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At least 1,153 records · Page 64Linked to original sources
PubMed1977

The interrelation between hypothalamically induced changes in sympathetic discharge to the gastrointestinal and cardiovascular systems.

In chloralose-anesthetized, adrenalectomized cats, the sympathetically conveyed effects of topical hypothalamic stimulations on gastric volume, blood pressure and heart rate were systematically explored. The vagal nerves were cut but could be kept active by graded efferent stimulation. In the absence of such vagal activity, hypothalamic stimulation had no appreciable influence on gastric volume, even though the stomach maintained considerable myogenic tone. When, however, a vagal excitatory activity was present, hypothalamic stimulation could markedly affect gastric tone, indicating that the sympathetic fibres exert their inhibitory influence on the stomach via its cholinergic intramural neurons. Hypothalamic stimulations that induced reductions in pressure or heart rate also usually caused an enhancement of gastric tone. Similarly, pressor responses were associated with decreases in gastric volume whereas stimulation-induced tachycardia was not linked to any particular type of gastric response. Thus, the hypothalamic sympathoinhibitory influences on the cardiovascular system seem closely connected to a supression of the sympathetic outflow to the stomach. There is, on the other hand, no regular association between hypothalamic sympathoexcitatory influences on the cardiovascular and gastrointestinal systems; in fact, there is in many areas even a suppression of sympathetic discharge to the stomach in association with cardiovascular stimulation.

Adrenalectomy↗
PubMed1979

The spinal origin of the sympathetic nerve fibres to the vascular and secretory components of the rat submaxillary salivary gland.

The spinal origin of the sympathetic vasoconstrictor and secretory fibres to the submaxillary gland of the rat was identified in the pithed rat preparation by means of selective stimulation of small segments of the spinal outflow. Secretory and vascular responses were similar following stimulation in pithed rats to those following stimulation of the isolated superior cervical nerve trunk in anaesthetized rats. The spinal origin of the secretory and vascular fibres was coincident and it is concluded that if a separate control of blood flow and secretion by sympathetic fibres does exist that it must occur at the level of C.N.S. but that the nerves share a common pathway to the gland.

Animals↗
PubMed1977

Prostaglandins in adrenergic transmission of isolated perfused rat pancreas.

In the isolated, perfused rat pancreas, prostaglandins (PGs) E1 and E2 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2alpha had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicylic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter three agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2alpha inhibited the vasoconstrictor responses to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1980

Prejunctional cholinergic modulation of adrenergic neurotransmission in the cardiovascular system.

In the heart and in the blood vessel walls, complex adrenergic-cholinergic interactions occur both prejunctionally, at the level of the autonomic nerve terminals, and postjunctionally, at the level of the responding cells themselves. The principal prejunctional interaction appears to be an inhibition of the release of norepinephrine from adrenergic nerve terminals by the acetylcholine liberated from nearby cholinergic nerve endings. This inhibitory effect is mediated by muscarinic receptors located on the postganglionic sympathetic nerve terminals. The inhibitory effect of acetylcholine on cardiac and vascular tissues are therefore achieved in part by a direct influence of the cholinergic neurotransmitter on the cardiac and vascular muscle cells, and in part by an indirect influence on sympathetic neurotransmission.

Acetylcholine↗
PubMed1981

Femoral circulatory responses to lumbar nerve stimulation in developing swine.

The maturation of femoral circulatory responses to efferent lumbar nerve stimulation was tested in 51 developing swine (1 day-3 mo old) under pentobarbital sodium anesthesia (10-30 mg/kg). Aortic pressure, heart rate, and femoral and carotid arterial flows (measured by electromagnetic flow transducers) were recorded simultaneously. Femoral vascular resistance was calculated as mean aortic pressure/mean flow. Transection of the lumbar nerve fibers below the last ganglion in the sympathetic chain did not after femoral resistance in day-old animals but decreased femoral resistance in swine 1 wk of age and older. Efferent lumbar nerve stimulation at various combinations of frequencies and intensities revealed an atropine-blockable vasodilator component in the femoral circulatory response in swine 1 mo of age and older. After alpha-adrenergic receptor blockade with phentolamine (0.25 or 0.5 mg/kg), femoral vasodilation occurred during low-frequency and -intensity stimulation of the lumbar nerve only in animals 1 mo of age and older. Acetylcholine (2 micrograms ia) caused a decrease in femoral resistance at all ages. Vasoconstrictor effects of high-frequency stimulation (5-10 Hz) were present at all ages and were age dependent. The results of these experiments suggest that the femoral circulation in swine at birth in innervated by functionally active vasoconstrictor fibers, which do not provide a tonic influence on femoral resistance until late in the first postnatal week. Furthermore, although femoral vascular cholinergic receptors are demonstrable at birth, there appears to be a delay in the maturation of functionally active vasodilator fibers.

Aging↗