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PubMed1985

Pharmacologic treatment of lower urinary tract dysfunction in the female patient.

As a result of the renewed interest in the neuropharmacology and neurophysiology of the urinary bladder and its outlet, pharmacologic therapy now exists that is helpful in the management of many types of voiding dysfunctions. This article summarizes the pharmacologic principles upon which this drug therapy is based and shows how pharmacologic treatment fits into a functional scheme of therapy for disorders of micturition, here specifically related to the female patient with lower urinary tract dysfunction.

Adrenergic alpha-Antagonists↗
PubMed1985

Ontogeny of gastric acidity in the ovine fetus.

Hypoacidity and hypergastrinaemia have been reported in the newborn human. However, little is known about in utero gastric acid secretion, and the relationship to fetal plasma gastrin levels. The longitudinal pattern of development of basal and stimulated gastric acid secretion in the non-anaesthetized fetal sheep has been studied during the last 45 days of gestation. Fetuses had cannulae inserted into the jugular vein, carotid artery and stomach. Gastric juice and blood was sampled daily from 101 days gestation until birth (145 days). Intermittent basal acid secretion began between 120 and 133 days of gestation. These fluctuations in gastric juice pH continued until birth. Overall there was a decline in gastric pH from 7.5 +/- 0.2 (SEM), for fetuses 101-105 days to 4.3 +/- 0.5 by 131-135 days. Mean fetal plasma gastrin was higher than maternal levels after 111-115 days but no correlation between fetal plasma gastrin levels and gastric pH could be demonstrated. Pentagastrin and histamine infusion did not stimulate acid secretion in fetuses younger than 115 days. After this age the fetuses became responsive to both pentagastrin and histamine. In contrast, cholinergic stimulation, using bethanechol, did not stimulate acid production until 10 to 15 days later, suggesting a hierarchy in the development of the control of acid secretion in the fetus. The lack of response to endogenous gastrin and the hierarchy in the control of acid secretion suggest either a lack of receptors on the parietal cell or the presence of an inhibitor of acid secretion. These studies are relevant to human physiology since the present findings show that the sheep and human have a similar gastrin/acid profile at birth.

Animals↗
PubMed1985

Possible inhibitory role of endogenous gamma-aminobutyric acid in the nonnicotinic functions of the dog cardiac sympathetic ganglia.

Participation of endogenous gamma-aminobutyric acid (GABA) in the functions of dog cardiac ganglia was investigated. The ganglionic stimulants as well as agents affecting GABA system were given directly into the cardiac sympathetic ganglia through the right subclavian artery (i.a.), unless otherwise mentioned. Inhibition of endogenous GABA degradation by the GABA-transaminase inhibitor, aminooxyacetic acid (AOAA) administered 10 mg/kg i.v. 2 hr before completion of surgical procedures did not alter the positive chronotropic responses to bethanecol (25 and 50 micrograms) and acetylcholine (25, 50 and 100 micrograms) but reduced markedly those to angiotensin II (1 and 2 micrograms). This reduction was antagonized by picrotoxin (5 mg). Diazepam given 10 mg/kg i.v. also inhibited the ganglionic responses to angiotensin II in both untreated and AOAA-pretreated dogs, this inhibition by diazepam being more marked in the AOAA-pretreated than in the untreated dogs. The same dose of diazepam did not affect the responses to acetylcholine but reduced to a certain degree of responses to bethanechol in the AOAA-pretreated dogs. These inhibitions by diazepam were also reversed by picrotoxin. After i.v. treatment with the glutamic acid decarboxylase inhibitors, 3-mercaptopropionic acid (50 mg/kg) or isoniazid (200 mg/kg), the ganglionic responses to angiotensin II were not altered, but inhibitory effects of diazepam on the responses to angiotensin II were eliminated after 3-mercaptopropionic acid but not after isoniazid. These results suggest that endogenous GABA may play an inhibitory role in the nonnicotinic ganglionic pathways and that diazepam probably exerts a ganglionic action through endogenous GABAergic mechanisms.

3-Mercaptopropionic Acid↗
PubMed1985

Drug pumps for treatment of neurologic diseases and pain.

Implanted drug pumps provide a new way to infuse medication chronically to the nervous system in a selective fashion. They have been of value in treating pain of cancer and spasticity through spinal subarachnoid catheters. Treatment of Alzheimer's disease is currently being investigated using intraventricular bethanechol.

Alzheimer Disease↗
PubMed1985

Neurally mediated nonadrenergic relaxation in cat airways occurs independent of cholinergic mechanisms.

Activation of the nonadrenergic noncholinergic (NANC) inhibitory system in cat airways causes coincident release of acetylcholine from vagal nerve terminals. The present study was undertaken to determine if neurally released acetylcholine is involved in initiating or modulating activity in the lung NANC inhibitory system. Electrical field stimulation experiments were performed on isolated segments of cat trachea and bronchi and additional studies were conducted in intact anesthetized, mechanically ventilated cats. In isolated airways, frequency-dependent NANC relaxations of bethanechol contracted tissues were identical to NANC responses of airways contracted with 5-hydroxytryptamine. This result suggested that muscarinic receptor activation did not influence NANC inhibitory system function. In additional studies where agents that inhibited or potentiated the actions of acetylcholine were used, similar results were obtained. Pretreatment of tissues with hexamethonium or atropine did not alter NANC frequency response curves. Contractile responses evoked by field stimulation were potentiated by neostigmine and abolished by hemicholinium treatment; NANC relaxation responses were not significantly affected by either agent. In intact cats, neostigmine pretreatment did not alter the magnitude or duration of vagally mediated NANC bronchodilation. Acetylcholine administered as an aerosol to cats treated with atropine did not mimic the NANC response. These findings suggest that NANC inhibitory system function in cat airways is neither dependent upon nor modulated by neurally released acetylcholine.

Acetylcholine↗
PubMed1985

An investigation of the mechanism of lead-induced relaxation of pigeon crop smooth muscle.

Lead-induced crop dysfunction is probably due to a direct action on the smooth muscle or the neural elements in crop tissue. Strips of crop tissue relax when exposed to lead chloride in vitro. We found that tetrodotoxin and the neurotransmitter antagonists propranolol, sotalol and apamin failed to alter lead-induced relaxation, suggesting that the effect is not neurally mediated. Lead, manganese, cadmium and theophylline inhibited calcium-induced contractions in depolarized crop tissue. However, lead, like the phosphodiesterase inhibitor theophylline and unlike the calcium-influx blocker verapamil, did not inhibit bethanechol- or potassium-stimulated contractions and calcium influx into crop tissue. This suggests that lead does not act by blockade of calcium influx. Lead stimulated cyclic AMP production in cell-free crop membrane preparations. Lead also enhanced manganese stimulation of cyclic AMP production. The results suggest that lead-induced relaxation may be due to stimulation of adenylate cyclase activity resulting in increased intracellular cyclic AMP levels.

Adenylyl Cyclases↗
PubMed1985

Effect of amino acids on isolated colonic smooth muscle from the rabbit.

The purpose of these studies was to evaluate the direct effect of amino acids on rabbit colonic smooth muscle. Isometric tension was measured in circular smooth muscle from the distal colon after the administration of 19 individual L-amino acids. L-Alanine, L-cysteine, L-serine and L-methionine stimulated a dose-dependent increase in isometric tension. The lowest concentration which increased tension of the tissue for each of these amino acids was between 1 X 10(-4) to 5 X 10(-4) M. At a concentration of 10(-3) M, each of these four amino acids stimulated smooth muscle to 40 to 60% of the maximum response to bethanechol (2050 +/- 105 mN/m2). The 15 other amino acids tested had less effect on the colonic smooth muscle. The smooth muscle response to the D-amino acids, D-alanine, D-cysteine or D-serine, was shifted 10-fold to the right. Neural blockade by tetrodotoxin, the alpha adrenergic receptor antagonist, phentolamine, or the alpha-2 antagonist, yohimbine, increased smooth muscle tension, but did not inhibit L-amino acid stimulation of the tissue. Atropine, naloxone or prazosin (alpha-1 adrenergic antagonist) had no effect on amino acid stimulation of the muscle. These data suggest that L-amino acids, alanine, serine, cysteine and methionine stimulate contraction of colonic circular smooth muscle, this response is stereospecific and amino acids appear to stimulate the smooth muscle directly and not through an effect on the myenteric neurons.

Amino Acids↗
PubMed1986

Desensitization within and between secretagogues of canine gastric acid and pepsin secretion.

Two types of desensitization, autodesensitization and cross-desensitization, of gastric secretory responses to cholinergic (bethanechol and vagal excitation) and noncholinergic stimuli (histamine and pentagastrin) were studied in groups of three to six conscious dogs with gastric fistula. Autodesensitization was manifested as fade of both acid and pepsin secretory responses by 10 to 20%/hr from peak output with all stimuli, histamine, pentagastrin and bethanechol. At the end of 4 hr of pentagastrin, 1.5 micrograms/kg X hr, doubling the dose of pentagastrin for 75 min reversed partly the trend of the acid fade, whereas adding an equipotent dose of histamine was much more effective, i.e., pentagastrin does not desensitize the stomach to histamine. When the three stimuli were given in sequence in random order for 2.5, 1.5 and 1.5 hr, respectively, to study cross-desensitization, histamine and pentagastrin reduced markedly the response of the parietal cells to either direct (bethanechol) or indirect (vagal) subsequent cholinergic stimulation. However, the parietal cells unresponsive to bethanechol remained fully responsive to histamine or pentagastrin, i.e., cholinergic stimulation did not desensitize the stomach to noncholinergic stimuli. From present and published data, neither auto- nor cross-desensitization is due to general, e.g. electrolyte and water depletion, or local, e.g. pH or osmolality, homeostatic consequences of secretion or to the drugs used, e.g. fall in blood pressure with histamine, but to cellular events. Inasmuch as the cell unresponsive to one stimulus may respond to another, a working hypothesis involving receptors is presented.

Animals↗
PubMed1985

Bethanechol versus antiacids in the treatment of gastroesophageal reflux.

To compare the efficacy of bethanechol in the treatment of gastroesophageal reflux with that of antiacids, a prospective, cross-over study was undertaken, in which 20 affected infants and children were randomized into two groups on 6-week alternate bethanechol and antiacids oral medication. Patients were evaluated clinically and by esophageal pH-metry before and after each treatment. Clinical score amelioration was achieved earlier than reflux number reduction and with similar incidence in both groups of patients, irrespectively to the initial medication; moreover, the differences in the degree of improvement between the two groups after either treatment were not found to be significant. These results fail to show that bethanechol is more effective than antiacids in controlling gastroesophageal reflux; moreover, bethanechol is more difficult to administer and offers a higher rate of undesired side effects.

Aluminum Hydroxide↗
PubMed1986

Functional effects of the purinergic innervation of the rabbit urinary bladder.

Although it is generally agreed that micturition is primarily under the control of the parasympathetic nervous system, there is good evidence that an atropine insensitive, nonadrenergic-noncholinergic neuronal component exists. Recent evidence indicates that the purinergic transmitter ATP (or an other purinergic analog) may be responsible for the atropine-insensitive portion of the contraction. Although isolated muscle strip studies have identified the purinergic response, the functional significance of this response has not been determined. Utilizing an in vitro whole-bladder model, we have investigated the functional ability of the purinergic component of field stimulation to empty the bladder under standard conditions. The results indicate: the response of the bladder to both cholinergic stimulation and field stimulation is characterized by a rapid rise in intravesical pressure followed by a prolonged plateau phase; expulsion of fluid from the bladder occurs primarily during the plateau phase of the contraction; in the presence of atropine, field stimulation produces only a transient rapid rise in tension, similar to the response to exogenous ATP; and this "purinergic" response does not result in significant bladder emptying. These results suggest that the bladder response to this purinergic stimulation may be complimentary to, but functionally different from that which occurs in response to cholinergic transmission alone.

Adenosine Triphosphate↗