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Bradykinin, oxytocin, physalaemin and some autonomic drugs were injected in to the common carotid artery. Physalaemin evoked secretion and a pressure rise in the submaxillary duct. A duct pressure rise could be elicited by bradykinin which did not evoke secretion. Autonomic blocking agents did not diminish secretion evoked by physalaemin and did not change pressure responses elicited by bradykinin or physalaemin. Neither secretion, nor duct pressure changes could be recorded after administration of oxytocin. In agreement with previous experiments secretion evoked by autonomic drugs was found to be mediated via cholinergic, alpha- and beta-adrenergic receptors, while motor effects were due to activation of cholinergic and alpha-adrenergic receptors.
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OBJECTIVE: To investigate the effects of autonomic drugs on the in vivo bladder base and proximal urethra in order to provide some reference materials for clinical usage of these drugs in the treatment of bladder outlet dysfunction. METHODS: In 35 dogs, the bladder base was separated from the bladder body and closed to constitute a small chamber. The changes of the pressure in the bladder base chamber and proximal urethra were recorded synchronously before and after administration of autonomic drugs. All data were analyzed with Student's t test. RESULTS: The bladder base had little response to acetylcholine (Ach) which however promoted a contraction of the proximal urethra. The effect of Ach on the proximal urethra was antagonized by phentolamine, but not by atropine. Isoprenaline resulted in relaxation of the bladder base, though it had little effect on the urethra. Norepinephrine (NE) produced contraction of the bladder base and urethra, while phentolamine caused a reduction in the bladder base and urethral pressure, and blocked the response of the bladder outlet region to NE. Angiotensin amide (AII) caused contraction of the bladder base and urethra, which was not obliterated by phentolamine. CONCLUSIONS: The cholinergic drug has no influence on the in vivo canine bladder base, but causes a contraction of the proximal urethra through indirect activation of alpha-receptors. The alpha-adrenergic agents have great effects on the bladder base and urethra by acting on alpha-receptors within the musculature in the outlet region. The beta-adrenoceptor agonist results in relaxation of the bladder base, but it has no effect on the urethra.
The contractile behaviour and effects of several autonomic drugs on the motor activity of human isolated ejaculatory ducts were investigated. Ejaculatory ducts exhibited spontaneous contractions characterised by an amplitude of 2.35 +/- 0.28 mN, a duration of 62. 9 +/- 3.72 s and a frequency of 0.64 +/- 0.014 waves min-1. Acetylcholine (10-5-10-4 m) induced a slight increase in basal tone and in the frequency of the contraction waves. These effects were suppressed by atropine (10-4 m). Noradrenaline (norepinephrine) increased the basal tone and frequency of spontaneous contractions in a dose-dependent manner. These responses were competitively inhibited by HEAT, a selective a1-adrenoceptor antagonist. These preliminary functional findings, indicating the presence of spontaneous motor activity of human ejaculatory ducts and its possible control by adrenergic agonists, suggests a physiological role for human ejaculatory duct in the propulsion of semen from the seminal vesicle towards the urethra.
Actions of some autonomic drugs on upper, middle and lower portion of isolated dog ureters under quiescent state were investigated quantitatively. Noradrenaline and adrenaline at lower concentrations evoked contractions in each portion of the ureters and increased the concentration-dependent frequency and tension of these contractions, but attenuated them at higher concentrations. Phentolamine significantly depressed these contractions, while propranolol enhanced them. Phenylephrine increased the concentration-dependent frequency and tension of contractions, which were suppressed by phentolamine. Acetylcholine at higher concentrations produced contractions of the ureters, and phentolamine or hexamethonium suppressed them. The results indicate that ureteral contractions may be stimulated through an activation of alpha-adrenoceptors and be attenuated through an activation of beta-adrenoceptors, and that acetylcholine may release noradrenaline from sympathetic nerve endings through an activation of presynaptic nicotinic receptors, resulting in ureteral contractions.
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Various autonomic drugs were placed on the peritoneal covering of the seminal vesicles of anaesthetized rats. Adrenaline (which stimulates the alpha-, beta 1- and beta 2-adrenoceptors) and phenylephrine (an alpha-stimulating agent) produced a sudden increase in tonus and in the amplitude and frequency of contractions. Phentolamine (an alpha-blocker) prevented these effects, whereas propranolol (a beta 1- and beta 2-blocker) did not. Phentolamine also abolished the seminal vesicle response to electrical stimulations. Terbutaline (a beta 2-stimulating agent) did not affect the spontaneous activity. There were no differences between the effects of terbutaline alone and those of terbutaline in the presence of propranolol. Moreover, propranolol did not block the contractile response of the gland to adrenaline or to electrical stimulation. These results indicate that alpha-adrenergic receptors are present in the muscle cell membrane of the rat seminal vesicle. The effects of acetylcholine were similar to those produced by adrenaline or phenylephrine although of smaller magnitude. Atropine prevented the effects of acetylcholine, indicating that they are of the muscarinic type.
Drugs that influence autonomic function are used more frequently than surgeons generally imagine. This article summarizes principles of autonomic pharmacology and highlights specific drugs that are useful to the practicing oral and maxillofacial surgeon.
The present study examined the effects of autonomic drugs and glucose on the insulin and glucose concentrations of sham-operated rats and of rats with ventromedial hypothalamic (VMH) lesions and obesity. In the basal condition both epinephrine and atropine significantly decreased serum insulin levels in VMH-lesioned but not sham-operated rats. During glucose stimulation of insulin secretion in VMH-lesioned rats, epinephrine inhibited the increase of insulin by 83% and atropine inhibited it by 42%; whereas in sham-operated rats, epinephrine inhibited it by 70% and atropine inhibited it by 34%. Epinephrine with atropine completely blocked the increase of insulin in response to glucose in both VMH-lesioned and sham-operated rats. In the basal condition, epinephrine together with propranolol significantly decreased serum insulin levels in VMH-lesioned but not sham-operated rats. Epinephrine with phentolamine, on the other hand, markedly increased insulin in the VMH-lesioned rats and to a lesser degree in the sham-operated rats. During glucose stimulation epinephrine with propranolol inhibited the increase of insulin in both groups. Epinephrine with phentolamine or isoproterenol markedly increased serum insulin in VMH-lesioned rats. These results suggest that stimulation of the vagus nerve and increased sensitivity of the beta-receptors on the beta-cells of the islet contribute to the development of hyperinsulinemia. The sympathetic contribution may also be through suppression of alpha-adrenergic receptors.
The effects of some autonomic drugs on the isolated human minor calyceal strips were investigated quantitatively. Norepinephrine, epinephrine and phenylephrine dose dependently increased the basal tone and the frequency of spontaneous contractions and decreased their amplitudes, which were depressed by phentolamine. Acetylcholine at high doses increased the basal tone and decreased the amplitude, which were depressed by atropine without changing the frequency. These findings indicate the existence of alpha-adrenoceptors and muscarinic receptors in the human minor calyceal smooth muscles.
Effects of some autonomic drugs on the isolated dog ureteral preparations showing spontaneous contractions were investigated quantitatively. Noradrenaline, adrenaline and phenylephrine produced increases in frequency and tension of the contractions which were reversed to decreases or depressed by phentolamine. Isoproterenol abolished the spontaneous contractions. Acetylcholine did not significantly change frequency and tension of the contractions. The results indicate that ureteral spontaneous contractions may be enhanced through an activation of alpha-adrenoceptors and be attenuated through an activation of beta-adrenoceptors. However, acetylcholine will not display an important role on the ureteral contractions.
The effects of various autonomic drugs and electroejaculation on the contractile activity of the rat prostate were registered in vivo by means of a video recording system. The changes in the glandular tone were measured by observing the modification of distance between two superficial paralel blood vessels used as references. Norepinephrine, epinephrine, acetylcholine and electrical stimulations produced an increase in the ronus. Since terbutaline had no effect, and phentolamine prevented the effects of both norepinephrine and epinephrine but propranolol did not, it resulted that contractility of the prostate is enhanced when the alpha-adrenoceptors are stimulated, and it is not affected by the stimulation of beta-adrenoceptors. The effects of acetylcholine were blocked by atropine, indicating that they are of the muscarinic type. The excitatory response of the prostate to electroejaculation appeared to be resistant to blockade by phentolamine and atropine.
To assess the influence of autonomic regulation on automaticity in patients with intrinsic sinus node dysfunction, heart rate responses to autonomic drugs were evaluated in 28 patients with sick sinus syndrome and in 8 normal subjects. Heart rates before and after intravenous administration of isoproterenol (Isp), propranolol, atropine, and methoxamine were measured. To compare the results with electrophysiologic data, heart rate and automaticity recovery time (ART) before and after pharmacologic autonomic blockade (AB) were evaluated. Seventeen patients without syncope showed a similar heart rate response after administration of Isp to that of normal subjects, but 11 patients with syncope showed a significantly lower response than patients without syncope. Responses to atropine and methoxamine were lower and response to propranolol was larger in patients as compared to normal subjects. However, no significant difference was observed between patients with and without syncope. Twelve patients showed severely prolonged max ART exceeding 5000 msec after AB. Seven of them showed preserved response to Isp and max ART before AB was significantly shorter than that after AB. The other 5 patients with lower response to Isp showed no significant change in max ART before and after AB. In conclusion, sympathetic regulation in patients with preserved response to Isp might compensate for the impaired intrinsic automaticity in preventing syncope even in patients with severely impaired intrinsic sinus node function.
The motility of the bile ducts of the pigeon and the effects of autonomic drugs on it were studied in vivo and in vitro. Peristalses which originated rhythmically at the hepatic end of the duct propagated to the duodenal end and excreted the bile into it. Antiperistalses did not occur in vivo. The intervals of peristalses of the duct in vivo changed variably while those of the spontaneous contractions in the isolated duct were fairly constant. No synchronization between the electrical activities recorded at the duodenal end of the duct and the duodenum close to the duct was observed. Cholinergic drugs increased motilities of the duct and duodenum. Adrenaline, noradrenaline and phenylephrine induced the excitation of the duct and isoprenaline slight inhibition. All of these sympathomimetic drugs inhibited duodenal motility. The excitatory effect was abolished by alpha-adrenergic blocking agent, and the inhibitory one was abolished by alpha- and/or beta- adrenergic blocking agents. These results suggest that the bile duct is functionally independent of the duodenum and responsibility of the adrenergic drugs are different between two organs.
The effects of the autonomic drugs (noradrenaline, isoproterenol and acetylcholine) and the urine volume change on the pacemaker of ureteral peristalsis were studied by our new method of the in vivo recording of electromyograms (EMGs) of canine renal pelvis. The EMGs of the pelvicalyceal region showed a two phasic slow-rising potential of amplitude of 20 microV and discharge interval of 5 s and was different from propagated waves and therefore considered to be the pacemaker potentials. In the diuretic state the pacemaker potentials kept a constant discharge interval. On the contrary, the discharge interval of the ureter EMG became shorter and finally corresponded to the pacemaker EMG one to one. These results suggest that the urine transport in the diuretic state is controlled by the change of efficiency of the peristaltic propagation and not by the changes of the discharge of the pacemaker itself. Noradrenaline promoted the ureteral peristalsis and isoproterenol inhibited the ureteral peristalsis. These two drugs had no effects on the pacemaker potentials. Acetylcholine had a great variety of the effects on the ureter EMG and the pacemaker EMG separately. These results suggest that the pacemaker of the ureteral peristalsis is controlled under the influence of the parasympathetic system and the ureter is controlled under the influence of both the sympathetic and parasympathetic system.
The effects of intravenously administered autonomic drugs on the intraluminal pressure and the excretion volume of the seminal vesicles in rats were studied. Both alpha 1-adrenergic and cholinergic stimulants produced a rapid increase in pressure and fluid excretion. alpha 1-Adrenergic stimulants elicited a sharp and single increase in pressure, while cholinergic stimulants caused a sharp increase with multiple peaks.