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At least 19 recordsLinked to original sources
PubMed1985

Mechanisms underlying changes in the contents of neuropeptide Y in cardiovascular nerves and adrenal gland induced by sympatholytic drugs.

Neuropeptide Y (NPY) is a recently isolated vasoactive peptide, which is present, together with catecholamines, in sympathetic nerves and in the adrenal medulla. In the present study, we report that pretreatment with sympatholytic agents influences the tissue levels of NPY-like immunoreactivity (NPY-LI) in the guinea-pig. Thus, 24 h after reserpine not only noradrenaline (NA), but also NPY-LI, was depleted in the heart, spleen and the adrenal gland. The levels of NPY-LI in the vas deferens and stellate ganglia, however, were unaffected by reserpine in spite of marked depletions of NA. The reserpine-induced depletion of NPY-LI was probably caused by enhanced nerve-impulse flow and subsequent release from cardiovascular nerves in excess of resupply, since it could be prevented by the ganglionic-blocking agent chlorisondamine. Long-term (6 days) treatment with chlorisondamine reduced the levels of NPY-LI in the stellate ganglion. Short-term treatment (48 h) with guanethidine partially prevented the reserpine-induced depletion of NPY-LI, probably due to inhibition of NPY release. Long-term guanethidine treatment depleted not only NA, but also NPY-LI from the spleen. Pretreatment with the alpha-receptor antagonist phenoxybenzamine did not influence the NA levels but reduced the content of NPY-LI in the spleen via a mechanism that was dependent on intact ganglionic transmission. Since NPY has several cardiovascular actions, changes in NPY mechanisms may contribute to the pharmacological and therapeutical effects of sympatholytic agents.

Adrenal Glands↗
PubMed1987

Neuropeptide Y and noradrenaline mechanisms in relation to reserpine induced impairment of sympathetic neurotransmission in the cat spleen.

The mechanisms underlying the reserpine-induced impairment of the functional responses to sympathetic nerve stimulation and output of noradrenaline (NA) and neuropeptide Y (NPY)-like immunoreactivity (-LI) were studied using the isolated blood-perfused cat spleen. Splenic nerve stimulation (10 Hz for 2 min) during control conditions caused perfusion-pressure increase, volume reduction and an increased output of NA and NPY-LI. After administration of phenoxybenzamine, the nerve stimulation-induced perfusion-pressure increase was almost abolished, the volume reduction inhibited and the output of NPY-LI enhanced. After subsequent addition of propranolol, a clear-cut increase in perfusion pressure upon nerve stimulation reappeared. Local infusion of NPY caused a potent, long-lasting, adrenoceptor-resistant increase in perfusion pressure and a relatively smaller volume reduction of the spleen. Twenty-four hours after reserpine pretreatment (1 mg kg-1 i.v.), which depleted the splenic content of NA greater than 95% and NPY-LI by about 50%, the functional responses upon nerve stimulation were markedly reduced. Preganglionic denervation or pretreatment with the ganglionic-blocking agent chlorisondamine did not influence the NA depletion after reserpine treatment. A considerable, adrenoceptor antagonist-resistant, long-lasting functional response as well as a markedly enhanced output of NPY-LI then occurred upon nerve stimulation. In conclusion, reserpine treatment combined with interruption of preganglionic impulse flow reveals non-adrenergic, nerve stimulation evoked splenic functional responses which could be mediated by release of a cotransmitter peptide like NPY.

Adrenergic alpha-Antagonists↗
PubMed1988

CRF activates autonomic nervous system and reduces natural killer cytotoxicity.

Corticotropin-releasing factor (CRF) acts within the brain to elicit changes in neuroendocrine, autonomic, and behavioral activity similar to those observed after stress. A reduction of immune function has also been described following central administration of CRF. In this study, we examined whether autonomic nervous system activation plays a role in CRF-induced suppression of natural killer (NK) cytotoxicity. synthetic rat CRF (1.0 microgram) microinjected into the lateral ventricle significantly increased plasma concentrations of norepinephrine and reduced splenic NK cell activity in the rat. Pretreatment of the animals with the ganglionic-blocking agent chlorisondamine completely abolished the CRF-induced increase in plasma norepinephrine levels and reduction in NK activity. However, CRF-induced elevations in plasma levels of adrenocorticotropic hormone and corticosterone were not affected by chlorisondamine. The results of this study suggest that activation of the sympathetic nervous system plays a role in CRF-induced suppression of NK cytotoxicity.

Adrenocorticotropic Hormone↗
PubMed1989

Effects of m-chlorophenylpiperazine on penile and bladder function in rats.

The effects of m-chlorophenylpiperazine (MCPP), a serotonin agonist, on spontaneous and evoked neural firing in nerves supplying the penis and bladder were examined in the urethan-anesthetized rat. MCPP (0.1-10 mg/kg iv) elicited, after a 2- to 4-min delay, an increase in spontaneous firing in cavernous nerves but no detectable firing in bladder nerves. The cavernous nerve firing was accompanied by an increase in intracavernous pressure and a depression of rhythmic bladder activity. Administration of ganglionic-blocking agents or transection of peripheral nerves revealed that the cavernous nerve discharge was mediated by activation of pre-ganglionic cholinergic pathways in the pelvic nerve. The effects of MCPP were noted in intact as well as in acute and chronic spinal rats and were prevented by the administration of the serotonin (5-HT) antagonist, metergoline (3 mg/kg im). These data indicate that pharmacological activation of 5-HT receptors, possibly of the 5-HT1B subtype, can facilitate the sacral preganglionic outflow to the penis and inhibit bladder activity.

Animals↗
PubMed1976

Barbiturates block calcium uptake by stimulated and potassium-depolarized rat sympathetic ganglia.

The effects of two barbiturates on calcium uptake by sympathetic ganglia have been examined. Sodium pentobarbital (0.4-0.75 mM) and sodium thiopental (0.3 mM) block the preganglionic stimulation-induced uptake of 45Ca by rat superior cervical ganglia but not action potential conduction in the presynaptic axons. The ganglionic-blocking agent, tetraethylammonium, does not inhibit stimulation-induced Ca uptake and does not prevent the blocking effect of thiopental. This effect is therefore probably presynaptic. Postassium-rich media also stimulate Ca uptake by the ganglia, and this effect is markedly inhibited by pentobarbital. Since the K stimulation effect is also observed in deafferented ganglia but not in guanethidine-denervated ganglia, this effect is probably associated primarily with postsynaptic elements. In sum, the data suggest that the barbiturates inhibit Ca permeability changes in both pre- and postsynaptic neurons.

Animals↗
PubMed1990

Intrinsic neuroregulation of ion transport in porcine distal jejunum.

The roles of spontaneous and electrically stimulated neural activity on mucosal ion transport were examined in the distal jejunum of the pig, an omnivorous species whose digestive function bears similarities to that of humans. Serosal administration of the neuronal conduction blocker tetrodotoxin (TTX; 0.1 mumol/l), the presynaptic Ca channel blocker omega-conotoxin GVIA (0.1 mumol/l) and the ganglionic-blocking agent hexamethonium (0.1 mmol/l) decreased basal short-circuit current (Isc) across sheets of jejunal mucosa-submusa in vitro. The TTX-induced change in Isc was attributable to an increase in net Cl absorption. Electrical transmural stimulation (ETS; 300 pulses at 0.5, 3 or 10 Hz, 0.5-msec pulse width, 2.8 mA cm-2) of the mucosa-submucosa produced a frequency-dependent increase in Isc and an increase in net anion secretion. TTX, conotoxin and hexamethonium produced concentration-dependent decreases of the ETS-evoked increase in Isc, indicating that ETS depolarizes enteric neurons and suggesting that cholinergic neurons synapsing with submucosal neurons play a significant role in mediating ETS-evoked ion transport. The ETS-induced Isc appears to be mediated by neurons containing acetylcholine but not substance P or vasoactive intestinal polypeptide. These results suggest that submucosal noncholinergic neurons tonically limit Cl but not Na absorption. Electrical depolarization of submucosal neurons evokes anion secretion which appears to be mediated by cholinergic neurons as well as neurons of unknown chemical identity.

Acetylcholine↗
PubMedDate not supplied

Hemodynamic, neural, and humoral mechanisms of aortic coarctation hypertension in the rat.

The present study was designed: (a) to examine the contribution of the renin-angiotensin system (RAS) to elevated regional vascular resistance during the onset of aortic coarctation hypertension, and (b) to determine the role of angiotensin II (Ang II)-neural interactions during the maintenance of high arterial pressure (AP). In the first study, rats were instrumented chronically with miniaturized pulsed Doppler flow probes on the right renal and superior mesenteric arteries 3 days prior to complete aortic ligation. After ligation, AP and renal and mesenteric vascular resistances increased significantly. In sham-ligated rats, small increases in AP and decreases in regional vascular resistances were observed. Captopril, administered 6 h postligation, reduced AP and regional vascular resistance in ligated rats to preligation levels, indicating that the RAS was responsible for these acute increases. In the second study, Ang II-neural interactions were examined by treating 12- to 14-day postligation hypertensive rats with captopril or with hexamethonium, a ganglionic blocker, followed by captopril. Depressor responses to captopril were also examined in aortic-ligated rats pretreated with hydralazine. Captopril alone and captopril after hydralazine caused similar reductions in AP (-26 +/- 2% and -27 +/- 1%, respectively). After ganglionic blockade, the depressor responses to captopril were attenuated (-13 +/- 2%). The marked differences in the efficacy of captopril to lower AP in the ganglionic-blocked group of rats suggested that the pressor actions of Ang II were mediated, in part, through indirect actions on the sympathetic nervous system.

Animals↗