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PubMed1981

A comparison of the effects of sympathomimetic agents on gastric acid secretion by the rat stomach in vivo and in vitro.

1. The action of isoprenaline on gastric acid secretion in rats with Heidenhain pouches has been compared with its action in a rat isolated stomach preparation. 2. Isoprenaline (40 micrograms kg-1 h-1) inhibited the acid secretion in response to pentagastrin (20 micrograms kg-1 h-1) in conscious rate with Heidenhain pouches. 3. This inhibition could be abolished by propranolol (2 mg kg-1) and butoxamine (8 mg kg-1) and partially reversed by practolol (8 mg kg-1). 4. Propranolol (2 mg kg-1) significantly increased the response to pentagastrin (20 micrograms kt-1 h-1) but butoxamine and practolol (both at 8 mg kg-1) and the inactive isomer (+)-propranolol (2 mg kg-1) were without any effect on the pentagastrin response in the rats with pouches. 5. In the rat isolated stomach preparation isoprenaline stimulated acid secretion over the range 10(-7) M-10(-3) M whereas phenylephrine and methoxamine were without effect. 6. Propranolol (2 X 10(-5) M) inhibited this stimulatory effect of isoprenaline in vitro but (+)-propranolol (2 X 10(-5) M), practolol and butoxamine (both at 10(-4) M) had no effect on the response. 7. Propranolol (2 X 10(-5) M) did not have any effect on the response of the isolated stomach to pentagastrin (5 X 10(-7) M) or bethanechol (1.7 X 10(-5) M). 8. Phenylephrine (2 X 10(-5) M) did not affect the in vitro responses to pentagastrin (2.17 X 10(-7) M), bethanechol (1.7 X 10(-5) M) or histamine (5.4 X 10(-5) M). 9. It is concluded that isoprenaline has a direct stimulatory effect and an indirect inhibitory effect on gastric acid secretion in the rat. Both effects involve stimulation of beta-adrenoceptors. The relative predominance of one or other of these two opposing effects may help to explain the contradictory results in the literature regarding the actions of beta-adrenoceptor agonists on gastric acid secretion.

Adrenergic alpha-Agonists↗
PubMed1986

Sympathomimetic pressor responses to thyrotropin-releasing hormone in rats.

Cardiovascular responses to centrally administered thyrotropin-releasing hormone (TRH) were studied in urethan-anesthetized rats to allow continuous recording of attendant changes in sympathetic nerve activity. Intracerebroventricular infusions of TRH (0.05-5.0 micrograms) consistently increased not only blood pressure and heart rate, but also spike frequency in splanchnic, renal, or cervical sympathetic nerves. Parasympathetic inhibition seemed unlikely because TRH responses were unaltered by cholinergic blockade with atropine, and efferent vagal nerve firing, instead of being reduced, was actually increased by TRH. An increased secretion of endogenous vasopressin also appeared unlikely, since TRH responses were essentially unaffected by either hypophysectomy or pretreatment with a vasopressin antagonist. Inasmuch as pharmacological ganglion blockade with pentolinium eliminated increases in splanchnic nerve firing but reduced the attendant tachycardia by only 50%, residual tachycardia after ganglion blockade was considered partly due to persistent sympathetic cardioaccelerator tone. On the other hand, because pressor responses to TRH were always accompanied by increased sympathetic nerve firing and were completely abolished after pentolinium-induced ganglioplegia, they were attributed solely to sympathetic hyperactivity.

Animals↗