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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In experiments lasting 8 h, low (0.5 mg kg-1) or medium (5 mg kg-1) subcutaneous doses of the angiotensin-converting enzyme inhibitor captopril were mildly dipsogenic in sham-operated rats, much more so in rats subjected to bilateral ureteric ligation and not at all in bilaterally nephrectomized rats. Rats with ligated ureters drank enough water to gain weight during the experiments. All other groups lost weight. The enhanced responsiveness of rats with ligated ureters, despite fluid retention, shows that captopril-induced drinking was not secondary to increased renal fluid loss. Ureteric ligation alone which caused some increase in renin secretion was mildly dipsogenic compared with sham operation. Captopril caused further increases in plasma renin concentration and more drinking suggesting that the captopril response is renin-dependent. The failure of the nephrectomized rat to drink after captopril also shows that the response is renin-dependent. The highest dose (50 mg kg-1) of captopril did not at first stimulate drinking, though water intake increased later. Slowness to drink was not the result of general depression of behaviour since drinking in response to subcutaneous hypertonic NaCl or intracranial angiotensin II was not inhibited by the highest dose. Slowness to drink after the highest dose was attributable to blockade of converting enzyme centrally as well as peripherally. This meant that the increased circulating angiotensin I resulting from peripheral blockade of converting enzyme was only slowly converted to angiotensin II in the brain. When cerebral conversion of angiotensin I was prevented by a single intracranial injection of 25 micrograms captopril, drinking in response to the lower doses of captopril was also inhibited in normal rats and in rats with ligated ureters. The same intracranial dose of captopril also inhibited drinking in response to intracranial injections of renin or angiotensin I, but not angiotensin II. The time course of inhibition of renin-induced drinking was similar to that of inhibition of subcutaneous captopril-induced drinking. In conclusion, subcutaneous captopril causes increased water intake through activation of the renal renin-angiotensin system, an effect that is enhanced when the system has already been partly activated by ureteric ligation. Increased circulating angiotensin I resulting from blockade of peripheral converting enzyme must be converted to angiotensin II in the brain in order to stimulate drinking. Drinking is not the consequence of increased fluid loss.
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PMID:Renin dependence of captopril-induced drinking after ureteric ligation in the rat. 635 61

The effect of humid heat (Ta = 43 degrees C, Pa = 32 Torr) on sweat rate, plasma renin activity and plasma levels of aldosterone and antidiuretic hormone (ADH) was studied in four male subjects before and after repeated heat exposures. Over-sweating and sweat drippage followed by hidromeiosis were observed in three subjects during initial heat exposure. With repeated humid heat exposures increased sweat rates were accompanied by a more intense sweat depression (hidromeiosis) in all four subjects. In our conditions, no changes in plasma levels of aldosterone and ADH or plasma renin activity were observed with hidromeiosis. Plasma renin activity was slightly depressed by repeated exposures, whereas plasma volumes were enhanced, with no significant changes in plasma Na or K. The results suggest that neither ADH nor the components of the renin-angiotensin aldosterone system are involved in the hidromeiotic phenomenon.
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PMID:Endocrine concomitants of sweating and sweat depression. 637 Jun 92

Superfusion of rat anterior pituitary cell aggregates with 10-min pulses of 0.1-10 nM angiotensin II (AII) resulted in a prompt and concentration-dependent rise of PRL release. The effect could be blocked by saralasin, an AII receptor antagonist. The response to AII, but not that to TRH, was rapidly desensitized: a 10 nM AII pulse caused an 80% depression of the response to a subsequent 10 nM pulse given 50 min later. The data provide a possible functional significance for the renin-angiotensin system recently demonstrated in the anterior pituitary.
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PMID:Stimulation of prolactin release by angiotensin II in superfused rat anterior pituitary cell aggregates. 641 Feb 99

Congestive heart failure is associated with ventricular hypertrophy and dilatation, increased circulating catecholamines, and peripheral vasoconstriction. The extent to which these changes occur, whether they are a favorable "compensatory mechanism" or contribute to cardiocirculatory dysfunction, depends on the cause and severity of the heart failure. The addition of new sarcomeres through ventricular hypertrophy distributes the excess workload of the failing ventricle over more contractile units. In ventricular pressure overload, hypertrophy primarily increases wall thickness and ventricular volume is not usually increased; the converse is true with ventricular volume overload. Hypertrophy can result in enhanced or depressed contractile performance, depending on the stimulus for hypertrophy and method by which contractility is evaluated. The "ventricular function curve," which relates stroke volume to ventricular filling pressure or volume, overestimates the role played by the "Starling principle" as a compensatory mechanism and underestimates how well contractile performance is preserved. The evaluation of end systolic pressure-volume relationships under conditions of variable afterload closely reflects the isometric length-tension relationship and is therefore a more accurate way to quantitate cardiac muscle performance. Pressure overload hypertrophy usually leads to a depression in contractility whereas volume overload may not. An exaggerated sympathoadrenal response is another hallmark of severe heart failure that enhances contractility, helps initiate hypertrophy, and maintains arterial perfusion pressure. A generalized increase in peripheral vascular resistance occurs and is most prominent in those circulations most susceptible to neurohumoral control (renal, splanchnic, cutaneous). This favors perfusion of the cerebral and coronary circulations. Vasoconstriction is further enhanced by the activation of the renin-angiotensin-aldosterone system and secretion of ADH. This results in sodium retention and plasma volume expansion. In early mild heart failure, vasomotor tone may be normal at rest; however, the sympathoadrenal response to exercise may be intense. Moderate alpha receptor stimulation reduces skeletal muscle blood supply and favors the intramuscular redistribution of blood flow from inactive to active muscle fibers, thereby maintaining a normal oxygen consumption. During the later stages of heart failure, increased vascular stiffness due to increased sodium content and excessive norepinephrine appears to restrict nutritional blood flow to exercising muscle at the conductance-vessel level. Vasodilator drugs may reduce aortic impedance and improve cardiac output, may lower ventricular filling pressure, and relieve congestive symptoms, and may result in complex but favorable changes in the distribution of blood flow to the regional circulations.
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PMID:Cardiocirculatory dynamics in the normal and failing heart. 645 90

This study was designed to more selectively investigate the dopaminergic regulation of 18-hydroxycorticosterone (18-OHB) and aldosterone production by the adrenal zona glomerulosa. Mature rhesus monkeys received either an infusion of dopamine (2 micrograms/kg/min) or 5% dextrose (0.2 ml/min) over a 60 min period (N=6). Dopamine had no effect on plasma levels of renin activity, cortisol, corticosterone, aldosterone or blood pressure. However, dopamine suppressed (p less than 0.05) plasma 18-OHB levels from a baseline of 31.6 +/- 3.5 ng/dl to 23.6 +/- 2.1 ng/dl at 60 min after onset of infusion. This observation is in agreement with some studies in humans but differs from others in which no depression in 18-OHB was observed following dopamine infusion. Dopamine infusion markedly (p less than 0.001) suppressed plasma PRL levels by 30 min after onset of infusion. Corticosteroid responses to metoclopramide (200 micrograms/kg) after dexamethasone 1 mg im every 6 h X 5 days or placebo treatment (vehicle im every 6 h X 5 days) was then evaluated. Dexamethasone significantly suppressed basal cortisol, corticosterone, 18-OHB and aldosterone. Although dexamethasone blunted the prolactin response, it did not inhibit the aldosterone response to metoclopramide. The 18-OHB response to metoclopramide was increased (p less than 0.01) following dexamethasone treatment. Following dexamethasone suppression, 18-OHB levels were still lowered (p less than 0.05) by dopamine infusion. These results suggest that dopamine selectively inhibits zona glomerulosa production of 18-OHB and aldosterone in rhesus monkeys.
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PMID:Evidence for direct inhibitory effects of dopamine on zona glomerulosa secretion of 18-hydroxycorticosterone in rhesus monkeys. 672 68

Oral contrceptives (OCs), usd by over 30% of reproductive aged women in Belgium, are by far the most widely used contraceptive in that country. The various types of OCs include monophasic, biphasic, and triphasic combinations of an estrogen and a progestin, sequentials containing estrogen only for 7-14 days followed by a progestin through the 21st day; macrodose or microdose progestin only formulations, 3-month injectable progestins, and the morning after pill. Side effects of OCs are mainly due to metabolic effects on coagulation factors, the renin-angiotensin system, glucose tolerance, or the lipid profile. Users of OCs face increased risks of cholelithiases, thrombophlebitis, thromboembolism, cerebrovascular accidents, myocardial infarcts (among smokers over 35 years of age), and hepatic adenomas. The most troubling secondary effect is the excess cardiovascular morbidity and mortality show by contraceptive users, not just those who are obese, hypertensive, or who have histories of vascular pathology, but also those over 40 years of age and smokers. Lenght of use of OCs does not increase vascular risks. Epidemiologic studies demonstrate that vascular risks are reduced in lower dose formulations. Absolute contraindications to OC use include serious cardiovascular problems, severe hepatic pathology, estrogen-dependent tumors, pregnancy and undiagnosed gynecologic problems, and significant hyperlipidemia. Relative contraindications include severe headaches, cholelithiase, previous cholestasis of pregnancy, severe renal disease, fibromyomas, benign breast disease, age over 40 years, smoking, surgery anticipated within 4 weeks, infectious mononucleosis, falciform anemia, and immediate postpartum and lactation. Epilepsy, diabetes, depression, and varicose veins are not strictly speaking contraindications but require additonal surveillance. Lower dose formulations should be prescribed if possible. OC users should be followed up every 6-12 months. Among other steroidal contraceptive methods, sequential OCs and high dose progestin-only formulations are used for short-term treatment of specific conditions. Progestin-only minipills are used when an OC is desired but estrogens are contraindicated. Injectable progestins should be reserved for patients who for cultural or medical reasons can use no other type of contraceptive. Morning-after pills should not be considered a regular form of contraception. If OCs are used in adolescents, a low dose pill is indicated. Low dose OCs may be indicated for diabetics because of the danger of infection with IUDs and the lesser efficacy of barrier methods. If OCs are used in epileptics, they should be regular dosed because of the danger of drug interactions. Only low-dose formulations and progestin-only minipills should be used by women over 40.
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PMID:[The choice of oral contraception in 1984: general indications and specific cases]. 672 93

The purpose of the study was to investigate the effects on urine flow and osmolar excretion of arachidonic acid (C20:4) infused in the renal artery of anaesthetized rats under conditions in which indomethacin previously was found to reduce urine flow and to prevent the development of a moderate saline diuresis. C20:4 caused a reversible increase in the urinary excretion rates of PGE2 and PGF2 alpha both in hydropenic rats and in rats during a saline diuresis. Renal venous plasma concentration of PGE2 increased significantly while the increase in PGF2 alpha was insignificant. C20:4 infusion was followed by an increase in urine flow and osmolar excretion rate in hydropenic rats, and it augmented urine flow (but not solute excretion) in saline-loaded rats. This latter effect was blunted by indomethacin treatment and inactin anaesthesia. Increased endogenous PG-levels were associated with only a modest (insignificant) increase in renin release under the present conditions. Saline loading acutely depressed PGE2 and PGF2 alpha urinary excretion rates and plasma renin concentration (PRC). The fall in PRC was unaffected by indomethacin. The main conclusions are that endogenous renal PG's have a diuretic effect in the amytal anaesthetized rat, while an effect on osmolar excretion rate is apparent only under hydropenic conditions. Acute saline loading depresses renal PG-synthesis, but this depression is not the only cause of the fall in PRC following saline loading. The saline diuresis is caused by a mechanism(s) not involving prostaglandins.
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PMID:A study of the effect of stimulated endogenous prostaglandin synthesis on urine flow, osmolar excretion rate, and renin release in hydropenic and saline loaded, anesthetized rats. 679 55

The effect of metoclopramide, a procainamide derivative with dopamine antagonistic properties, and L-dopa on plasma renin activity (PRA) was studied in adult rats. Following an intravenous bolus of metoclopramide (200 microgram/kg) to the American Wistar rat there was a significant (p less than 0.05) elevation in PRA at 10 min and a maximum response at 30 min. There was a significant depression (p less than 0.05) in PRA at 15 through 40 min following an intravenous bolus of L-dopa (30 mg/kg). Pre-administration of L-dopa delayed and blunted the PRA response to metoclopramide. However, the PRA response to this dopamine antagonist was not altered by beta blockade with propranolol and alpha blockade with phentolamine. Administration of metoclopramide resulted in considerably greater (p less than 0.01) PRA responses in spontaneously hypertensive rats than in Wistar Kyoto (WKY) normotensive controls. Administration of L-dopa resulted in similar suppression of PRA in the two groups. These results indicate that there is a dopaminergic inhibitory control mechanism for renin secretion. Dopaminergic control of renin release appears to be altered in the spontaneously hypertensive rat.
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PMID:Dopaminergic modulation of renin release. 700 2

The renal clearance of endogenous creatinine, inulin and para-aminohippurate was measured in 10 healthy human volunteers taking aspirin during severe dietary sodium restriction (10 meq/d) to clarify the clinical significance and pathophysiology of aspirin-induced changes in renal function. Sodium restriction alone had no effect on renal clearances but did increase plasma renin activity and urinary prostaglandin E excretion. The addition of aspirin decreased the urinary clearance of prostaglandin E but not plasma renin activity, and caused a significant fall in both endogenous creatinine (from 92.3 +/- 4.1 SE ml/min . 1.73 m2 body surface area to 80.8 +/- 4.4 mL/min . 1.73 m2, p = 0.02) and inulin (from 95.3 +/- 7.0 mL/min . 1.73 m2 to 80.9 +/- 7.0 mL/min . 1.73 m2, p less than 0.001). The fall in inulin clearance was directly related to the salicylate level. The clearance of para-aminohippurate showed only a slight, statistically insignificant decline with aspirin. The results of this study suggest that aspirin-induced depression of glomerular filtration rate may be independent of total renal plasma flow. Aspirin should be used cautiously, with careful attention to dosage, in sodium-restricted patients whose glomerular filtration rate may, in part, be under the homeostatic control of renal prostaglandins.
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PMID:Aspirin-induced depression of glomerular filtration rate in normal humans: role of sodium balance. 701 93

1. Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Increased sodium appetite, characteristic of sodium depletion, was assessed by operant behaviour where scoring of panel pressing for NaHCO(3) rewards showed change in sodium appetite.2. Sodium-depleted calves readily drank the calculated ionic deficit as a hypertonic solution (4 l.) in a few minutes, or as an isotonic solution (16 l.) usually within 30 min.3. When the ionic deficit was restored by either i.v. infusion or drinking, sodium appetite was reduced significantly. The suppression of sodium appetite was more rapid when the depleted ions were replaced by drinking (30 min) than by i.v. infusion (2 hr) but in both circumstances the effect was short lived since sodium appetite redeveloped within 3 hr.4. The rapid return of sodium appetite following restoration of the ionic deficit occurred even when the plasma sodium level was normal. Other biochemical changes resulting from sodium depletion, such as acidosis and reduced salivary sodium, could not be correlated with variation in sodium appetite.5. Rapid infusion of Ringer saline (4 l.) did not inhibit the sodium appetite, which suggests that neither vascular volume changes per se nor vascular baroreceptors control sodium appetite in sodium-deficient calves.Plasma aldosterone fell rapidly following infusion of the hypertonic solution but only slightly with the isotonic infusion. The change in plasma hormone level was not related to changes in sodium appetite.6. Drinking the hypertonic solution produced a marked reduction in panel pressing for NaHCO(3) with a rapid rise in plasma sodium. Consumption of the larger volume of isotonic solution also inhibited sodium intake but plasma sodium remained low. A secondary increase in plasma renin activity (p.r.a.) occurred following ingestion of the hypertonic solution, but both p.r.a. and aldosterone fell to normal levels over the next 6 hr when the cattle again showed marked sodium appetite. It is possible that these effects may be due to ion and fluid movement between gut and extracellular fluid and reflect osmolality changes or tissue dehydration.7. It is concluded that the sodium appetite of sodium deficient cattle is only temporarily alleviated by restoration of the depleted ionic loss, and that the behavioural response to seek sodium rewards is independent of plasma sodium, p.r.a., aldosterone and volume changes in the gut and vascular system.8. Recent reports suggest that sodium appetite may be controlled by receptors in the hypothalamus or by angiotensin II in the brain. In cattle the capacious gut may also be involved, since sodium appetite is inhibited more rapidly when the depleted ions are taken orally than by i.v. infusion.
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PMID:The effect on salt appetite and the renin-aldosterone system on replacing the depleted ions to sodium-deficient cattle. 702 8


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