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PubMed1981

Characterisation of the cyclic AMP response to thyrotrophin in monolayer cultures of normal human thyroid cells.

The cyclic AMP response to thyrotrophin (TSH) has been investigated in cells prepared from human thyroid tissue obtained during surgery for subtotal laryngectomy, and maintained under in vitro conditions as primary monolayer cultures. When cells were incubated with 1.0 mU TSH/ml, a maximal level of intracellular cyclic AMP was reached after 20 min of incubation in the presence of 0.5 mM 3-isobutyl-1-methyl xanthine (MIX). This level of cyclic AMP was sustained for at least 2 h. Half-maximal stimulation of cyclic AMP was produced by TSH doses of between 1 and 5 mU/ml. In a study of a series of eight groups of monolayer cultures, each derived from a single, different thyroid gland, the mean stimulation of cyclic AMP given by 50 mU TSH/ml was 37.8-fold greater than in non-stimulated cell monolayers. Significant stimulation of 50 microunits TSH/ml was observed in some monolayers and the precision of measurement of TSH was better than 15% over the TSH dose range 0.2-1.0 mU/ml. The magnitude of the cyclic AMP response to TSH was unaffected by the presence in the incubation medium of 20% (v/v) normal human serum. A cyclic AMP response to TSH was still demonstrable in cells that had been maintained for a period of 22 days in monolayer culture, although the response was reduced in comparison with that given by 4-5 day old cultures.

Biological Assay↗

PubMed1983

Effect of multiplication-stimulating activity (MSA) on the cyclic AMP level and proteoglycan synthesis in cultured chondrocytes.

Multiplication-stimulating activity (MSA), a somatomedin purified from conditioned medium of Buffalo rat liver cells, had little effect on the intracellular level of cyclic AMP when it markedly enhanced the synthesis of sulphated glycosaminoglycans in rabbit chondrocytes in culture. In addition, MSA did not inhibit prostaglandin E1- or parathyroid hormone-induced accumulation of cyclic AMP in the chondrocytes. On the contrary, MSA slightly decreased stimulation of cyclic AMP accumulation by prostaglandin in human fibroblasts. Dibutyryl cyclic AMP and MSA increased the incorporation of [35S]sulphate and [3H]serine into proteoglycans synthesized by rabbit chondrocytes, and their effects were additive. These findings suggest that somatomedin and dibutyryl cyclic AMP enhance sulphate proteoglycan synthesis through different mechanisms. The lack of inhibitory effect of MSA on cyclic AMP accumulation may be favourable for producing additive effects with cyclic AMP on proteoglycan synthesis and DNA synthesis in chondrocytes.

Alprostadil↗

PubMed1975

Hyperreactive arterial endothelial cells in atherogenesis and cyclic AMP phosphodiesterase inhibitor in prevention and treatment of atherosclerotic disorders.

The hyperreactive arterial endothelial cells have been introduced in this paper. They are characterized by their ability to transport particles too large for the small holes of the internal elastic lamina locating underneath the endothelial cells, such as carbon particles with the similar size of LDL, floating beta-lipoprotein, Lp(a) and especially of VLDL, into the subendothelial space from the blood stream by their abnormally strong contracting and phagocytosis-like activity. Large particles such as carbon particles with a size of 200 to 700 angstrom are too large to penetrate further through holes of the internal elastic lamina from the subendothelial space to muscular layers of the arterial wall, resulting in stagnating for a long time in the subendothelial space, thus showing the atherogenic property of the hyperreactive arterial endothelial cells. Such endothelial cells appear spotty and streaky in the localized endothelial lining of predominantly susceptible parts to atherosclerosis in susceptible animal species such as rabbit, chicken, and rhesus monkey especially densely in their atheromatous lesions, but do not generally appear in non-susceptible animals to atherosclerosis like rate and dog. They are extremely few in infant rabbit, but increase by age.They appear in hypertensive rat, showing a characteristic distribution even in small groups of arteriessuch as the circle of Willis. Cyclic AMP, and especially dibutyryl cyclic AMP, exhibited an inhibitory effect on the hyperreactivity of those cells. Cyclic AMP phosphodiesterase inhibitors, EG467 and eg626, exhibited a powerful inhibitory effect on the contracting and phagocytosis-like activity of those cells, as in the case of pyridinolcarbamate, which enhances enzymes to produce ATP and inhibits slightly cyclic AMP phosphodiesterase, although its inhibitory effect on cyclic AMP phosphodiesterase is weaker than that of EF467 and EG626. The usefulness of the inhibitors on cyclic AMP phospodiesterase of arterial endothelial cells and platelets and on that of brain, such as EG467 AND EG626, has been suggested in the treatment of atherosclerotic disorders, especially of cerebral atherosclerosis. Some of the hitherto desperate mental disability of the aged seem to be a promising target for treatment with cyclic AMP phosphodiesterase inhibitors.

Actomyosin↗

PubMed1975

Responsiveness of urinary cyclic AMP and phosphate to parathyroid extract in patients with parathyroid disorders.

Responsiveness of urinary cyclic AMP and phosphate to 200 units of parathyroid extract was evaluated in 5 normal subjects, 2 patients with idiopathic hypoparathyroidism, 4 patients with pseudohypoparathyroidism and 3 patients with primary hyperparathyroidism. Among them, 3 patients with pseudohypoparathyroidism were examined prior to and during therapy with vitamin D. Two patients with primary hyperparathyroidism were examined before and after removal of adenomas. In control subjects, percent increase in cyclic AMP after parathyroid extract administration was 7265 plus or minus 3312%, and in phosphate 290 plus or minus 72%. It was found that in idiopathic hypoparathyroidism the response of cyclic AMP was in the normal range, though that of phosphate was higher than normal. In pseudohypoparathyroidism, as distinguished from what Drezner et al. called pseudohypoparathyroidism type II, the response of cyclic AMP was uniformly low, while that of phosphate was variable. Similar results were obtained during treatment with vitamin D. In primary hyperparathyroidism, the responses of both cyclic AMP and phosphate were lower than normal. After removal of adenomas, the response of phosphate became norma., but the response of cyclic AMP rose to a subnormal level in one patient, and remained low in the other. For the diagnosis of pseudohypoparathyroidism, the response in cyclic AMP was considered to be a more reliable index than that in phosphate whether the patient was being treated with vitamin D or not.

Adenoma↗

PubMed1976

Venous plasma cyclic AMP in acute cerebrovascular disease.

Antecubital venous blood was sampled from stroke patients in the presence of disodium ethylenediamine tetraacetate. Plasma was analyzed for cyclic AMP applying a competitive protein binding method without any special pretreatment. In mild hemispheric infarction as manifested by moderate hemiparesis and/or dysarthria, plasma cyclic AMP remained in the normal range (8-18 picomoles/ml). In most of the cases with moderate infarction, the cyclic AMP level was distinctly below the normal range several days after the onset of symptoms. However, cyclic AMP remained in the normal range in severe infarction with signs of brain edema, and in two cases with moderately severe symptoms. One of the two cases suffered from later development of brain edema, and the other revealed a large lesion in brain scintigrams. The sizes of the lesion revealed in brain scintigrams were smaller in the moderate cases and larger in the severe cases, except in one of the cases mentioned above. It appeared that with plasma cyclic AMP levels we could predict the extent of the lesion, and perhaps the subsequent development of impending brain edema in a few days after the onset of cerebral infarction. In moderate cases of cerebral hemorrhage, judged from the consciousness, cyclic AMP decreased to a subnormal level 2-4 days after the onset. In severe cases it remained in the normal range. Subarachnoid hemorrhage showed significantly elevated cyclic AMP levels in the early stage.

Aged↗

PubMed1981

Lack of effect of angiotensin on levels of cyclic AMP in isolated adrenal zona glomerulosa cells from the rat.

The effects of pure [Asp1,Val5]- and [Asn1,Val5]-angiotensin II and also [des-Asp1,Ile5]-angiotensin II (angiotensin III) on cyclic AMP and steroid outputs by dispersed rat capsular cells, comprising 95% zona glomerulosa and 5% zona fasciculata cells, have been studied. The results showed that [Asp1, Val5]-and [Asn1, VAl5]-angiotensin II, at doses between 2.5 X 10(-11) and 2 X 10(-4) mol/l, which produced typical increases in steroidogenesis, failed to increase output of cyclic AMP. This lack of effect was observed whether the nucleotide was measured by radioimmunoassay or by adrenal binding protein and under the same conditions in which 8.4 mM-K+ consistently increased the output of cyclic AMP. Instead the results showed a small but significant decrease in cyclic AMP output with angiotensin II. Similar results were obtained with incubations for 60 rather than 120 min and with medium containing a concentration of 5 or 40 g bovine serum albumin/l. Although the levels of cyclic AMP were generally higher in the presence of the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, the same decrease relative to basal outputs was observed with angiotensin II which increased steroidogenesis. Angiotensin III also failed to increase output of cyclic AMP at doses (2.5 X 10(-9) to 2.5 X 10(-6) mol/l) which produced increases in steroid output equivalent to those with angiotensin II. These results indicate that angiotensin II and III can act through a cyclic AMP-independent mechanism.

Adrenal Glands↗

PubMed1982

Dopamine-induced cyclic AMP increase in canine myocardium, kidney and superior mesenteric artery.

The effect of dopamine on cyclic AMP levels in tissue slices of canine myocardium and kidney, and in chopped superior mesenteric arterial wall was investigated to identify dopamine receptors. Tissues were incubated in modified Krebs-Henseleit Ringer bicarbonate solution at 37 degrees C for 20 min with test drugs, after 20-min preincubation. In the presence of 3-isobutyl-1-methylxanthine (IBMX), dopamine and apomorphine caused dose-dependent increases in cyclic AMP levels in the myocardium, kidney and superior mesenteric artery. Phentolamine significantly intensified the cyclic AMP-increasing effect of dopamine in the superior mesenteric artery, but it did not influence the cyclic AMP increase caused by dopamine or apomorphine in the myocardium and kidney. Propranolol markedly blocked the effect of dopamine on cyclic AMP levels in all tissues studied. Haloperidol slightly inhibited the effect of dopamine and completely blocked the effect of apomorphine in the myocardium and kidney. These data suggest that dopamine increases cyclic AMP levels by activating predominantly beta-adrenergic receptors and partly dopamine receptors in the canine myocardium, kidney and superior mesenteric artery. The present results also suggest that dopamine acts not only on beta-adrenergic and dopamine receptors but also on alpha-adrenergic receptors in the superior mesenteric artery. Contrary to the activation of beta-adrenergic and dopamine receptors, the activation of alpha-adrenergic receptors resulted in a decrease in cyclic AMP levels in this tissue.

1-Methyl-3-isobutylxanthine↗

PubMed1994

Repeated application of anodal direct current produces regional dominance in histamine-elicited cyclic AMP accumulation in rabbit cerebral cortex.

A unilateral 30-min application of anodal direct current to the promotor cortex of rabbits was repeated 10 times, and cyclic AMP accumulation in response to histamine was investigated in slices of different cortical areas. Polarization with 1.0 microA decreased the cyclic AMP accumulation in the cortical area contralateral to the polarization, by which regional dominance in cyclic AMP accumulation was produced in the polarized cortex. In contrast, the regional difference in cyclic AMP accumulation was reversed when 10.0 or 30.0 microA was applied. The histamine-elicited accumulation of cyclic AMP was almost completely inhibited by the selective H2-receptor antagonist cimetidine. These results suggest that repeated anodal polarization regionally alters H2-receptor-mediated cyclic AMP generation in the cortex depending on the intensity of the polarizing currents and this pattern of cyclic AMP accumulation is responsible for the characteristic motor behavior induced by anodal polarization.

Animals↗

PubMed1983

Plasma cyclic AMP responses to adrenaline administration in patients with spinocerebellar degeneration, bronchial asthma, and diabetes mellitus--a preliminary report of a clinical test for detecting beta-adrenergic dysfunctions.

Plasma cyclic AMP responses to adrenaline administration in normal volunteers, patients with spinocerebellar degeneration, bronchial asthma, pulmonary emphysema, and diabetes mellitus were studied. Intramuscular administration of low doses (0.1--0.4 mg/person) of adrenaline caused a dose-dependent increase in plasma cyclic AMP. The increase in cyclic AMP was completely prevented by propranolol, while it was not affected by phentolamine or atropine. In patients with spinocerebellar degeneration, the concentrations of plasma cyclic AMP both before and after adrenaline administration were lower than in normal subjects. In asthmatic patients, the plasma cyclic AMP increase after adrenaline administration was smaller than that of the healthy controls. The plasma concentration of cyclic AMP in patients with insulin-dependent diabetes reached the peak level more slowly than in diabetic patients with dietary control alone. Examining changes in the plasma cyclic AMP level after adrenaline administration appears to be a useful means for assessing the degree of beta-adrenergic dysfunction.

Adult↗

PubMed1989

Role of cyclic AMP in proliferation of lung tissue in organ culture.

The role of cyclic AMP in cell proliferation and division has been the subject of study by a number of investigators in the past 30 years, but the argument of whether cyclic AMP is a negative or a positive regulator has not been settled. We studied the effect of cyclic AMP on proliferation of normal and postpneumonectomized lung tissues in young adult rats by measuring the incorporation of tritiated thymidine into lung DNA in organ culture. In normal lung tissues the incorporation of [3H]thymidine was increased by exogenous dibutyryl cyclic AMP, or by isoproterenol or forskolin to stimulate adenylate cyclase, or by caffeine, which inhibits cAMP phosphodiesterase. The effect of isoproterenol, but not forskolin, was abolished by the beta-adrenergic blocking agent propranolol. The effect of caffeine on [3H]thymidine incorporation was further enhanced in normal lung tissues in the presence of dibutyryl cyclic AMP and in postpneumonectomized lung tissues. Imidazole, a cAMP phosphodiesterase stimulator, also increased [3H]thymidine incorporation in culture, but the effect was not magnified in the presence of exogenous dibutyryl cyclic AMP, nor in postpneumonectomized lung tissues. The data suggest that cyclic AMP acts as a positive regulator in proliferation of lung tissues.

Animals↗

PubMed1992

Rabbits have a circadian rhythm of aqueous humor cyclic AMP.

Rabbits have circadian rhythms of intraocular pressure (IOP) and aqueous flow. The dark phase increases of IOP and flow are associated with increased aqueous cyclic AMP. If the daily rhythm of aqueous cyclic AMP reflects changes of tissue levels of cyclic AMP which mediate one of the mechanisms which control the rhythms of IOP and aqueous flow, then it must be a circadian rhythm as are the rhythms of IOP and flow. A recent report showed no change in aqueous cyclic AMP from 2 hrs before to 2 hrs after the beginning of subjective dark in animals housed in constant dark. Because the increase of intraocular pressure at the same times did persist in constant dark, the authors concluded that a significant portion of the circadian rhythm of IOP is unrelated to cyclic AMP mediated ocular mechanisms. However, if an inhibitor of cyclic nucleotide phosphodiesterase is added to aqueous samples after harvesting by paracentesis, it is possible to show that most of the increase of aqueous cyclic AMP from mid-light phase to mid-dark phase persists in constant dark and is therefore likely to reflect a circadian rhythm of tissue cyclic AMP.

1-Methyl-3-isobutylxanthine↗

PubMed1977

Cyclic AMP and adenyl cyclase in brain tumors.

Some of the regulatory mechanisms of cyclic adenosine monophosphate (AMP) production in human brain tumors were investigated by assessing both cyclic AMP levels and adenyl cyclase activity. A large disparity was found between the levels of cyclic AMP of normal brain and brain-tumor tissue. Cyclic AMP levels were much lower in brain tumors (25.8 pmoles (picomoles)/mg protein) than in normal brain (98.8 pmoles/mg protein). These studies also show that the abnormally low levels of cyclic AMP in tumors parallel those of adenyl cyclase. The mean adenyl cyclase activity of brain tissue was found to be 111.0 pmoles of cyclic AMP/min/mg protein, while that of the tumor was only 23.0 pmoles/min/mg protein. Levels of cyclic AMP and adenyl cyclase activity were inversely related to the degree of malignancy. Attempts to stimulate adenyl cyclase in homogenates of human brain and brain tumors resulted in a similar response in both tissues. Norepinephrone was the most effective stimulant and produced a two- to threefold increase in cyclic AMP production, while histamine had no effect. It is concluded that one of the factors governing tumor growth may be a defect in the adenyl cyclase system.

Adenylyl Cyclases↗

PubMed1978

A rapid, simple determination of plasma cyclic AMP.

Plasma cyclic AMP content was determined without being extracted, using binding protein obtained from rat liver. EDTA was suitable as an anticoagulant for cyclic AMP estimation. Cyclic AMP further added to EDTA plasma was able to be estimated. The estimated values by plasma dilution were almost the same as the expected values. It was thought that the direct assay was useful for determination of plasma cyclic AMP. Isoproterenol (50 microgram/kg, iv) produced an increase of plasma cyclic AMP level accompanied with a decrease of blood pressure and an increase of heart rate in anesthetized dogs. Cyclic AMP level of peripheral venous plasma was 18.6 +/- 1.32 p mole/ml in human (N=25), 21.6 +/- 3.04 P mole/ml in dogs (N=7) and 50.6 +/- 4.59 p mole/ml in rabbit (N=9). Plasma cyclic AMP level of rabbit was higher than those of human and dog.

Animals↗

PubMedDate not supplied

Effects of calcium ions and substances affecting Ca2+ -related mechanisms on histamine-evoked stimulation of cyclic AMP formation in chick pineal gland.

In avian central nervous system (CNS), and particularly in the pineal gland, histamine (HA) potently stimulates synthesis of cyclic AMP in intact tissue, and only weakly affects adenylyl cyclase activity in membrane preparation. In this work, we focussed on calcium (Ca2+) as a possible link in the mechanism through which HA affects cyclic AMP generation in the chick pineal. The problem was studied in two sets of experiments where the action of HA on the pineal cyclic AMP was tested: (1) in the incubation medium containing various compounds influencing Ca2+ influx and/or Ca2+ intracellular concentration/action (Ca2+ -ionophore calcimycin, Ca2+ -channel agonist Bay-K 8644, Ca2+ -channels blockers: diltiazem, verapamil, nifedipine and omega-conotoxin-GVIA, CaCl2, EGTA in the absence of CaCl2 in the incubation medium, as well as calmodulin inhibitors: calmidazolium and W-7), and (2) in a CaCl2-free incubation medium yet containing different concentrations of BaCl2, CdCl2, CoCl2, MgCl2, and NiSO4. The results of the first series were mostly negative; an exception was the inhibiton of the HA-evoked cyclic AMP formation observed in the presence of 5.2 and 10.4 mM CaCl2 In the second series of experiments, divalent cations (however with the exception of Mg2+, which was inactive at concentrations up to 15.6 mM) inhibited the HA-evoked cyclic AMP production, with the following rank order of potency: Cd2+ >> Co2+ >> Ni2+ > Ba2+. The inhibitory effect of CdCl2 was prevented by nifedipine. Taken together, the present data suggest that intracellular Ca2+ -related mechanisms are not of major importance in the HA action on cyclic AMP synthesis in the chick pineal. It could be suspected that the inhibition of the HA-driven cyclic AMP formation by high concentrations of Ca2+, and other divalent cations, probably resulted from their direct inhibitory interaction with the catalytic site of the pineal adenylyl cyclase.

Animals↗

PubMedDate not supplied

Adaptive responses of brain cyclic AMP-generating systems to alterations in synaptic input.

The concept of subsensitivity and supersensitivity as a mechanism of neuronal adaptation to alterations in synaptic activity in the brain is an attractive one. However, the complexity of the central nervous system has made it difficult to determine the cellular basis of apparent changes in neuronal excitability resulting from alterations in synaptic input (cf. ref. 83). It now seems that, at least for inhibitory central pathways in which cyclic AMP-generating systems mediate postsynaptic receptor-responses, alterations in synaptic input lead in rat cortex to predictable super- or subsensitivity of the norepinephrine-sensitive cyclic AMP-systems. Supersensitivity of histamine-sensitive cyclic AMP-systems also occurs in rat cortex as a result of apparent lesions of histaminergic tracts. The reason that supersensitivity does not develop to norepinephrine and histamine in guinea pig cortex after similar "denervations" is not known, but is central to an understanding of the factors involved in the role of cyclic AMP-mechanisms to the adaptive plasticity of the central nervous system. However, even before an understanding of all the factors involved in alterations in cyclic AMP-responses in brain tissue is obtained, studies on the effects of environmental and drug-manipulations can provide insights both into the central roles for cyclic AMP-mechanisms and into the nature of drug action. Clearly, an understanding of the interelationships of synaptic input and adaptive changes in postsynaptic cyclic AMP-systems and the exploitation of such knowledge for the elucidation of central adaptive function is an exciting challenge for future research.

Adenosine↗

PubMed1992

A method to simultaneously investigate histamine-induced cyclic AMP and aminopyrine accumulation in isolated gastric mucosal cells from human biopsies.

A method has been developed to simultaneously measure two parameters of histamine-induced gastric secretion, cyclic AMP and aminopyrine accumulation, in gastric mucosal cells from human biopsies. Histamine stimulated cyclic AMP and aminopyrine accumulation with different time courses. Cyclic AMP production reached a maximum at 30 min, whereas maximal aminopyrine accumulation was obtained after the cells had been incubated for 90 min in presence of 100 mcM histamine. Histamine was more potent in stimulating aminopyrine than cyclic AMP accumulation. The ED50 values for histamine-induced aminopyrine accumulation were estimated to be 0.88 +/- 0.02 and 25.53 +/- 8.75 mcM for cyclic AMP production, respectively. The aminopyrine accumulation was more than half-maximally increased at 1 mcM histamine without significant effects on the cyclic AMP basal level. It remains to be elucidated whether this finding indicates, besides cyclic AMP, the involvement of calcium in histamine stimulus. The histamine H2-receptor antagonists cimetidine and ranitidine inhibited both in vitro parameters, whereas the gastric proton pump inhibitor omeprazole only affected aminopyrine accumulation. Our method might be a valuable tool for in vitro pharmacological and clinical investigations on histamine-induced gastric secretion in human biopsies.

Adult↗

PubMed2005

[Family of AMP-deaminase genes].

AMP-deaminase (AMP-aminohydrolase, EC 3.5.4.6), a highly regulated oligomeric enzyme catalyzing the irreversible deamination of adenylic acid (5'-AMP), is located at a branch point of adenylate nucleotide catabolism. It plays an important role in the stabilization of adenylate energy charge (AEC) and the regulation of the purine nucleotide pool in several types of animal tissue. Tissue- and stage-specific isoforms of AMP-deaminase were described in mammals. In humans, three isozymes of AMP-deaminase, i.e. M (muscle), L (liver), and E (erythrocyte), exhibiting different physical, catalytic, and regulatory properties, were identified. AMP-deaminase activity is encoded by a multigene family in which two genes produce at least three mRNAs through alternative splicing of one of the primary transcripts. In this study we present all found and so far unpublished detailed knowledge about AMP-deaminase gene structures. We also present basic information on the effects of these gene mutations.

AMP Deaminase↗

PubMed1975

Relationship between cyclic AMP metabolism and inotropic response of perfused rat hearts to phenylephrine and other adrenergic amines.

A positive correlation between inotropic response and increment of cyclic AMP levels and labeling (from 14-C-adenine in the perfusate) was found after isoprenaline, dopamine, and phenylephrine alone, and after isoprenaline in the presence of chlorpromazine. 2. a lack of correlation between contractile activity and cyclic AMP levels and labeling was found when the hearts were exposed to phenylephrine in the presence of propranolol. The contractile activity increased, but the parameters for cyclic AMP did not change. These resuls together with findings by other workers indicate that the inotropic response to beta-stimulation always is associated with cyclic AMP accumulation, while the inotropic response to alpha-stimulation (when present) is not correlated to cyclic AMP elevation. Other differences between alpha- and beta-adrenergic effects on heart (course of development of the inotropic response, effect of theophylline on the response, effects on relaxing processes, action potential, and on refractory period) also indicate different mechanisms of action. On the basis of the available data we suggest as a conclusion that the inotropic response after alpha-adrenergic stimulation does not involve cyclic AMP as a mediator whereas beta-adrenergic effects are mediated by cyclic AMP. This means that the naturally occurring adrenergic amines norepinephrine and epinephrine, both of which are able to stimulate both alpha and beta myocardial receptors (twenzel and Su, 1966), elicit the inotropic response through two different mechanisms. Usually the beta-adrenergic effect on the heart is the more important. The contribution from alpha-stimulation, however, may increase under certain conditions: hypothyroidism or proplythiouracil treatment per se (Nakashima et al., 1971) or hypothermia (Kunos and Szentiványi, 1968; Buckley and Jordan. 1970; Benfey et al., 1973; Kunos, Yong, and Nickerson, 1973; Nickerson, 1973). Thus a single physiologic response may be mediated by more than one mechanism. Multiple mechanisms of action for one agent might have more general biologic significance; e.g., they may serve to maintain the responsiveness of a tissue under various conditions.

Animals↗