Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method of preparing a suspension of cells of the zona glomerulosa from rat adrenal capsules treated with crude collagenase is described. The cells responded to ACTH, angiotensin II and serotonin by increased production of aldosterone. Pooled human sera or individual human sera (from healthy normal or non-psychiatric in-patients) to a final concentration of 30% had no effect on ACTH-stimulated production of aldosterone. Many serum samples from five patients with manic-depressive psychosis, however, caused a reduction in aldosterone production; 65% of those samples taken during depression, 44% of the samples taken during manic episodes and 23% of the samples taken when the mood was normal. Sera from manic-depressive patients also reduced the production of aldosterone caused by angiotensin II or serotonin. This effect of serum from manic-depressives in vitro may be related to the abnormalities of aldosterone control in such patients.
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PMID:Inhibition of aldosterone production in adrenal cell suspensions by serum from patients with manic-depressive psychosis. 21 27

Among the newer antihypertensive agents are the beta-blocking drugs, such as propranolol. These agents are useful as second-step drugs to be used if diuretic therapy alone is not effective. In mild to moderately severe hypertension, propranolol, in does of up to 480 mg/day in combination with a thiazide diuretic, has been found to be effective in over 80% of patients on long-term therapy. This degree of response is essentially similar to that noted with a combination of reserpine and a diuretic agent. Although some observers believe that propranolol produces many fewer side effects than the other step 2 drugs (reserpine and alpha-methyldopa), there are some patients who do experience restlessness, insomnia, and depression. Clonidine may be substituted for another step 2 drug, is of moderate potency, but may not be tolerated by a large number of patients because of the severe dry mouth and drowsiness that it produces. Prazosin appears to be a suitable substitute for hydralazine as an effective vasodialator if thiazides plus propranolol or thiazides plus reserpine or alpha-methyldopa are not effective. In some instances, it many be an acceptable second-step drug because of its alpha-adrenoreceptor-blocking properties. The angiotensin II competitive inhibitors or converting enzyme inhibitors may in the future have some place in the management of hypertension.
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PMID:Propranolol and newer antihypertensive drugs in the management of hypertension. 42 60

The changes in breathing accompanying increases in arterial pressure caused by intravenous injections of angiotensin II were examined in dogs anaesthetized with chloralose, and in unanaesthetized rabbits. They were compared with the effects on breathing caused when the alpha-adrenergic vasoconstrictor, phenylephrine, or inflation of an aortic balloon were used to raise blood pressure to comparable levels. Phenylephrine and balloon inflation always depressed breathing: this depression was secondary to the increase in arterial pressure and was abolished by denervation of the arterial baroreceptors. In every animal ventilation was greater with angiotensin II than it was at a comparable blood pressure achieved with phenylephrine or balloon inflation. When compared with control levels of ventilation, however, angiotensin II sometimes caused an increase in breathing, sometimes a reduction, and sometimes had little effect. When both carotid sinus and vagus nerves were cut, angiotensin II consistently stimulated breathing. This shows that angiotensin II has an independent stimulating effect on ventilation which cannot be attributed to inhibition of any baroreceptor-mediated respiratory restraint nor to stimulation of either arterial chemoreceptors or intrathoracic receptors which run to the CNS through the vagus.
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PMID:Respiratory stimulation by angiotensin II. 44 87

We present evidence in accord with the observations of S. Kalsner (Br. J. Pharmacol. 36: 582-593, 1969) that in the rabbit aorta, desoxycorticosterone (DOC) potentiates the contractile response to certain catecholamines by inhibiting their degradation by catechol-O-methyltransferase. In contrast, DOC depresses the contractile responses in rat aorta and tail arteries. To elucidate the mechanism of this depression the effect of DOC was evaluated under various conditions. DOC depressed the contractile response to epinephrine, phenylephrine, KCl, and angiotensin II. The depression was unaltered by ouabain or by a potassium-free solution, indicating that DOC did not produce its depression by altering Na-K-ATPase activity. The depression is unaltered in a chloride-free solution, demonstrating that the DOC effect is not caused by a change in membrane permeability to chloride. Radioisotope studies demonstrate that DOC does not alter membrane permeability to potassium. Removal of extracellular calcium with EGTA (ethylene glycol-bis (beta-aminoethyl ether) N, N'-tetraacetic acid) significantly reduced the magnitude of the DOC depression. Indirect evidence is presented suggesting that DOC might increase calcium binding to the plasma membrane, resulting in its stabilization and hence in a depression of the contractile response.
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PMID:In vitro effects of desoxycorticosterone on vascular smooth muscle. 46 13

The undecapeptide eledoisin caused vigorous and copious drinking within a minute or two of injection into the pigeon forebrain. Systemic injections of the same doses were ineffective. The relative efficacy of eledoisin and angiotensin II as dipsogens in the pigeon was similar to that of carbachol and angiotensin II in the rat. The related peptides eledoisin hexapeptide, physalaemin and substance P also caused some drinking, but they were less effective than eledoisin. In the rat none of these substances caused drinking. On the contrary eledoisin and substance P were found to depress angiotensin-induced drinking, but carbachol-induced drinking was not depressed to the same extent by these peptides. The preferential depression of angiotensin II-induced drinking resembles the effects of other vasoplegic drugs on this response in the rat, and may be related to the potent vasodilator properties of these peptides.
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PMID:Eledoisin, substance P and related peptides: intracranial dipsogens in the pigeon and antidipsogens in the rat. 67 89

1. Dose-response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2-5% (w/w) or 0-007% (w/w) sodium and administered in various sequences. 2. Dose-response curves were shifted to the left in rats on a high-, compared with a low-, sodium intake. This response was maintained for 7 days on changing from high to low sodium. 3. There was no difference in the relation between the fall of cardiac output and the rise of blood pressure in any of the experimental groups. 4. Dose-response curves for peripheral resistance showed the same directional change as seen for the pressor response in rats on high- and low-sodium diets. Since depression of cardiac output was proportional to the pressure rise, the absolute change in peripheral resistance was greater than the blood pressure response. The proportional changes were similar. 5. It is concluded that alterations in the pressor response to angiotensin caused by changes in sodium loading are attributable to changes in peripheral resistance and not to changes in the cardiac output response to the acute rise in blood pressure.
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PMID:The effect of dietary sodium intake on the blood pressure and cardiac output responses to angiotensin II in unanaesthetized rats. 88 29

Left ventricular injection of meglumine diatrizoate caused an initial (1-10 minute) decrease in renal vascular resistance followed by a late (30-minute) increase in renal vascular resistance. The late renal vasoconstrictor response was not blocked by bilateral cervical vagotomy, by renal adrenergic blockade or by renal alpha adrenergic receptor blockade; it was blocked by prior extracellular fluid volume expansion and blockade of the response of the kidney to angiotensin II. There was no effect on intrarenal distribution of blood flow. In the kidney perfused at constant flow, injections of meglumine diatrizoate into the kidney resulted in early renal vasodilation (1-5 minutes) with a return to control renal vascular resistance by 7 minutes; no vasoconstriction was observed. The renal vasodilatation was not abolished by prior treatment with atropine. Vasodilator responses identical to those observed with meglumine diatrizoate were obtained with 4.5% NaCl (equiosmolar to meglumine diatrizoate); no response was obtained with 0.9% NaCl. When given into either the left ventricle or the renal artery, meglumine diatrizoate caused an early reversible depression in renal extraction of para-aminohippurate; both 0.9 and 4.5% NaCl were without effect. The renal vasodilation produced by meglumine diatrizoate initially appears to be caused by its hyperosmotic properties; the late renal vasoconstrictor response appears to be mediated via an activation of the renin-angiotensin system. The depressive effect of meglumine diatrizoate on the renal extraction of para-aminohippurate is not related to its osmotic properties but rather to an effect of the organic iodinated molecule on cellular transport of para-aminohippurate.
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PMID:The renal vascular effects of meglumine diatrizoate. 115 40

Inotropic effects of angiotensin II were studied in 26 anesthetized dogs with different conditions of autonomic activity. The values of maximal velocity of contraction (Vmax TP) were compared before and 10 minutes after the arterial pressure was elevated by the infusion of the drug. In eight dogs, previously treated with atropine and reserpine, the administration of angiotensin had no effect on mean values of Vmax TP. Nine animals submitted to ganglionic blockade by hexamethonium presented an improvement of myocardial contractility when angiotensin was infused. In nine dogs studied with intact nervous system, infusion of the drug was accompanied by decrease of mean values of the index. It was concluded that the polypeptide exerts no important physiological effects upon myocardial contractility without the mediation of the autonomic nervous system. It was considered that the positive inotropic effect verified in dogs under ganglionic blockade was due to adrenergic hyperactivity induced by angiotensin. The depression of the contractile state observed in intact animals was supposed to be mediated by variations of autonomic nervous system activiity consequent to baroreceptor reflex.
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PMID:Role of the autonomic nervous system in the inotropic variations induced by the infusion of angiotensin II. 123 24

Elementary Na+ currents were recorded at 19 degrees C in cell-attached and inside-out patch-clamp experiments to study the influence of the vasoactive peptide angiotensin II (A II) and of the diacylglycerol analogue OAG (1-oleoyl-2-acetyl-sn-glycerol) on open probability and gating properties of single cardiac Na+ channels from cultured neonatal rat cardiocytes. Treating the cardiocytes with A II caused Na+ channel activation: reconstructed peak INa increased to 137 +/- 17.5% of control at 3 mumol/liters and to 176 +/- 42% at 30 mumol/liter. This NPo increase developed without major changes in open state and burst activity, even at 30 mumol/liter. OAG (6 mumol/liter) did not mimic this A II action. By contrast, OAG treatment of the cardiocytes had the opposite effect on NPo and diminished reconstructed peak INa to 67 +/- 4.9% of the control. The putative protein kinase C inhibitor staurosporine (0.2 mumol/liter) abolished this INa depression and led to a normalization of NPo. OAG had the same effect on isolated Na+ channels. Exposure of the cytoplasmic surface of inside-out patches to 1 mumol/liter OAG reversibly depressed, in the simultaneous presence of 50 mumol/liter Mg-ATP, the reconstructed peak INa to 40 +/- 9.7% of the control but left unit, tau open and burst activity unaffected. No NPo depression was obtained in the absence of Mg-ATP indicating that Mg-ATP may serve as phosphate donor. Obviously, after phosphorylation by protein kinase C, cardiac Na+ channels attain a reduced open probability but appear to preserve their kinetic properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Opposite effects of angiotensin II and the protein kinase C activator OAG on cardiac Na+ channels. 133 16

Cardiac hypertrophy is an adaptive response to an increased load imposed on the myocyte which allows the heart to perform increased work while maintaining normal myocardial fiber stress and shortening in systole. A deleterious consequence of pressure-overload hypertrophy is the prolongation of Ca(2+)-sensitive force inactivation (impaired myocardial relaxation) which is related to intrinsic alterations in cytosolic Ca2+ transport and reuptake in diastole. Additional factors appear to adversely modify myocardial relaxation in the hypertrophied heart, including the imposition of ischemia. There is also evidence that the expression and activity of the cardiac tissue renin angiotensin system (RAS) may be modified in the hypertrophied heart and contribute to diastolic dysfunction. Recent studies have demonstrated the presence of increased cardiac angiotensin converting enzyme (ACE) mRNA expression and activity in animal models of hypertrophy, including the aortic-banded rat with compensatory pressure-overload hypertrophy and rats with post-infarction remodeling. In the beating, isovolumic aortic-banded rat heart, the increased intracardiac activation of angiotensin I to II has been shown to be associated with a dose-dependent depression of diastolic relaxation. Preliminary studies suggest that the depression of diastolic function by angiotensin II in the hypertrophied heart can be prevented by the specific inhibition of cardiac ACE. In addition, the well-recognized susceptibility of the hypertrophied heart to severe ischemic diastolic dysfunction also appears to be favorably modified by the inhibition of cardiac ACE activity. The mechanisms responsible for the adverse effects of angiotensin II on diastolic relaxation in the hypertrophied heart are likely to be complex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: current concepts. 133 63


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