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PubMed1986

Influence of basal perfusion pressure on vasoconstrictor and vasodilator responses induced sympathetically and reflexly in pump-perfused rat hindquarters.

The hindquarters of Wistar rats, under pentobarbital anesthesia, were vascularly isolated and perfused at a constant flow rate (6.25 ml/min) with autologous blood. Basal perfusion pressure varied from 60 to 140 mm Hg during the experimental procedure and among individual rats. The magnitude of the constrictor effect of i.a. norepinephrine was virtually constant and independent of the basal pressure. I.A. injection of acetylcholine and histamine; i.v. injection of norepinephrine; and stimulation of the lumbar sympathetic nerves with pulses of 0.03 msec or less, produced dilator responses in the perfused extremities. Stimulation with pulses of 0.1 msec or more resulted in a constrictor response followed by a dilator response. These dilator responses increased linearly and the constrictor responses decreased linearly as the basal pressure increased. Thus, the law of initial value of resistance held true for all dilator responses tested and for the constrictor responses evoked by stimulation of the lumbar sympathetic nerves. This result permitted normalization of these responses to predicted values at a reference perfusion pressure (100 mm Hg) by statistical analysis. The dilator response elicited by stimulation with shorter pulses and the constrictor response elicited by longer pulses had the same time course, which suggests that the constrictor response is probably compounded by a synchronous dilator mechanism. Hexamethonium, guanethidine and prazocin abolished the dilator responses elicited by neural stimulation and those induced by i.v. norepinephrine. These results indicate that the responsiveness of pump-perfused rat hindquarters varies with the existing perfusion pressure in a linear fashion according to the law of initial value of resistance except in the case of i.a. norepinephrine. Both the electrically- and reflexly-evoked dilator responses require intact ganglionic and alpha-adrenergic transmission.

Acetylcholine↗
PubMed1984

Pharmacologic identification, activation and antagonism of two muscarine receptor subtypes in the lower esophageal sphincter.

Lower esophageal sphincter pressures were monitored with water-filled catheters in anesthetized opossums. Muscarinic agonists McN-A-343 and bethanechol were administered in the arterial supply of the sphincter. McN-A-343 caused relaxation after a brief contraction of the sphincter. Bethanechol caused a dose-dependent contraction. Tetrodotoxin antagonized the inhibitory effect of McN-A-343 but did not antagonized sphincter contraction caused by McN-A-343 or bethanechol. The mean ED50 values were 6.9 nmol/kg i.a. for McN-A-343-induced relaxation, 10.5 nmol/kg i.a. for McN-A-343-induced contraction and 0.4 nmol/kg i.a. for bethanechol-induced contraction. Atropine caused a dose-dependent rightward shift in the dose-response curves of inhibitory and excitatory effects of the two muscarinic agonists. Pirenzepine caused a dose-dependent rightward shift in the dose-response curves of McN-A-343-induced relaxation. Pirenzepine did not modify sphincter contraction caused by the muscarinic agonists. 4-Diphenylacetoxy-N-methylpiperidine methiodide, on the other hand, did not modify McN-A-343-induced sphincter relaxation but caused dose-dependent rightward shifts in the dose-response curves of sphincter contraction caused by McN-A-343 or bethanechol. These studies suggest that there are two distinct types of muscarine receptors in the opossum lower esophageal sphincter. The M1 muscarine receptors are present on the inhibitory neurons and participate in the synaptic transmission between vagal preganglionic and intramural postganglionic inhibitory neurons. They are activated by McN-A-343 and antagonized by pirenzepine. The M2 muscarine receptors are located directly on the sphincter muscle. They are also activated by McN-A-343, but are selectively activated by bethanechol and are antagonized by 4-diphenylacetoxy-N-methylpiperidine methiodide.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗