3- or by the membrane-impermeable anion isethionate. Alternatively, extracellular Na+ (100 mmol/l) was substituted by the membrane-impermeable cation choline. The effects of these ion substitutions on basal and stimulated renin secretion were then examined. Renin secretion was stimulated by the adenylate cyclase activator forskolin (10 microM), the NO donor sodium nitroprusside (SNP, 100 microM), the calmodulin antagonist calmidazolium (10 microM), by lowering extracellular Ca2+ concentration ([Ca2+]e) with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) (2 mM), and by increasing [Ca2+]e from the normal value of 0.5 to 3 mM. Substitution of extracellular Cl- by isethionate, but not by NO3-, inhibited basal renin release over 20 h of incubation. NO3- also did not change renin secretion stimulated by forskolin, SNP, calmidazolium, EGTA, or by increased [Ca2+]e. Isethionate, on the other hand, markedly attenuated the effects of EGTA and of increased [Ca2+]e, but not the stimulatory effect of forskolin, calmidazolium, or SNP. Substitution of Na+ by choline also attenuated basal renin secretion and renin secretion stimulated by lowering or raising [Ca2+]e. These findings suggest that, with respect to the dependency on permeable ions, at least two different pathways of regulated renin secretion from JG cells exist: a cation- and anion-dependent Ca(2+)-related pathway and a less ion-sensitive pathway for renin secretion activated by adenosine 3',5'-cyclic monophosphate and NO.
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PMID:Role of membrane-permeable ions in renin secretion by renal juxtaglomerular cells. 763 33


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