Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.
 ...
PMID:The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1. 2 69

The present study was conducted to examine the roles of hormonal factors in plasma potassium alterations in acute respiratory acidosis. Respiratory acidosis (pH, 7.07-7.10) induced by the inhalation of 10% CO2, 20% O2 and 70% N2 mixed gas caused an increase in the plasma potassium concentration beyond that of the control of 3.44 +/- 0.12 (mean +/- SE) to 4.36 +/- 0.07 mEq/l (p less than 0.01) within 180 min. The plasma norepinephrine concentration was also noted to significantly increase at the same time. Phentolamine (40 micrograms/kg/min i.v.) did not affect the degree of acidosis or acidosis-induced hyperkalemia. No significant changes in the plasma levels of epinephrine, insulin, glucagon, cortisol or aldosterone could be detected. Hormonal factors would thus appear not to be essential to potassium movement from intracellular to extracellular compartments in acute respiratory acidosis.
 ...
PMID:Roles of hormones in plasma potassium alteration in acute respiratory acidosis in dogs. 140 6

1. Male rats (110-140 g body wt.) were restrained by a standard laboratory technique, by wrapping in a linen towel, and subjected to a constant intravenous infusion of saline (0.15 M-NaCl) for periods of 1 or 6 h. Fractional rates of protein synthesis (ks, %/day) were estimated at the start and at the end of the infusion period, by injection of a large concentration of [3H]phenylalanine. 2. In fed and overnight-fasted rats, restraint and infusion of saline for 1 and 6 h decreased ks in skeletal muscle by 15-20% and 30-35% respectively. Plasma glucose, insulin, glucagon and corticosterone concentrations in restrained and infused rats were not characteristic of immobilization stress. 3. Restrained rats responded to nutrient administration; ks in skeletal muscle increased by 35-40% after infusion of a mixture of amino acids and glucose for 1 or 6 h, as compared with saline-infused rats. 4. Restraint and infusion for 1 or 6 h did not overtly decrease ks and kRNA (protein synthesis per unit of RNA) in hypoxaemia-sensitive tissues, such as heart and liver. Restraint and infusion in an open cage, or in a cloth of open weave, did not decrease ks in muscle after 1 h. Blood gas measurements showed that rats restrained in a linen cloth were hypercapnic and acidotic compared with rats in an open cage. 5. It was concluded that respiratory acidosis, rather than hypoxia, resulting from restraint in a linen cloth decreases muscle protein synthesis.
 ...
PMID:The influence of restraint and infusion on rates of muscle protein synthesis in the rat. Effect of altered respiratory function. 313 2

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23