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Biomedical subjects

L W Frazier

Publications and source records attributed to L W Frazier.

At least 37 records · Page 2Linked to original sources
PubMed1985

Characteristics of proton excretion in normal and acidotic toad urinary bladder.

This study, performed on the urinary bladder of Bufo marinus, was to investigate the characteristics of H+ excretion in the normal and metabolic acidotic toad. Experiments were run in modified Ussing chambers in the presence and absence of exogenous CO2. Amiloride in the mucosal medium (1.5 X 10(-4) M) inhibited H+ excretion in the acidotic bladder but this inhibition was reversed in the presence of 5% CO2. Na+-free mucosal medium revealed a component of H+ excretion in the normal toad that is Na+-dependent and not reversed by 5% CO2. Acetazolamide (10(-3) M) had no effect on H+ excretion in normal toad but inhibits excretion in the acidotic toad both in the presence and absence of exogenous CO2. In both the presence and absence of exogenous CO2 and in the presence of varying pH gradients, the bladders from acidotic toads excreted H+ at a greater rate and were able to generate greater pH gradients than in normal bladders. Voltage clamp experiments revealed that H+ excretion in the acidotic toad was inhibited by a mucosal potential difference of -20 to -100 mV but this inhibition was completely reversed by 5% CO2. In the normal toad bladder H+ excretion was stimulated by a mucosal potential difference of -20 to -100 mV in both the presence and absence of exogenous CO2. Our evidence suggests the possibility of two H+ excretory mechanisms in toad urinary bladder each with its' own set of characteristics dependent on the acid-base state of the animal. Proposed models are presented for these mechanisms.

Acidosis↗
PubMed1984

Increased Na+ excretion by the skin of Rana pipiens after NaCl loading.

In vivo the frog skin excretes sodium and the sodium excretion is increased in response to a NaCl load. The sodium excretion can be demonstrated in vitro, and the rate of excretion is greater in skin from NaCl-loaded animals than from control, non-loaded animals. Unidirectional 22Na flux experiments on paired frog skins, as well as 22Na and 24Na bidirectional flux experiments measured in vitro, confirm the above finding that net sodium excretion occurs in response to the NaCl load.

Animals↗
PubMed1983

The effect of catecholamines on H+ and NH+4 excretion in toad urinary bladder.

The catecholamines epinephrine and norepinephrine, when placed on the toad urinary bladder in vitro, at a final concentration of 50 microM, caused a significant increase in H+ and NH+4 excretion by the bladder. Isoprenaline in a final concentration of 50 microM also increased H+ and NH+4 excretion in the bladder. Propranolol at a concentration of 50 microM blocked the stimulation of H+ excretion by isoprenaline but propranolol at 100 microM was required to block the stimulation of NH+4 by isoprenaline. The dose-response analysis indicates that the concentration of epinephrine used (50 microM) is at or near the maximal effective dose. These findings indicate that catecholamines stimulate H+ and NH+4 excretion in the toad urinary bladder and evidence suggests this may be mediated via the beta receptor mechanism.

Adrenergic alpha-Antagonists↗
PubMed1983

The role of the adrenal gland in control of H+ and NH4+ excretion by toad urinary bladder.

The urinary bladder of Bufo marinus has been shown to excrete H+ and NH4+ and this excretion is increased by metabolic acidosis. The involvement of the adrenal gland and its steroid secretions in the adaptation for increased acid and ammonia excretion by the bladder was tested during the course of this study. Groups of toads were adrenalectomized and maintained in chronic NH4Cl-induced acidosis. Three other groups of toads were adrenalectomized and put in acidosis but repleted with 2.5 mg/day of either cortisol (CT), dexamethasone (Dexa), or deoxycorticosterone acetate (DOCA). All control groups were sham-operated. The bladders were excised after 3 days and mounted between 2-ml Lucite chambers. Net H+ and NH4+ fluxes into the mucosal media were measured and reported in units of nanomoles per 100 mg bladder per minute. In control acidotic toads H+ excretion was 20.1 +/- 2.0 and the adrenalectomized nonreplete group H+ excretion was 14.2 +/- 1.87 (P less than 0.04). For the same groups NH4+ excretion was 2.90 +/- 0.26 for the controls and 1.38 +/- 0.19 for the adrenalectomized (P less than 0.001). The H+ excretion in CT-, Dexa-, and DOCA-repleted toads was not significantly different from the control group. NH4+ excretion, however, showed a 55% decrease (P less than 0.001) in the CT group, and a 45% decrease (P less than 0.05) in the Dexa group. The NH4+ excretion in the DOCA repleted group was significantly different from the control group. Therefore, we conclude that the adrenal gland plays a role in the adaptive increase of H+ and NH4+ excretion by the urinary bladder in acidosis through the secretion of steroid hormones. The increase in NH4+ excretion appears to be a mineralocorticoid-stimulated process. We were not able to determine in this study if the steroid hormones had an exacting regulatory role or one of a permissive role over H+ and NH4+ excretion in the toad urinary bladder.

Acid-Base Equilibrium↗
PubMed1979

Action of steroids on H+ and NH+4 excretion in the toad urinary bladder.

This study was done to determine if steroid compounds will stimulate the urinary bladder of the toad to increase its capacity to acidify the urine and excrete NH+4. Aldosterone, 17 beta-estradiol, dexamethasone, pregnenolone, and cholesterol were tested on the bladder. All compounds tested were found to stimulate the rate of acidification by the bladder, above that of a paired control hemibladder. In contrast, only the steroids aldosterone and 17 beta-estradiol were found to stimulate NH+4 excretion in the bladder. Cycloheximide was found to block the action of aldosterone on the NH+4 excretion, but did not have a significant effect on the stimulation of acidification by aldosterone. We conclude that steroids stimulate H+ and NH+4 excretion in the toad urinary bladder. In addition, the NH+4 excretory system seems to be more specific to this effect than is the H+ excretory system.

Aldosterone↗
PubMed1979

Stimulation of ammonium ion excretion in the toad urinary bladder by an extract of human urine.

It is well known that ammonium ion excretion is increased during metabolic acidosis in mammals. The purpose of this study was to determine whether we could isolate from human urine during metabolic acidosis a factor that would stimulate NH+4 and/or H+ excretion in toad urinary bladder. Extracts of urine from six human subjects collected during NH4Cl-induced acidosis were prepared. These extracts were tested for their effect on NH+4 excretion in hemibladders mounted between plastic chambers. The extracts significantly increased NH+4 excretion in the toad urinary bladder. We found no effect on H+ excretion by these extracts. This ammoniuretic activity was not present in the urine when the same individuals were in metabolic alkalosis. We conclude that during metabolic acidosis a humoral factor is present which stimulates the excretion of NH+4. The factor could act as a permease in the bladder cell or as a stimulator of an NH+4 transport system.

Acid-Base Equilibrium↗
PubMed1978

Cellular changes in the toad urinary bladder in response to metabolic acidosis.

The urinary bladder of Bufo marinus excretes H+ and NH+4, and the H+ excretion is increased when the animal is placed in metabolic acidosis. The mitochondria-rich (MR) cells mediate the H+ excretion by the bladder. The purpose of this study was to determine if there is a change in MR cells of the bladder during metabolic acidosis. Bladders from normal toads and from toads that had been placed in metabolic acidosis were used. The bladders were mounted between plastic chambers and H+ excretion measured. The bladder was then fixed and prepared for scanning (SEM) and transmission (TEM) electron micrograph studies. SEM's at low magnification were used to count the various cell types and the TEM's were used to confirm the different cell types. Fields were randomly selected and a total of 2500 cells counted in each group. The bladders from toads in metabolic acidosis had a consistently higher ratio of MR cells to granular cell than did the normal bladders. These results indicate that during metabolic acidosis there is an increased number of MR cells in the bladder, and this increased the bladder's capacity to excrete H+.

Acidosis↗
PubMed1976

Effects of parathyroid hormone on H+ and NH+4 excretion in toad urinary bladder.

The urinary bladder of Bufo marinus excretes H+ and NH+4, and the H+ excretion is increased after the animal is placed in metabolic acidosis. The present study was done to determine if parathyroid hormone could stimulate the bladder to increase the excretion of H+ and/or NH+4. Parathyroid hormone added to the serosal solution in a final concentration of 10 mug/ml was found to increase H+ excretion by 50 per cent above the control hemibladders, while there was no effect on NH+4 excretion. Parathyroid hormone had no effect on H+ excretion when added to the mucosal solution. We also performed experiments utilizing theophylline and dibutyryl cyclic AMP which mimicked those of the parathyroid hormone experiments. A dose-response analysis was performed and the results indicate that 1 mug/ml of parathyroid hormone was the minimal effective dose. These results suggest that parathyroid hormone can stimulate H+ excretion in the toad urinary bladder and this effect seems to be mediated by cyclic AMP. In addition, it was found that parathyroid hormone has no effect on NH+4 excretion.

Ammonia↗
PubMed1976

The effect of angiotensin II on electrolyte excretion by the renal tubules.

In vivo studies were done on mongrel dogs to determine the effect of angiotensin II on renal electrolyte excretion. Angiotensin II was infused directly into the left renal artery at a rate of 1 ng/kg/min. Angiotensin produced consistent reductions in the excretion of Na+, K+, and Cl- in the left kidney. These reductions could not be attributed to decreases in GFR or RPF. Electrolyte excretion by the right kidney was constant. These data are consistent with the hypothesis that angiotensin II may function as an intrarenal, antinatriuretic hormone.

Angiotensin II↗