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The effects of carbachol, propranolol and isoproterenol on tonin concentrations in rat saliva have been investigated. The results suggest that the activity of this enzyme in rat saliva is dependent on activity of beta-adrenergic receptors.
The cardiovascular effects of phenylephrine or ephedrine alone and after autonomic blockade was studied in the chronically cannulated fetal lamb (100-145 days), the newborn lamb, and adult sheep. As gestation advanced, phenylephrine and ephedrine produced an increasing pressor response before and after pretreatment with atropine (1 mg/kg). Compared with the fetus, the magnitudes of the pressor responses were somewhat greater in the newborn and much larger in the adult. Both drugs produced a reflex bradycardia in the unatropinized fetus which in the case of ephedrine was followed by a tachycardia. Pretreatment with atropine resulted in an immediate tachycardia after ephedrine but not after phenylephrine administration. Pretreatment with phentolamine (0.15 mg/kg) produced about a 55% inhibition of the phenylephrine pressor response in both the fetus and adult, suggesting a linear relationship between body weight and number of alpha-adrenergic receptors. Pretreatment with metoprolol blocked the tachycardia associated with ephedrine administration to unatropinized fetuses. In summary, the increase in the magnitude of the pressor response to phenylephrine suggested development of the receptor-effector system. The greater development of the response to ephedrine suggested that there was an increasing amount of noradrenaline being released with advancing gestation.
Hypothermia increases the sensitivity of isolated cardiac muscle to stimulation by beta-adrenoceptor agonists. The purpose of this study was to determine pharmacologically whether this supersensitivity is associated with a change in the affinity of agonists for the receptor. The positive inotropic and chronotropic responses of guinea-pig paced left and spontaneously beating right atria were recorded. Cumulative dose--response curves to noradrenaline (or adrenaline) were compared with isoproterenol in each tissue. At 38 degrees C, the rate curves were to the left of the tension curves, with lower mean effective concentration (EC50) values. However, this difference was less for noradrenaline and adrenaline which were therefore tension selective relative to isoproterenol. Lowering the temperature to 25 degrees C induced supersensitivity, all dose--response curves being displaced to the left. In the presence of carbachol the curves were shifted to the right with depression of the maxima. Dissociation constants (KA) were calculated from plots of reciprocals of equiactive concentrations obtained before and in the presence of carbachol. KA values for rate and tension responses of each agonist were identical at 38 degrees C, indicating that the rate selectivity was not due to affinity differences. The efficacies (er) of noradrenaline and adrenaline were greater than isoproterenol for tension, but smaller for rate responses, which may explain their relative tension selectivity. At 25 degrees C, the KA values of all agonists were reduced approximately 10-fold. Hypothermia-induced supersensitivity is therefore associated with an increase in affinity for the cardiac beta-adrenoceptor.
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BACKGROUND: Celiprolol, a newer beta-blocking agent, has been reported to have vasodilatory capacity which may be due to partial beta-2-receptor agonistic activity or to alpha-receptor antagonistic or central sympathoinhibitory effects. METHODS: To more critically assess the physiologic effects of celiprolol, we measured sympathetic nerve activity to muscle (MSNA), forearm blood flow (FBF), blood pressure (BP), central venous pressure, and heart rate (HR) in 10 normal volunteers at rest, during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP), and during a cold pressor test (CPT). Responses were compared with those seen with metoprolol and with placebo, i.e. each subject was studied three times. RESULTS: Celiprolol did not alter resting levels of hemodynamics, FBF, and MSNA nor did it alter responses to LBNP or the CPT. In contrast, metoprolol produced significant decreases of FBF and HR, and increases of forearm vascular resistance and BP, but had also no effect on responses to the applied stress tests. CONCLUSIONS: The lack of peripheral vasoconstriction seen after acute administration of celiprolol is most likely due to its partial beta-2-receptor agonistic effect and does not seem to be due to a central or reflex action or to an alpha-blocking effect. Both beta-blockers do not impair fundamental neural mechanisms involved in circulatory homeostasis.
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Apomorphine administered in reserpine-induced as well as in restraint ulcers in rats, failed to afford protection. Pimozide, moperone, trifluperidol and chlorpromazine fail to influence the development of the experimental ulcers. Pimozide and moperone although antagonizing the behavioral changes of amphetamine, maintained its antiulcer activity. Amitryptiline, cocaine and morphine had a protective activity. L-Dopa afforded a significant protection which was abolished if this compound was administered together with FLA-63, a specific dopamine-beta-hydroxilase inhibitor. These results were explained by admitting that not dopamine, but noradrenaline was responsible for the antiulcer activity. alpha-Methyl-dopa produced a significant protection in both experimental models.
Pancreatic secretion in anesthetized rats with acute fistulas was provoked by caerulein, acetylcholine, electrical stimulation of the vagus nerves or by 2-deoxy-D-glucose (2-DG). Venous infusions of norepinephrine, isoprenaline or dopamine inhibited the 2-DG-stimulated enzyme secretion but not that provoked by caerulein, acetylcholine or vagal electrical stimulation. Intracerebroventricular administration of norepinephrine or isoprenaline also inhibited 2-DG-stimulated enzyme secretion. It was confirmed that the amines stimulated water and electrolyte secretion by the pancreas in the order of potency isoprenaline greater than norepinephrine greater than dopamine. The results are consistent with a model whereby norepinephrine and isoprenaline exert their effect on pancreatic secretion via a central inhibition of vagal drive to the pancreas, together with a direct stimulating effect on water and electrolyte secretion at the level of pancreatic cells.
Single intraperitoneal doses of phenylephrine (PE), phenylpropanolamine (PPA) and pseudoephedrine (PSD) have differing effects on blood glucose in stressed, normal and goldthioglucose (GTG) mice. PE in normal and GTG mice caused a pronounced but temporary rise in blood glucose while PPA failed to show a significant effect on resting blood glucose in either animal. PSD, in normal and GTG mice, caused a hyperglycemia at 2 h after treatment. Reduced stress conditions (nonrepeated orbital sinus blood sampling) or adrenalectomy eliminated the PSD delayed hyperglycemia in normal mice. PSD did not alter immunoreactive insulin levels at 2 h; however, PSD caused significantly higher corticosterone levels in normal and GTG mice at 2 h. PPA, which did not cause hyperglycemia, had no effect on corticosterone levels at 2 h in normal mice.
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