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PubMed1995

Effects of pinacidil on arterial and venous resistances and mean circulatory filling pressure in rats.

1. The effects of the potassium channel opener, pinacidil, on mean arterial pressure (MAP), mean circulatory filling pressure (MCFP), total peripheral resistance (TPR), cardiac output (CO) and resistance to venous return (Rv) were studied in rats. 2. In pentobarbitone-anaesthetized rats given mecamylamine (ganglionic blocker, 3.7 micrograms kg-1) and noradrenaline (1.5 micrograms kg-1 min-1) to suppress autonomic reflexes, pinacidil (60 and 180 micrograms kg-1 min-1), relative to the vehicle, reduced MAP and TPR in a dose-dependent manner but did not significantly alter CO, MCFP or RV. 3. Pinacidil (10-300 micrograms kg-1 min-1) caused similar increases in MCFP, an inverse index of venous compliance, and similar dose-dependent reductions in mean arterial pressure (MAP) in conscious, intact rats and rats infused with the ganglionic blocker, hexamethonium (150 micrograms kg-1 min-1). In rats with vasomotor tone elevated by the infusion of noradrenaline (1.5 micrograms kg-1 min-1), pinacidil caused markedly greater depressor responses but did not significantly alter MCFP. 4. Our results show that pinacidil is an efficacious vasodilator of arterial resistance blood vessels but has little venodilator activity.

Anesthesia↗
PubMed2006

Role of beta-endorphin, corticotropin-releasing hormone, and autonomic nervous system in mediation of the effect of chronic ethanol on natural killer cell cytolytic activity.

BACKGROUND: We have recently shown that alcohol feeding suppresses natural killer (NK) cell cytolytic activity partly by decreasing the function of hypothalamic beta-endorphin (beta-EP) neurons. The neuronal mechanism by which hypothalamic beta-EP communicates with the spleen to regulate the action of ethanol on NK cells is not known. In the present study, we evaluated the roles of beta-EP neurons, corticotropin releasing hormone (CRH) neurons, and the autonomic nervous system (ANS) in regulation of the ethanol effect on splenic NK cell cytolytic function. METHODS: Male rats were fed an ethanol-containing liquid diet or control diets. These rats were used to determine the hormone release from the paraventricular nuclei (PVN) of the hypothalamus or used to determine the splenic NK cell cytolytic function after PVN administration of CRH or intraperitoneal (i.p.) administration of a ganglionic blocker chlorisondamine. The release of hormones from the PVN was measured using the push-pull perfusion method. Splenic cytolytic activity was determined using the 4-hour (51)Cr release assay against YAC-1 lymphoma target cells. RESULTS: Alcohol feeding decreased the amount of beta-EP but increased the amount of CRH in the push-pull perfusate (PPP) samples collected from the PVN. When exogenous beta-EP was perfused into the PVN, it suppressed the release of endogenous CRH found in PPP samples of the PVN. Conversely, perfusion of an opiate antagonist naltrexone into the PVN increased the levels of endogenous CRH in PPP samples of the PVN. In addition, administration of exogenous beta-EP in the PVN stimulated the cytolytic function of NK cells, an action that was antagonized by CRH as well as by ethanol. Corticotropin-releasing hormone and ethanol alone also had an inhibitory action on NK cells. Finally, the ganglionic blocker used prevented the effect that ethanol, beta-EP, and CRH had on NK cells. These data suggest that ethanol inhibits the function of NK cells partly by suppressing the influence of the beta-EP-CRH-ANS signal to the spleen.

Animals↗
PubMed1995

Activation of the micturition reflex by NK2 receptor stimulation in the anaesthetized guinea-pig.

1. The mechanisms underlying stimulation of bladder contractions and bronchoconstriction by the selective NK2 receptor agonist, [beta-Ala8]NKA(4-10), were examined in the anaesthetized guinea-pig. 2. Atropine, alpha,beta-methylene-ATP and ganglion blocking agents were used to examine the contribution of reflex arc activation and/or potentiation of efferent mechanisms to the NK2 receptor-mediated responses seen in these two tissues. 3. [beta-Ala8]NKA(4-10)-induced bronchoconstriction was immediate, dose-dependent and was unaffected by pretreatment with ganglion blockers (hexamethonium or chlorisondamine), blockade of muscarinic receptors by atropine, or desensitization of P2 purinoceptors by alpha,beta-methylene-ATP. 4. At does of 5 micrograms kg-1 and above, [beta-Ala8]NKA(4-10) induced bladder contractions that appeared to be of an 'all-or-nothing' nature. These contractions occurred after a delay of 10 to 30 s and were often biphasic, comprised of an initial rapid component followed by a slower tonic component. 5. Pretreatment of the animals with either atropine or the desensitizing purinoceptor agonist alpha,beta-methylene-ATP, resulted in partial inhibition of bladder contractile responses to [beta-Ala8]NKA(4-10). The combination of atropine and alpha,beta-methylene-ATP pretreatment resulted in additive inhibition leading to complete blockade of the response. 6. The bladder responses to [beta-Ala8]NKA(4-10) (5 micrograms kg-1) were inhibited by pretreatment with the ganglion blockers, hexamethonium and chlorisondamine, indicating a preganglionic mechanism of action. 7. These findings demonstrate the indirect nature of the bladder contractions induced by activation of NK2 receptors in the anaesthetized guinea-pig. Contractions occur secondary to the release of endogenous cholinergic and NANC transmitters by activation of neuronal NK2 receptors located at apreganglionic site, possibly on capsaicin-sensitive sensory afferent nerves, where NK2 sites have been demonstrated autoradiographically. In contrast, [beta-Ala8]NKA(4- 10)-induced bronchoconstriction in the anaesthetized guinea-pig is a direct smooth muscle contractile response that is unaffected by ganglionblockade or blockade of muscarinic receptors.

Animals↗
PubMed1986

Dopamine, noradrenaline and isoprenaline: secretory and electrophysiological effects in vitro on mouse pancreas.

The amylase release from mouse pancreatic fragments was studied after dopamine (DA), and alpha- or beta-sympathomimetic agonist application. The electrical parameters of the acinar cell membrane were also monitored. Both DA (from 5 X 10(-6) to 10(-4) M) and beta-stimulants (isoprenaline from 5 X 10(-6) to 5 X 10(-5) M; noradrenaline from 3 X 10(-4) to 10(-3) M) evoked an increase in amylase release, while noradrenaline in alpha-receptor stimulating doses failed to have any effect. The stimulatory effect of DA was blocked by ganglion blockers (Arfonad 10(-5) M; pentamethonium 3 X 10(-5) M) in a competitive manner and a dual antagonism was observed with atropine (10(-7) M, 10(-9) M). An alpha-receptor antagonist (phentolamine 10(-5) M) and a beta-receptor antagonist (propranolol 10(-5) M) had no influence on the dopamine response. Moreover, the DA-induced stimulation was dependent on the presence of extracellular calcium. Perfusion with 10(-4) and 10(-3) M-DA or local application (from 77 micrograms to 4.3 mg), resulted in marked membrane depolarization with diminution of the input resistance. This effect was blocked by atropine (10(-5) M) and pentamethonium (10(-4) M), but not by propranolol (10(-5) M) or phentolamine (10(-5) M). The isoprenaline- (IP) and noradrenaline- (NA) induced increase in amylase release was competitively blocked by propranolol (10(-5) M) but not by phentolamine (10(-5) M). Atropine caused a dose-dependent (10(-7) M, 10(-6) M) decrease in the maximal response (non-competitive antagonism), while the ganglion blocker pentamethonium (10(-4) M) was without effect. NA caused membrane depolarization accompanied by a decrease in the input resistance after local application (from 77 micrograms to 1.6 mg). This effect persisted in the presence of 10(-5) M-phentolamine but was abolished by 10(-5) M-propranolol. IP perfusion (10(-4) and 10(-3) M) or local application (0.3 M; from 32 to 130 micrograms) caused the same electrical changes as those induced by NA and DA. The effect of IP persisted in the presence of 10(-5) M-phentolamine, 10(-4) M-pentamethonium and 10(-4) M-domperidone, but was abolished by propranolol (10(-5) M) and tetrodotoxin (5 X 10(-6) M) and markedly diminished by atropine (10(-5) M).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1990

Vagal afferent-mediated inhibition of a nociceptive reflex by intravenous serotonin in the rat. I. Characterization.

The effect of intravenous (i.v.) serotonin (5-HT) on nociception and blood pressure was examined in male Sprague-Dawley rats. Intravenous 5-HT produced a dose-dependent (6-192 micrograms/kg, i.v.) inhibition of the nociceptive tail-flick (TF) reflex in lightly pentobarbital-anesthetized (ED50 = 40 micrograms/kg) and conscious rats (ED50 = 44 micrograms/kg). In the lightly pentobarbital-anesthetized rat, the blood pressure response to i.v. 5-HT was typically a triphasic response with a marked Bezold-Jarisch reflex-induced decrease in pressure (associated with a brief period of apnea) followed by a pressor phase and a subsequent delayed hypotension. In the conscious rat, the response was typically biphasic with the late hypotensive phase absent. A variety of anatomical and pharmacological manipulations were performed to characterize the 5-HT-induced inhibition of the TF reflex and associated changes in blood pressure. Prevention of 5-HT-induced reflex apnea by artificial ventilation did not affect inhibition of the TF reflex produced by 5-HT. Pharmacological manipulations were performed to mimic, as closely as possible, the acute increases and decreases in blood pressure associated with i.v. 5-HT. Nitroprusside (8 micrograms/kg, i.v.) produced a decrease in blood pressure of similar magnitude and rate as that associated with the Bezold-Jarisch reflex-induced decrease in pressure produced by 72 micrograms/kg 5-HT, but did not change TF latency from baseline. Similarly, acute increases in pressure produced by phenylephrine (8 micrograms/kg, i.v.), intended to mimic the secondary pressor effect of 5-HT, did not change TF latency. The short-acting ganglion blocker trimethaphan (5 mg/kg, i.v.) closely mimicked the late hypotensive phase produced by 5-HT, but again resulted in no change in TF latency. Pretreatment with the ganglion blocker chlorisondamine (2.5 mg/kg) abolished all depressor responses to 72 micrograms/kg 5-HT, but did not significantly affect the TF reflex. These results indicate that acute changes in blood pressure and respiration associated with i.v. 5-HT do not contribute to inhibition of the TF reflex. This conclusion was confirmed in experiments in which bilateral vagotomy abolished approximately 70% of the 5-HT-induced inhibition of the TF reflex (and all depressor responses), and resulted in a significantly greater pressor response. Finally, low thoracic spinal cord transection (T9-10) abolished the inhibition of the TF reflex produced by i.v. 5-HT. Therefore, 5-HT stimulates vagal afferents and inhibits the TF reflex by activating descending inhibitory systems from the brainstem.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1982

A rat model for predicting orthostatic hypotension during acute and chronic antihypertensive drug therapy.

An experimental model has been developed to determine postural hypotension in chloralose-urethane-pentobarbital (CUP) anesthetized rats. Using this technique, mean arterial pressure, heart rate, and blood pressure compensation to 60 degree tilt were examined in rats treated acutely and chronically with a spectrum of standard antihypertensive agents. The results closely parallel the orthostatic profiles seen clinically with these drugs. Significant orthostatic hypotension was seen with the acute intravenous administration of the alpha-adrenergic antagonists phenoxybenzamine, phentolamine, and prazosin, the neuronal suppressant guanethidine, and the ganglionic blockers hexamethonium and chlorisondamine. The central antihypertensive clonidine displayed mild, acute orthostasis that dissipated by 1 hr. The vasodilator minoxidil was entirely free of postural effects. Chronically, guanethidine, the ganglionic blocker mecamylamine, and a high dose of reserpine all resulted in significant postural hypotension after 4 days of oral administration. Prazosin's acute orthostasis had largely dissipated by this time. Chronic minoxidil resulted in slight overcompensation to tilt. Based on the consistency to these data relative to the clinical profiles of these standard antihypertensive agents, it would appear that the CUP anesthetized rat is an accurate, efficient test model for identifying orthostasis in novel hypotensive agents under acute and chronic drug treatment conditions.

Anesthesia↗
PubMedDate not supplied

Capsaicin-sensitive primary afferents are involved in the hypotensive effect of neurotensin in ganglion-blocked guinea pigs.

The mechanism of the blood pressure (BP)-lowering effect of neurotensin (NT) in the anesthetized, ganglion-blocked guinea pigs was further examined using animals in which the basal BP was artificially raised by an IV infusion of noradrenaline (NA) to overcome the BP-lowering effect of the anesthesia as well as of the ganglion blocker. The animals were also vagotomized and given atropine at the beginning of the experiments to prevent potential baroreceptor-mediated vagal reflexes and/or activation of muscarinic receptors by endogenous acetylcholine. Under these experimental conditions, the IV bolus injections of NT as well as of capsaicin (a reference drug) produced dose-dependent hypotensive effects and variable levels of tachycardia. Omitting the ganglion blocker from the animal drug regimen attenuated but did not abolish the BP-lowering effect of NT and of capsaicin. Neither the hypotensive nor the tachycardic effects of NT and of capsaicin in ganglion-blocked guinea pigs were affected by prior animal treatment with propranolol (a beta adrenoceptor blocker), antihistaminics (mepyramine, cimetidine) or indomethacin (a cyclooxygenase inhibitor). Morphine was found to slightly reduced the hypotensive effect of NT without altering its slight tachycardic effect. Both the hypotensive and tachycardic effects of NT and of capsaicin, in contrast to those elicited by substance P (SP) and calcitonin gene-related peptide (CGRP), were inhibited in ganglion-blocked guinea pigs pretreated four days previously with capsaicin.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1995

Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata.

The cholinergic agonist-induced secretion of catecholamines from chromaffin cells in the American eel, Anguilla rostrata, was assessed using a saline-perfused posterior cardinal vein preparation. Direct membrane depolarization with 60 mmol.l-1 K+ caused a significant release of catecholamines (adrenaline+noradrenaline) into the perfusate which was unaffected by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The nicotinic receptor agonist, 1,1-dimethyl-4-phenyl-piperazinium iodide, evoked catecholamine release in response to several doses exceeding 10(-7) mol; at 10(-5) mol the response was abolished by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The muscarinic receptor agonist, pilocarpine, did not elicit catecholamine release in response to any of the doses administered (10(-8)-10(-4) mol). A single injection of the mixed nicotinic/muscarinic cholinoceptor agonist, carbachol (10(-5) mol), caused the release of catecholamines which was abolished by pre-treatment with hexamethonium but which was unaffected by pre-treatment with the muscarinic receptor antagonist atropine (final concentration = 10(-5) mol.l-1). The results of this study indicate that the process of cholinergic agonist-induced catecholamine secretion from the chromaffin cells in the American eel is mediated exclusively by activation of nicotinic receptors with no involvement of the muscarinic receptor.

Animals↗
PubMed1998

Sensitivity to voltage-independent inhibition determined by pore-lining region of the acetylcholine receptor.

Some noncompetitive inhibitors (e.g., ganglionic blockers) exhibit selectivity for the inhibition of neuronal nicotinic acetylcholine receptors (nAChRs). This study characterizes the mechanism of selective long-term inhibition of neuronal and muscle-neuronal chimeric nAChRs by bis(2,2,6,6-tetramethyl-4-piperidinyl) sebacate (bis-TMP-10 or BTMPS), a bifunctional form of the potent ganglionic blocker tetramethylpiperidine. Long-term inhibition of neuronal nAChRs by bis-TMP-10 has been previously demonstrated to arise, at least in part, from the binding of the bis compound to neuronal beta-subunits. In this study, long-term inhibition is demonstrated to be dependent upon the presence of sequence element(s) within the pore-lining second transmembrane domain (tm2) of neuronal beta-subunits; however, the inhibitor binding site itself does not appear to be contained within the segment of the channel pore influenced by the membrane electric field. Specifically, our results imply that bis-TMP-10 interacts with an activation-sensitive element, the availability of which may be regulated by a sequence in the tm2 domain. Furthermore, we demonstrate a compound length requirement for long-term inhibition that would be consistent with binding to multiple sites located on the extracellular portion of the receptor.

Acetylcholine↗
PubMed1997

Effect of ganglionic blocking compounds on in-vivo fluid secretion in the rat small intestine.

It is well-known that enteric, secreto-motor nerves mediate cholera toxin-induced fluid secretion in the rat small intestine. This notion is, in part, derived from experiments on anaesthetized animals in which the response to cholera toxin was antagonized by the ganglionic nicotinic receptor antagonist, hexamethonium. In the current study, such anti-secretory action of ganglionic blocking compounds was analysed in an experiment designed to minimize any possible negative effect of general anaesthesia on intestinal secretion. Rats were anaesthetized with ether for 5-10 min, during which time a jejunal loop (10-12 cm) was constructed. The loop was challenged with one of the secretagogues, cholera toxin, prostaglandin E1 (PGE1) or okadaic acid. Saline (control) or either of the ganglionic blockers, hexamethonium and chlorisondamine, was administered intravenously. The rats were killed 5 h (cholera toxin) or 1.5 h (PGE1 and okadaic acid) after challenge, and the amount of fluid accumulated in the loops was determined. Cholera toxin-induced secretion was unchanged by hexamethonium but reduced by approximately 80% by chlorisondamine. The difference in effect between the two blockers might relate to the duration of ganglionic blockade. Chlorisondamine blocked secretion induced by either PGE1 or okadaic acid by approximately 60%. It is suggested that the anti-secretory effect of ganglionic blocking compounds might be a result of blockade of secreto-motor nerves but other mechanisms, for example interference with haemodynamic factors, cannot be ruled out.

Alprostadil↗
PubMed1994

Does the spinal cord generate functionally significant sympathetic activity in the awake rat?

Previous studies reach conflicting conclusions regarding the presence of physiologically significant sympathetic nerve activity (SNA) in conscious rats with transection of the cervical spinal cord (CST). The objective of the current study was to determine whether either spinally generated SNA or nonspecific effects of antagonists are responsible for the natriuresis and decreased heart rate that accompany adrenergic blockade in CST rats. To test the first possibility, adrenergic antagonists (phentolamine and propranolol) were administered to three groups of CST rats: 1) renal denervated, 2) adrenalectomized or sham-adrenalectomized, and 3) rats who received the ganglionic blocker hexamethonium. Neither renal denervation, adrenalectomy, nor ganglionic blockade prevented either the three- to fivefold increase in sodium excretion or the 25-50 beats/min decrease in heart rate previously reported. We then administered combinations of different adrenergic antagonists to CST rats to test for nonspecific effects of the drugs. Whereas idazoxan+propranolol reproduced the natriuresis seen with phentolamine+propranolol, prazosin+yohimbine+propranolol did not. We conclude that there is no evidence for functionally significant spinally generated SNA in conscious CST rats and that the natriuresis observed with phentolamine administration is due to imidazoline binding.

Adrenalectomy↗
PubMed1982

Antihypertensive treatment and fetal welfare in essential hypertension in pregnancy: a retrospective survey of experience with various regimes at National Women's Hospital, Auckland, 1970-80.

A series of 184 pregnancies in 161 hypertensive women was classified according to the regimen of antihypertensive treatment used during pregnancy. In 72 pregnancies management was with bed rest alone, attaining a mean gestation of 37.8 +/- 0.4 weeks, a mean birthweight of 2941 +/- 97 g with 38 percent of infants below the 25th percentile. Late deterioration of hypertension with development of proteinuria occurred in 16.6 percent with fetal mortality of 6.9 percent. Antihypertensive therapy involved methyldopa, thiazide diuretics, sympathetic ganglion blockers, hydralazine, beta-adrenergic blockers and the combination of oxprenolol and prazosin. Fetal growth was compared in pregnancies that reached term on the various regimens. Significantly better growth was achieved where debrisoquine plus a thiazide were used (3617 +/- 113 g in six subjects) and oxprenolol/prazosin (3411 +/- 72 g in 14 subjects) compared to 11 comparably hypertensive patients on bed rest alone (2975 +/-87 g). Therapy with the ganglion blocker plus thiazide was complicated by the deterioration of hypertension with proteinuria in 37.2 percent of women; this did not occur in patients receiving oxprenolol/prazosin. Maternal age had no effect on fetal growth, but smoking more than 10 cigarettes per day caused significant growth retardation.

Antihypertensive Agents↗
PubMed1989

Pharmacological distinctions between functional nicotinic acetylcholine receptors on the PC12 rat pheochromocytoma and the TE671 human medulloblastoma.

Some properties of functional nicotinic acetylcholine receptors (nAcChoR) expressed by the PC12 rat pheochromocytoma or the TE671 human medulloblastoma were studied by the use of an isotopic rubidium ion efflux assay. The assay involves active uptake of 86Rb+ via a ouabain-sensitive mechanism to load cells with isotopic tracer and the subsequent release of ion from cells through agonist-activated opening of nAcChoR-coupled ion channels. For either cell line the rate of receptor-mediated ion efflux is time-dependent and falls as duration of exposure to agonist increases. However, dose-response curves for agonist activation of receptor function (or for antagonist blockade of agonist activation) are temporally invariant. Dose-response curves have characteristic shapes for a given agonist, and the relative and absolute potencies of agonists differ between TE671 and PC12 cells. Most notably, nicotine and cytisine are more potent activators of receptor function on the PC12 cell line whereas TE671 cell nAcChoR are more sensitive to activation by isoarecolone and suberyldicholine. PC12 cell nAcChoR are more sensitive to blockade by the classic "ganglionic" blockers, mecamylamine and hexamethonium, and by the molluscan substance, neosurugatoxin, than are nAcChoR on TE671 cells. The results, illustrating differences in the pharmacological profiles of drugs acting as functional nAcChoR on TE671 and PC12 cells, suggest that structural differences exist in nAcChoR active site(s) and are consistent with the notion that functional nAcChoR are a heterogeneous family of macromolecules.

Animals↗
PubMed1988

Adrenal proenkephalin-derived peptides during postnatal development in spontaneously hypertensive rats.

Adrenal enkephalin and enkephalin-containing peptides were studied during postnatal development in normotensive (WKY) and spontaneously hypertensive rats (SHR). The effect of chronic treatment with the ganglionic blocker chlorisondamine (5 mg/kg) was also assessed. Free enkephalin immunoreactivity and total enkephalin immunoreactivity, as determined by enzymatic digestion of large enkephalin containing fragments, were quantitated in the adrenal glands at 11 days and 7, 16, and 24 weeks of age. Both total and free metenkephalin were significantly diminished in the adrenal of SHR when compared to WKY at all ages tested. The analysis of the chromatographic profile showed that SHR displayed reduced levels of high and low molecular weight materials at 11 days and 16 weeks of age; however intermediate compounds were high in the glands of these animals. Similar increased values for free met-enkephalin were found in adrenals of WKY and SHR after ganglionic blocker treatment, which means that the relative increase was larger in SHR than WKY; while for total enkephalin the relative increase and the concentration reached in SHR was about half of those presented in WKY. These and other results presented suggest that the basic alteration of the adrenal proenkephalin system of SHR may be due to a genetic reduction of proenkephalin levels. Otherwise, the free enkephalin decrease could be related to changes in nervous input to the adrenal gland.

Adrenal Glands↗
PubMed1990

Effects of alpha 1- and alpha 2-adrenoceptor antagonists on venous tone in conscious rats.

The dose-response effects of hexamethonium, prazosin and rauwolscine - a ganglionic blocker, alpha 1- and alpha 2-adrenoceptor antagonists, respectively - on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of body venous tone, were examined in conscious and unrestrained rats. Prazosin and rauwolscine were also administered to rats after venous tone was elevated by drug-induced hypotension via the infusion of the vasodilator drug hydralazine. The effects of these drugs were compared with those of the vehicle, acidified glucose solution, administered to control rats. In intact rats, i.v. infusions of prazosin and rauwolscine dose dependently decreased MAP; the highest dose of rauwolscine, but not prazosin slightly reduced MCFP. The i.v. infusion of hexamethonium reduced MAP and caused a marked dose-dependent decrease in MCFP. After venous tone was raised by hydralazine, both prazosin and rauwolscine dose dependently decreased MCFP. The decrease in MCFP caused by rauwolscine was significantly greater than that caused by prazosin. Our results show that in the basal condition, the capacitance vessels are somewhat resistant to the effects of alpha-adrenoceptor antagonists in contrast to the effects of ganglionic blockers. After venous tone was raised by reflex mechanisms, both alpha-adrenoceptor antagonists were effective in lowering venous tone, however, the effect of alpha 2-adrenoceptor antagonist is significantly greater than that of alpha 1-adrenoceptor antagonist.

Adrenergic alpha-Antagonists↗
PubMed2004

Parasympathetic control of the heart. II. A novel interganglionic intrinsic cardiac circuit mediates neural control of heart rate.

Intracardiac pathways mediating the parasympathetic control of various cardiac functions are incompletely understood. Several intracardiac ganglia have been demonstrated to potently influence cardiac rate [the sinoatrial (SA) ganglion], atrioventricular (AV) conduction (the AV ganglion), or left ventricular contractility (the cranioventricular ganglion). However, there are numerous ganglia found throughout the heart whose functions are poorly characterized. One such ganglion, the posterior atrial (PA) ganglion, is found in a fat pad on the rostral dorsal surface of the right atrium. We have investigated the potential impact of this ganglion on cardiac rate and AV conduction. We report that microinjections of a ganglionic blocker into the PA ganglion significantly attenuates the negative chronotropic effects of vagal stimulation without significantly influencing negative dromotropic effects. Because prior evidence indicates that the PA ganglion does not project to the SA node, we neuroanatomically tested the hypothesis that the PA ganglion mediates its effect on cardiac rate through an interganglionic projection to the SA ganglion. Subsequent to microinjections of the retrograde tracer fast blue into the SA ganglion, >70% of the retrogradely labeled neurons found within five intracardiac ganglia throughout the heart were observed in the PA ganglion. The neuroanatomic data further indicate that intraganglionic neuronal circuits are found within the SA ganglion. The present data support the hypothesis that two interacting cardiac centers, i.e., the SA and PA ganglia, mediate the peripheral parasympathetic control of cardiac rate. These data further support the emerging concept of an intrinsic cardiac nervous system.

Animals↗
PubMed1983

Dopaminergic inhibition of aldosterone secretion in man is independent of the autonomic nervous system.

To determine whether the plasma aldosterone response to metoclopramide, a dopamine antagonist, is mediated by the autonomic nervous system in man, five healthy male volunteers were injected with metoclopramide during an infusion of either 5% dextrose in water or trimethaphan, a ganglionic blocker. Despite evidence of ganglionic blockade during the trimethaphan infusion, the aldosterone response to metoclopramide remained intact. This suggests that the aldosterone response to metoclopramide is not mediated by the autonomic nervous system in man as it appears to be in the sheep, and suggests species variation in the mechanism of this this mineralocorticoid response.

Adult↗
PubMed1984

Role of autonomic nervous system in the time-dependent hyperglycemia induced by intracranial injection of D-mannitol and D-glucose.

Intracranial injection of D-mannitol (MA) or D-glucose (GL) caused photoperiodic hyperglycemia in rats; MA injection elicited hyperglycemia only in the light period, while GL injection induced it only in the dark period. To elucidate the mechanisms of these hyperglycemias, we examined the effect of the autonomic nervous system on them in rats under the L:D (12:12) condition. Propranolol, a beta-adrenergic blocker, and hexamethonium, a ganglion blocker, effectively inhibited hyperglycemia induced in either the light (MA) or dark (GL) period. In contrast, phenoxybenzamine, an alpha-adrenergic blocker, and atropine, a cholinergic blocker, inhibited hyperglycemia induced in the light period (MA), but not that induced in the dark period (GL). These findings suggest that alpha and beta-adrenergic and cholinergic mechanisms are involved in the hyperglycemia induced by MA in the light period, while only the beta-adrenergic mechanism is involved in the hyperglycemia induced by GL in the dark period.

Animals↗