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Biomedical subjects

M J Fregly

Publications and source records attributed to M J Fregly.

At least 181 records · Page 10Linked to original sources
PubMed1979

Use of an iodide-specific electrode to study lactoperoxidase-catalyzed iodination of l-tyrosine.

An in vitro method employing an iodide-specific electrode for monitoring lactoperoxidase-catalyzed iodination is described. The method utilized lactoperoxidase, potassium iodide, and a glucose--glucose oxidase system for the generation of hydrogen peroxide and l-tyrosine. As iodination of l-tyrosine proceeded, the free iodide concentration in solution decreased and was monitored by an iodide-specific electrode. The iodide electrode was reliable when compared to a 131I-method for measuring free iodide changes in solution. Increasing concentrations of resorcinol, a well-known inhibitor of thyroid peroxidase-catalyzed iodination, in the reaction mixture resulted in graded inhibition of the initial rate of lactoperoxidase-catalyzed l-tyrosine iodination. This in vitro system can be used to assess inhibitory activity of various antithyroid substances.

Catalysis↗
PubMed1979

Effect of an angiotensin converting enzyme inhibitor (SQ 14,225) on beta-adrenergic and angiotensin-induced thirsts.

The effect of acute administration of SQ 14,225, a new angiotensin converting enzyme inhibitor, on the drinking response of female rats administered either isoprenaline, angiotensin I, or angiotensin II was studied during 2 h after treatment. Administration of isoprenaline (25 micrograms/kg body wt) was accompanied by a significant increase in water intake when compared with saline-treated controls. Acute administration of a constant dose of isoprenaline (25 micrograms/kg body wt) and increasing doses of SQ 14,225 (5--50 mg/kg) was accompanied by a dose-related, linear decrease in water intake. Acute administration of either angiotensin I or angiotensin II (200 micrograms/kg body wt) was accompanied by a significant increase in water intake. The dipsogenic response to angiotensin II was not affected by acute administration of 35 mg SQ 14,225/kg body wt. However, at the same dose of SQ 14,225, angiotensin I-induced thirst was attenuated. Since isoprenaline-induced and angiotensin I-induced, but not angiotensin II-induced, thirsts are blocked by SQ 14,225, the results suggest that isoprenaline-induced thirst is mediated by way of the renin--angiotensin system.

Angiotensin I↗
PubMed1979

The effect of ambient temperature on beta-adrenergic responsiveness in rats.

The responses of tail skin and colonic temperatures of female rats to ambient temperatures of 20, 22, 24, 26, 28, and 30 degrees C were measured. Within this range, colonic temperature was stable while tail skin temperature increased linearly with increasing ambient temperature. Administration of the beta-adrenergic agonist, d,l-isoproterenol, at 10.0, 25.0, and 62.5 micrograms/kg, sc, at each ambient temperature was accompanied by increases in tail skin and colonic temperatures that were dependent on both the dose of isoproterenol administered and the ambient temperature. The integrated responses of tail skin temperature following administration of the three doses of isoproterenol were maximal at an ambient temperature of 26 degrees C while the integrated responses of colonic temperature were maximal at 30 degrees C. The results suggest that tests of beta-adrenergic responsiveness using this technique should be performed at an ambient temperature of 26 degrees C for maximal sensitivity.

Animals↗
PubMed1979

Tolerance of estrogen-treated rats to acute cold exposure.

Female rats treated chronically with ethynylestradiol (36 micrograms/kg per day) alone, and in combination with the progestational agent, norethynodrel (253 micrograms/kg per day), cooled significantly faster than controls when lightly restrained and exposed to air at 5 degrees C. Rate of cooling of rats given only norethynodrel was similar to that of the control group. In other studies, rate of oxygen consumption was determined for all groups during acute exposure to cold (14 degrees C). All estrogen-treated groups achieved the same maximal rate of oxygen consumption as control and norethynodrel-treated groups during cold exposure, but cooled significantly faster. Two groups of female rats were treated chronically with ethynylestradiol at two separate doses (36 and 61 micrograms/kg per day). An untreated group served as controls. Rate of oxygen consumption of all animals were measured during restraint and exposure to cold (18 degrees C). The estrogen-treated groups again achieved the same maximal rate of oxygen consumption as the control group, but also cooled significantly faster despite the fact that the cold stress was less severe than in the previous experiment. That estrogen-treated rats cooled faster than controls in both studies despite achieving a maximal rate of heat production which did not differ from controls suggests that reduced cold tolerance of estrogen-treated rats may be related to increased heat loss.

Animals↗
PubMed1979

Effect of clonidine on the contractile responsiveness of aortic smooth muscle to norepinephrine.

A length-tension relationship was established for aortic smooth muscle of rats by means of membrane depolarization with KCl. Maximal tension was developed by aortic rings when the preload initial tension was 8--9 g. Two aortic rings (4 mm thick) were removed from segments of the aorta cut 1.5 (upper) and 2.4 cm (lower) below the aortic arch. Upper rings appeared to develop a greater tension than lower rings during depolarization with KCl. However, in spite of this quantitative difference between rings from upper and lower segments of the aorta, there were no qualitative differences observed. Clonidine, an antihypertensive agent, induced a contraction in aortic smooth muscle, apparently by way of alpha-adrenoreceptor stimulation. Clonidine also attenuated significantly the development of active tension by norepinephrine but did not inhibit significantly the development of active tension following membrane depolarization with KCl. This suggests that there is a partial antagonism between norepinephrine and clonidine, presumably at the site of the receptors on smooth muscle, and that clonidine does not interfere with the contractile mechanism, per se.

Animals↗
PubMed1979

Adrenergic activity of ortho-, meta-, and para-octopamine.

DL-o-, and p-octopamine were tested for beta- and alpha-adrenergic activity in rats. When compared to DL-isoproterenol, a beta-adrenergic agonist, all three isomers failed to show significant beta-adrenergic activity as assessed by intiation of thirst and by increase in tail skin temperature. All three isomers increased mean blood pressure in pentolinium-blocked rats. Of the three isomers, m-octopamine possessed the greatest alpha-adrenergic activity. When the responses were compared with those induced by L-norepinephrine, the order of activities was: 1:0.01 :0.0005 :0.0007 for norepinephrine, m-, p- and o-octopamine, respectively. Thus, DL-m-octopamine has about 1/100th the alpha-adrenergic activity of L-norepinephrine.

Adrenergic alpha-Agonists↗
PubMed1979

Effect of chronic treatment with desoxycorticosterone on the dipsogenic response of rats to isoproterenol and angiotensin.

Administration of desoxycorticosterone (DOC) at a dose of 0.5 mg/kg/day to male rats for 6 weeks attenuated significantly the drinking response to acute subcutaneous administration of 5, 10 and 20 microgram isoproterenol/kg body weight. Chronic administration of DOC did not prevent the drinking response to acute intraperitoneal administration of angiotensin II (200 microgram/kg body weight). In contrast, the drinking response was enhanced compared with that of control rats given angiotensin II acutely. While attenuation of the drinking response to isoproterenol in DOC-treated rats may be attributed to depletion of renin from their kidneys, the mechanisms responsible for the enhanced drinking response to angiotensin II are not clearly understood.

Angiotensin II↗
PubMed1979

Relationship between thermogenic drinking and plasma renin activity in the rat.

The spontaneous water intake of rats increases when they are transferred abruptly from a cold (5 degrees C) to a neutral (25 degrees C) environment. This has been termed thermogenic drinking. Treatment of cold-acclimated rats with SQ 14,225, an angiotensin converting enzyme inhibitor, at 10-50 mg/kg of body weight prior to removal from cold, inhibited the thermogenic drinking response in a dose-dependent manner. Plasma for determination of plasma renin activity (PRA) was obtained by cardiac puncture from methoxyflurane anesthetized rats maintained chronically at both 25 degrees and 5 degrees C. In addition, plasma was obtained from cold-acclimated rats 15 min after removal from 5 degrees to 25 degrees C. PRA values were 2.2 +/- 0.4 (S.E.) ng/ml/h for control rats; 1.9 +/- 0.8 ng/ml/h for cold-acclimated rats and 8.5 +/- 1.7 ng/ml/h for cold-acclimated rats removed from cold for 15 min. Thus, PRA was significantly increased in rats removed acutely from cold. These data suggest that thermogenic drinking may be mediated by the renin-angiotensin system.

Acclimatization↗
PubMed1979

Time for loss of increased cardiac responsiveness to isoproterenol in cold-acclimated rats after removal from cold.

Female rats exposed to air at 5 +/- 1 degree C for 12 weeks had a greater increase in heart rate in response to s.c. administration of d,l-isoproterenol (8 microgram/kg body weight) than warm-acclimated controls when both were tested in air at 25 +/- 1 degree C. After removal from cold for 24, 48, or 72 h, cold-acclimated rats still showed a greater responsiveness of heart rate to s.c. administration of isoproterenol (8 microgram/kg body weight) when compared with warm-acclimated controls. However, by 96 h after removal from cold, the responsiveness of heart rate to isoproterenol in the cold-treated group no longer differed from that of the warm-acclimated group. Hence, the increased beta-adrenergic responsiveness of heart rate in cold-acclimated rats was lost at some time between 72 and 96 h after removal from cold.

Acclimatization↗
PubMed1978

Attenuation of angiotensin-induced water intake in estrogen-treated rats.

Chronic treatment with either estradiol benzoate (31 and 57 microgram/kg/day) or ethynyl estradiol (30 and 72 microgram/kg/day) attenuated the drinking responses of female rats to acute administration of either isoproterenol (25 microgram/kg, SC) or synthetic angiotensin II (100 and 200 microgram/kg, IP). While these studies do not rule out the possibility that attenuation of isoproterenol-induced drink in estrogen-treated rats may be associated with a defect in renin release, attention is also apparently associated with a reduced responsiveness to angiotensin II. This may be related to reduced permeability of angiotensin II at the level of the circumventricular organs of the brain; to hyporesponsiveness of receptors for angiotensin II mediating thirst in the central nervous system, or to mechanism beyond the receptor that are responsible for the conscious behavioral changes which normally accompany angiotensin II-induced thirst.

Angiotensin II↗
PubMed1978

Mediation of isoproterenol-induced thirst in rats by beta2-adrenergic receptors.

Isoproterenol-induced thirst in rats has been attributed to the activation of beta-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into beta1 and beta2 types, experiments were performed using several beta-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The beta1- and beta2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 microgram/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little beta-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 microgram/kg). Practolol (125 mg/kg), a beta1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective beta2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 microgram/kg), a beta2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that beta2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

Albuterol↗
PubMed1978

Reversal by theophylline of some changes characteristically accompanying hypothyroidism in rats.

Chronic dietary administration of theophylline (0.625, 1.25 or 2.50 g/kg food) for 7--9 weeks prevented the decrease in resting oxygen consumption, heart rate and systolic blood pressure characteristically observed in rats treated simultaneously with either of the antithyroid drugs, aminotriazole (ATZ; 0.25 g/kg food) or propylthiouracil (1.0 g/kg food). However, theophylline failed to restore both the food intake and growth rate of hypothyroid rats to that of euthyroid controls. Measurements of 131I uptake by the thyroid gland, thyroid acinar cell height and protein-bound iodine failed to reveal an effect of theophylline in either control or hypothyroid animals although theophylline increased thyroid to body weight ratio in both groups. Thus, the restoration of rate of oxygen consumption, heart rate and systolic blood pressure of hypothyroid rats to that of euthyroid controls was apparently not exerted through an increase in thyroid activity. The reduction in rate of oxygen consumption, heart rate and systolic blood pressure, generally associated with lack of thyroid hormone, appear more likely to be associated with reduced responsiveness to catecholamines in the hypothyroid rats. The results suggest that an increase in the half-life of cAMP by administration of theophylline to hypothyroid rats returned these functions to the level of euthyroid controls.

Amitrole↗