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)

1. The ability of maturing rats to excrete a sodium load was studied by micropuncture and clearance procedures. 2. During control conditions, no change of glomerular filtration rate or sodium excretion was observed for the time period of the entire procedure (P greater than 0-20). During the infusion of hypertonic (4%) sodium chloride, fractional sodium excretion was 0-08 +/- 0-01 in rats 21-30 days old and 0-14 +/- 0-01 (P less than 0-01) in adults. However, the depression of proximal tubular water re-absorption was equal in both groups (P greater than 0-20). 3. Proximal glomerulotubular balance for water re-absorption was similar in all groups (P less than 0-20). Since end proximal tubular water excretion and depression of fractional water excretion were the same in all animals, differences of urinary sodium excretion during development are probably due to differences of function of segments beyond the proximal tubule during development. 4. Fractional potassium excretion was reduced in young rats (0-17 +/- 0-04) during hypertonic sodium chloride infusion, compared to adults (0-24 +/- 0-01, P less than 0-05). 5. Passage time of fast green through cortical segments in seconds is prolonged in young rats during control conditions. Similar decreases of passage time were seen in all groups during hypertonic sodium chloride infusion. No segmental differences of passage time were seen during developmental. 6. No difference in the relationship between fractional sodium and water excretion was seen during development of the renal response to hypertonic sodium chloride infusion. Thus, altered sensitivity to sodium chloride osmotic diuresis does not exist during maturation in rats.
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PMID:Maturation of the renal response to hypertonic sodium chloride loading in rats: micropuncture and clearance studies. 94 39

Postexcitatory depression (PED) and adaptation were examined in slowly adapting aortic baroreceptors of normotensive rats (NTR) and spontaneously hypertensive rats (SHR); an aortic arch-aortic nerve preparation in vitro was used. PED was elicited either mechanically by employing single or double pressure steps, or electrically by antidromic stimulation of the aortic nerve. During PED the axon of the receptor was capable of conducting action potentials and the receptor itself could respond to increased pressures. The relationship between duration of PED and number of impulses preceding it was hyperbolic. In NTR's and SHR's PED was abolished by ouabain or solutions containing no potassium, neither of which affected the steady state pressure-volume relationship of the aorta. These interventions, which are known to block electrogenic pumps, also lowered the pressure threshold and increased the curvature of the steady state pressure-frequency curve. Furthermore, lithium, another agent that blocks electrogenic pumps, also abolished PED. Thus, PED is attributed mainly to an electrogenic sodium pump which operates normally in baroreceptors. We found that adaptation from peak transient to steady state frequency did not appear to be altered significantly when the pump was blocked. Blockage of the pump by ouabain is responsible for the baroreceptor reflex effects elicited by this drug. We conclude that resetting and reduced sensitivity in SHR baroreceptors are not attributed to significant differences in electrogenic pump activity.
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PMID:An electrogenic sodium pump and baroreceptor function in normotensive and spontaneously hypertensive rats. 96 33

1 The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep. 2 Adrenalectomized sheep were infused with 0.43 M KCl at 2 ml/min for 2-2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute-free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (COsm) and solute-free water reabsorption (TcH2O) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration. 3 After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute-free water reabsorption to values above those anticipated from the pre-vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period. 4 Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returnied to values which approximated the pre-vasopressin relations between plasma potassium and the urinary excretions of these ions. 5 Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant. 6 The large increments in potassium excretion (averaging greater than 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.
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PMID:The effect of high rates of vasopressin administration on renal potassium and sodium excretion during potassium loading in the sheep. 97 79

In 30 experiments in isolated canine hearts perfused with whole donor blood disorders in myocardial contractions were studied following the termination of paired stimulation. It was concluded that the cause of depression of cardiac contractions following paired stimulation is not myocardial hypoxia and energy reserve exhaustion during enhanced mechanical activity of the heart, but a dissociation of the electric and mechanical processes in the myocardium; switching off the second (stand-by) action potential together with the termination of the paired stimulation caused disorders in the regimen of coupling processes that have established themselves under this form of electric stimulation. This suggestion is supported by the fact that repeated paired stimulation during depression is capable of producing the same stimulating effect upon the cardiac contractions as the initial one. The depression was eliminated by the administration of potassium ions and catecholamines.
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PMID:[Analysis of depression of contractions of the isolated dog heart following paired stimulation]. 101 51

To determine the effect of high extracellular potassium concentration ([K]o) on the membrane current of the sinoatrial node cell, voltage clamp experiments were conducted using the double microelectrode technique. When depolarizing clamp pulses were applied, a transient inward current was followed by an outward current and an outward current tail flowed after the pulse. The amplitude of both the transient inward current and the outward current tail were markedly reduced with increasing [K]o, but the magnitude of the outward current during depolarization scarcely changed. The inward current during hyperpolarizing clamp pulses increased in magnitude at higher [K]o and the reversal potential for the inward current change decreased with increasing [K]o. From these results it was concluded that the suppression of the sinoatrial node automaticity at higher [K]o was due to the decrease in magnitude of both the transient inward current and the outward current tail. As the cause of the depression of the transient inward current, its inactivation through depolarization, increased outward leak current and some direct inhibitory effect of K were proposed. The reduction of the outward current tail was attributed to the decrease in the driving force of the K current.
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PMID:Mechanisms underlying cessation of rabbit sinoatrial node pacemaker activity in high potassium solutions. 103 Jul 49

Because of the multiplicity of disease conditions and diminished tolerance for drugs in the aged, it is necessary to know concomitant pathologic conditions to determine which antihypertensive drug to use. In the Philadelphia Geriatric Center, there are about 1,000 residents, between 70 and 100 years of age. About 40% have hypertension; almost 50% have or once had depression; there are many cases of hiatal hernia and/or peptic ulcer; in one subdivision of residents, almost 40% have renal disease with BUN above 30 mg/100 ml. In antihypertensive treatment, some individuals respond fairly well to reassurance and weight reduction, when obese, even without drugs. All are given a low-salt diet. A diuretic is first used--thiazide in cases of good renal function, furosemide with impaired renal function. Liquid potassium supplements are given. If there is but little reduction in blood pressure in several weeks, methyldopa is added in ascending doses, in cases with or without renal impairment. In hypertension with impaired renal function, furosemide and/or methyldopa were especially valuable. Furosemide as an antihypertensive drug was also noted to delay the onset of congestive heart failure. Since reserpine can aggravate peptic ulcer and can precipitate or aggravate depression, it should seldom be used to treat hypertension in the aged. Guanethidine is rarely used, since it can cause cerebrovascular insufficiency and marked weakness. High blood pressure should be reduced slowly in the aged, to avoid untoward effects.
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PMID:An approach to the treatment of hypertension in the aged. 105 27

The effects of meperidine and naloxone, and their interaction effects on action potential production in frog's sartorius muscle fibres, were studied with intracellular micro-electrode techniques. 1. Meperidine, a narcotic analgesic drug, depressed the rate of rise, the rate of fall and the amplitude of the action potentials. 2. At a meperidine concentration of 0-35 mM, the depression in the action potential maximum rate of rise followed a diphasic time course. At first there was a rapid reduction in the maximum rate of rise which was levelling off at about 60% of control 60-90 min after drug application. This was followed by the second phase during which there was an initial rapid decrease in the maximum rate of rise and all surface fibres were inexcitable by 180 min. 3. The addition of naloxone, a narcotic antagonist, in low concentrations (3 X 10(-5) to 3 X 10(-4) mM) at 70-90 min blocked the second phase of the meperidine-induced depression. 4. With lower concentrations of meperidine (0-18 and 0-07 mM) the depression usually developed more slowly (up to 6 hr with the latter dose) and the addition of low naloxone concentrations partially antagonized the effects of meperidine. However, under no conditions was it possible to completely antagonize the effects of meperidine by the addition of naloxone. 5. A linear relation was found between action potential amplitude and the action potential maximum rate of fall. 6. Meperidine caused a shift in the relation of rate of fall against amplitude to higher action potential amplitudes, indicating that the drug inhibited the increase in potassium conductivity (gK) associated with the falling phase of the action potential. 7. When low naloxone concentrations antagonized the effects of meperidine on the rate of rise and restored action potential amplitudes to control levels, the effect of meperidine on the maximum rate of fall was not antagonized. 8. Larger naloxone concentrations (1-5 X 10(-2) mM or more) depressed the action potential rate of rise but did not alter the relation between action potential amplitude and the maximum rate of fall. 9. It is proposed that meperidine blocks action potential production by two mechanisms: (i) a non-specific mechanism in which the increases in both gNa and gK ar depressed and (ii) an opiate drug receptor mediated mechanism causing a specific depression of gNa. 10. The impression gained from the results is that there are opiate drug receptors located on the inner surface of the muscle membrane associated with the 'sodium channels' and that drug activation of these receptors by either meperidine or high naloxone concentrations interferes with the opening of the 'sodium channels' normally produced by membrane depolarization.
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PMID:Two mechanisms for the meperidine block of action potential production in frog's skeletal muscle; non-specific and opiate drug receptor mediated blockade. 108 25

1. Using the isolated spinal cord of bullfrogs (Rana catesbeiana), intracellular correlates of habituation-like depression of the monosynaptic response elicited in motoneurons by lateral column (LC) stimulation were investigated. The following properties of the motoneuron were compared before and after response depression produced by stimulation of the LC at 0.5/s: resting membrane potential, membrane conductance, critical firing level, and rheobasic current. No alteration was found in any of these parameters. 2. To determine whether transmitter release mechanisms were changing over trials, the LC was stimulated with pairs of stimuli separated by 6 ms presented at 0.5/s. While the amplitude of the first EPSP declined (74% of initial value), the amplitude of the second EPSP increased (111% of initial value). Facilitation ratios thus increased. 3. The following conclusions can thus be drawn: 1) habituation involves a process intrinsic to the LC-motoneuron synapse; 2) habituation is not totally mediated by receptor desensitization; 3) habituation is not mediated by a mechanism extrinsic to the LC-motoneuron synapse that depolarizes terminal endings, e.g., presynaptic inhibition or accumulation of extracellular potassium; 4) habituation is not produced by transmitter depletion. Any of these possibilities has as a necessary consequence that facilitiation ratios remain unchanged. 4. Possible mechanisms that could mediate habituation are: 1) alterations in mobilization and/or release of transmitter; 2) decreased probability of invasion of terminal branches of the presynaptic fiber by the action potential.
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PMID:Habituation of a monosynaptic response in frog spinal cord: evidence for a presynaptic mechanism. 108 14

A patient is described who developed hypoglycemia and generalized neurologic depression after cardiac surgery, while receiving an infusion of glucose, insulin, and potassium (GIK). Hypoglycemia as a complication of the use of GIK solution in patients with hepatic dysfunction, malnutrition and low cardiac output is discussed.
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PMID:Hypoglycemia complicating the use of solution of glucose, insulin and potassium. 111 35

Cardiac arrest developed in two patients after the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal.
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PMID:Cardiac arrest due to oral potassium administration. 111 63


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