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PubMed1991

Neuropsychiatric considerations in the treatment of hypertension.

Algorithms have been developed to guide the treatment of simple hypertension. The basic algorithms are modified in the face of concurrent medical conditions, taking into account the various pharmacological effects of antihypertensive agents. This article reviews the neuropsychiatric effects of the major classes of antihypertensive agents (ganglionic blockers, centrally acting agents, diuretics, vasodilators, beta-blockers, calcium channel blockers and angiotensin converting enzyme inhibitors). The purported efficacy of some antihypertensive agents in the treatment of psychiatric conditions is also discussed. Beneficial as well as adverse neuropsychiatric effects are reviewed. In this way, guidelines for the treatment of hypertension are suggested which take into account a broad spectrum of neuropsychiatric considerations.

Antihypertensive Agents↗

PubMed1984

Ultrastructural study of the effect of acute hyper- and hypotension on the stria vascularis and spiral ligament.

The effects of acute hyper- and hypotension on the stria vascularis and spiral ligament of the rat were studied electron microscopically with the horseradish peroxidase (HRP) tracer method. Acute hypertension was induced by i.v. infusion of methoxamine chloride (Mexan), and acute hypotension by i.v. infusion of a ganglion-blocker (Arfonad) and by venesection. In both acute hyper- and hypotensive experiments, a large amount of leaked HRP spread into the intercellular spaces until it was stopped by tight junctions bordering the stria vascularis. The stria capillary endothelium displayed a dense distribution of labelled vesicles, which suggests increased vesicular transport. There was no extravasation of HRP from capillaries in the spiral ligament, despite the presence of some labelled pinocytotic vesicles. The present paper deals with the discovery of enhanced capillary permeability of the stria vascularis under acute hyper- and hypotension, and makes comparison between acute hyper- and hypotension in order to define the function of the stria vascularis.

Animals↗

PubMed1986

Involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate and sodium ricinoleate.

Rat small intestine was continuously perfused for up to 3 h with two different concentrations of sodium deoxycholate (4 and 8 mM) or with sodium ricinoleate (6 mM). The 4-mM bile salt solution produced a secretion that developed to a maximal rate within 3 h, whereas the maximal rate was reached within 1 h with the 8-mM bile salt solution. Hexamethonium, a ganglionic blocker, and lidocaine, a local anesthetic, always reduced the net fluid secretion to approximately zero irrespective of the rate of bile-salt-induced secretion, the concentration of the bile salt, or the perfusion time. Fluid secretion induced by sodium ricinoleate was, like the bile-salt-induced secretion, markedly inhibited by hexamethonium and lidocaine but not by atropine. It is concluded that the rate of secretion induced by the bile salt is related to the monomer concentration of free bile salt molecules in close proximity to or within the intestinal epithelium. The intestinal fluid secretion is mainly due to stimulation of an active secretory process via an activation of enteric nerves. Sodium ricinoleate evokes secretion via similar nervous reflex mechanisms.

Animals↗

PubMed1981

Effect of peripheral cholinergic activation on the adrenal cortex function.

The adrenocortical response to cholinergic agonist and antagonist agents were investigated in intact, hypophysectomized and medullectomized rats. The administration of peripherally active compound neostigmine, was found to cause a significant rise of corticosterone in the intact, and the hypophysectomized animals but not in the medullectomized animals. Meanwhile, the centrally and peripherally active cholinergic agent physostigmine caused a significant rise in the intact, hypophysectomized and medullectomized animals. The results also show that the administration of the ganglionic blocker (e.g. tetraethylammonium or hexamethonium), the muscarinic agonist (pilocarpin) or the muscarinic antagonist (atropin) did not result in any significant changes in corticosterone levels. The results of these experiments might indicate that peripheral cholinergic pathway is involved in the regulation of the adrenal cortex function.

Adrenal Cortex↗

PubMed1995

Age-dependent alterations in Na+, K(+)-ATPase activity in the central nervous system of spontaneously hypertensive rats: relationship to the development of high blood pressure.

We have previously demonstrated that cerebroventricular administrations (i.c.v) of potassium chloride solutions (KCl; 0.375-1.25 mumoles/5 microliters) elicit ouabain-sensitive, concentration-dependent decreases in the blood pressure and heart rates of anesthetized, normotensive Sprague-Dawley (SD) rats. These studies have suggested an inverse relationship between Na(+)-pump activity in the central nervous system (CNS) and central sympathetic outflow. Such a view is further supported by the present studies showing that i.c.v. injections of KCl failed to produce any alterations in the blood pressures of rats pretreated with an autonomic ganglionic blocker, chlorisondamine. In the present studies, depressor responses to i.c.v. potassium chloride were considered as functional indices for evaluation of neuronal Na(+)-pump activity in 8 and 12 week old (8 wk and 12 wk) SHR, WKY and Sprague-Dawley (SD) rats. Basal arterial blood pressures of 8 wk-old SD and SHR, and the responsiveness of these two groups to i.c.v. potassium chloride solutions are similar and they both are significantly greater than that of age matched WKY. However, in the 12 wk-old groups, arterial pressure of SHR was significantly greater than that of WKY as well as SD, whereas the depressor responses to KCl in SHR were significantly greater than that of only WKY. Pretreatment of the rats with i.c.v. ouabain abolished the differences in the hypotensive responses to i.c.v. potassium chloride that existed between various groups but not the differences in the basal blood pressures. Evaluation of these data suggest that a) the centrally mediated hypotensive responses to K+ in various groups could depend upon Na+, K(+)-pump activity in C.N.S. and/or on basal central sympathetic discharge; b) central sympathetic activity is greater in SHR only when compared to WKY but not to SD; c) since the central Na(+)-pump activity and sympathetic tone appears to be similar in SHR and SD, mechanisms other than the increases in sympathetic activity must play a prominent role in the development of spontaneous hypertension; d) attenuation of neuronal Na(+)-pump activity cannot account for greater sympathetic tone in SHR and SD-rats when compared to WKY.

Aging↗

PubMedDate not supplied

Central nervous system noradrenergic control of sympathetic outflow in normotensive and hypertensive humans.

We applied transmitter washout methodology, sampling internal jugular venous plasma via a percutaneously placed catheter, to study CNS norepinephrine release in humans and its relation to peripheral sympathetic activity. Norepinephrine overflows into the venous drainage of the brain, as do its precursor, DOPA, and metabolites DHPG and MHPG, indicating that the blood-brain barrier provides an incomplete impediment to their outward flux from the brain. Pharmacological testing with two drugs which altered CNS norepinephrine turnover, the tricyclic antidepressant desipramine and the ganglionic blocker, trimethaphan, demonstrated a direct relation existed between CNS norepinephrine release and sympathetic nerve firing rates. In essential hypertension, the sympathetic activation commonly present was associated with, and possibly caused by increased CNS release of norepinephrine, manifested in elevated overflow of norepinephrine, MHPG and DHPG from the brain. Bilateral jugular sampling, coupled with a cerebral venous sinus scan to delineate the drainage pattern, demonstrated that this increased norepinephrine release was confined to subcortical forebrain regions.

Blood Pressure↗

PubMedDate not supplied

Central nervous system monoamine neurotransmitter turnover in primary and obesity-related human hypertension.

Recent experiments in laboratory animals have challenged the conventional view that the dominant effect of CNS noradrenergic neurons in cardiovascular control is sympathetic nervous inhibition and blood pressure reduction, describing instead sympathetic activation. We have tested whether such a stimulant effect on sympathetic outflow is also evident in human hypertension. CNS norepinephrine turnover was estimated from the combined overflow of norepinephrine, MHPG and DHPG into the internal jugular veins. Cerebral blood flow scans allowed differentiation between cortical and subcortical jugular venous drainage. In patients with pure autonomic failure, jugular overflow of norepinephrine and metabolites was not reduced, indicating brain neurons and not cerebrovascular sympathetics was the source. In healthy men, CNS norepinephrine turnover and muscle sympathetic nerve activity were directly related (p < 0.02). Administration of the ganglion blocker, trimethaphan, caused a compensatory five-fold increase in jugular overflow of MHPG. Conversely, intravenous clonidine reduced CNS norepinephrine turnover by approximately 50%, this possibly representing a mechanism of drug action. In cardiac failure patients, sympathetic nervous activation was associated with a trebling of CNS norepinephrine turnover (p < 0.01). In untreated patients with essential hypertension, the sympathetic activation present was associated with 250% higher CNS norepinephrine turnover (p < 0.01), but in subcortical brain regions only. A close and direct relation exists between brain norepinephrine turnover and human sympathetic nervous activity. CNS release of norepinephrine, presumably in the forebrain where noradrenergic neurons are sympathoexcitatory and pressor, mediates increased sympathetic nerve firing in patients with essential hypertension.

Animals↗

PubMed1989

Influence of hypothyroidism on the ontogenic development of tyrosine hydroxylase induction in the adrenal glands of the rat.

The ontogenic development of the transsynaptic induction of adrenal tyrosine hydroxylase (TH), evoked by reserpine and nicotine was studied in control and hypothyroid young rats, aged 3-52 days. The enzymatic induction was measured as an increase in the enzyme activity, since this increase was shown to be impaired either by an inhibitor of RNA synthesis or by a ganglionic blocker. In the control animals, TH induction elicited by reserpine increases between 3 and 32 days of age. In the hypothyroid rats, the enzymatic induction is impaired up to 32 days; at 52 days the induction is similar in both groups of animals. When nicotine is used as a stimulating agent, hypothyroidism still impairs the enzymatic induction at 5 and 21 days, indicating that at least one of the mechanisms inhibited by hypothyroidism is localized in the adrenal chromaffin cells. The present results, taken together with previous findings dealing with adrenal epinephrine secretion, show that the thyroid hormones play a crucial role in the responses of the adrenal medulla to a stimulation in the developing rat, while they have no effect in the adult.

Adrenal Glands↗

PubMed1999

Potent mast cell degranulation and vascular permeability triggered by urocortin through activation of corticotropin-releasing hormone receptors.

Urocortin (Ucn) is related to corticotropin-releasing hormone (CRH), and both are released in the brain under stress where they stimulate CRH 1 and 2 receptors (CRHR). Outside the brain, they may have proinflammatory actions through activation of mast cells, which are located perivascularly close to nerve endings and degranulate in response to acute psychological stress. Here, we report that a concentration of intradermal Ucn as low as 10 nM induced dose-dependent rat skin mast cell degranulation and increased vascular permeability. This effect appeared to be equipotent to that of calcitonin gene-related peptide and neurotensin. Ucn-induced skin vasodilation was inhibited by pretreatment with the mast cell stabilizer disodium cromoglycate (cromolyn) and was absent in the mast cell-deficient W/Wv mice. The selective nonpeptide CRH receptor 1 antagonist, antalarmin and the nonselective peptide antagonist astressin both reduced vascular permeability triggered by Ucn but not that by Substance P or histamine. In contrast, the peptide antagonist alpha-helical CRH-(9-41) reduced the effect of all three. The vasodilatory effect of Ucn was largely inhibited by pretreatment with H1 receptor antagonists, suggesting that histamine is the major mediator involved in vitro. Neuropeptide depletion of sensory neurons, treatment with the ganglionic blocker hexamethonium, or in situ skin infiltration with the local anesthetic lidocaine did not affect Ucn-induced vascular permeability, indicating that its in situ effect was not mediated through the peripheral nervous system. These results indicate that Ucn is one of the most potent triggers of rat mast cell degranulation and skin vascular permeability. This effect of Ucn may explain stress-induced disorders, such as atopic dermatitis or psoriasis, and may lead to new forms of treatment.

Animals↗

PubMed1976

Cardiovascular reactivity and neurogenic tone in unilateral renovascular hypertension in the rat.

The role of some mechanisms in the development of hypertension due to unilateral renal artery stenosis is influenced by the presence or absence of the intact opposite kidney. In this paper: a) the cardiovascular reactivity (CR) to norepinephrine (NE) and b) the effect of a ganglionic blocker (pentolinium, P) during the early (first two weeks) and later periods (ten weeks) of hypertension elicited by unilateral renal ischemia in the presence of the untouched contralateral kidney in the rat have been reported. Neither the threshold doses nor the dose-pressor response curves have shown a greater reactivity of the cardiovascular system to NE in this specific type of renovascular hypertension. An increase in the activity of the nervous system apparently contributes in early and late periods to the fuller development of high arterial pressure (AP).

Animals↗

PubMed1999

Excitation of dorsal motor vagal neurons evokes non-nicotinic receptor-mediated gastric relaxation.

Vagal stimulation results in both gastric motor excitatory and non-adrenergic non-cholinergic (NANC) inhibitory responses. The NANC pathway involves preganglionic cholinergic neurons, which act through nicotinic receptors to ultimately evoke gastric smooth muscle relaxation via release of nitric oxide (NO) and other neurotransmitters. Within the dorsal motor nucleus of the vagus (DMN), some preganglionic neurons also contain NO synthase. The NO synthase-containing neurons innervate the gastric fundus where adaptive relaxation occurs. This study tests the hypothesis that chemical stimulation of vagal motor neurons in animals, in which nicotinic receptors are blocked, evokes an NO-dependent gastric relaxation. A cell body excitant, N-methyl-D-aspartate (NMDA, 0.03-3 nmol), was microinjected into the DMN in anesthetized rats while recording intragastric pressure (IgP). The first group received NMDA before and after administration of a ganglionic blocker, hexamethonium bromide (15 mg/kg, i.v.) and atropine (1.0 mg/kg). Significant dose-dependent increases in IgP and gastric motility occurred before hexamethonium after the 0.3 and 3 nmol doses of NMDA. After hexamethonium, 0.3 and 3 nmol NMDA evoked significant decreases in IgP. A second group of rats was hexamethonium-pretreated and received NMDA microinjection into the DMN before and after an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (10 mg/kg, i.v.). The NMDA-evoked decrease in IgP was completely abolished by the NO synthase inhibitor. These data support the novel idea that NO synthase-containing preganglionic neurons mediate gastric relaxation that is independent of nicotinic receptors.

Animals↗

PubMed1999

Excitation of dorsal motor vagal neurons evokes non-nicotinic receptor-mediated gastric relaxation.

Journal Article↗

PubMedDate not supplied

[Antiarrhythmic properties of a cannabinoid (CB) receptor agonist].

The cannabinoid (CB1) receptor agonist HU-210 (0.5 mg/kg, i.v.) exhibited a pronounced antiarrhythmic effect in rats with the adrenaline (epinephrine) and aconitine induced arrhythmia models. At the same time, the intracerebrovascular introduction of HU-210 (500 or 5000 ng) did not affect the adrenaline-induced arrhythmia. The CB1 receptor pretreatment (blocking) with the SR 141716 antagonist (3 mg/kg) and the introduction of a ganglion blocker (hexamethonium, 10 mg/kg) did not inhibit the antiarrhythmic effect of HU-210. It is concluded that the antiarrhythmic effect of intravenously injected HU-210 is neither related to the CB 1 receptor activation nor mediated by the autonomous (vegetative) nervous system.

Aconitine↗

PubMed2001

Mecamylamine, a nicotinic receptor channel antagonist, affects amylase secretion by isolated pancreatic acinar cells.

It is well established that CCK is a potent stimulator of amylase secretion from the pancreatic acinar cells, while nicotine is an effective inhibitor of such secretion. The present study was conducted to determine whether mecamylamine, a well-established ganglionic blocker drug, could influence amylase secretion from the pancreas. Male Sprague-Dawley rats were fasted, sacrificed, the pancreas removed, and pancreatic acinar cells isolated and purified. The cells were equally divided into 4 different flasks and treated with the following solutions: (control), 10 mM nicotine, 10 microM mecamylamine or 100 microM mecamylamine. The cells were washed twice after 30 min incubation at 37 degrees C, resuspended in HR buffer, and amylase release in response to graded doses of CCK-8 was measured in cells from each flask. The study was repeated four times. Basal amylase release was not different by treatment with nicotine or different doses of mecamylamine. In response to CCK-8, amylase release was decreased by nicotine and by mecamylamine (100 microM) when compared with control. Amylase release was similar between control and mecamylamine (10 microM). Peak amylase released with the maximal dose of CCK-8 (1 x 10(-10) M) was less in cells treated with nicotine when compared with those measured cells treated with saline or with the two doses of mecamylamine. The release of amylase was suppressed in a similar manner in all treatment groups in response to supramaximal (3 x 10(-10) to 1 x 10(-9) M) doses of CCK-8. Mecamylamine, at the high dose, acts on isolated pancreatic acinar cells to decrease amylase release in a manner similar to that found with nicotine. Both of these drugs, nicotine and mecamylamine, may act via CCK receptors via two different intracellular mechanisms.

Amylases↗

PubMed1993

Blood Pressure, Memory, and Electroconvulsive Therapy.

Blood pressure changes recorded during electroconvulsive therapy (ECT) in 23 psychiatric in-patients with major depressive disorders correlated with and predicted the degree of anterograde memory changes measured 48-72 h after ECT. The Randt memory test was the principal measure of memory change. A subgroup of older patients with cardiovascular illness received trimethaphan, a ganglionic blocker that impedes a hypertensive surge during the treatment. They did not differ in memory function from a younger subgroup that did not receive trimethaphan. Control of the hypertensive response in the older age group counterbalanced the additional memory dysfunction that was anticipated as a result of advanced age and cardiovascular pathology.

Journal Article↗

PubMed1975

[Functional state of baroreceptors of the aortic arch in experimental hypertension].

The bioelectrical activity of the aortic nerve was studied in normal rabbits and in those with experimentally induced hypertension. Electroneurograms of the aortic nerve of rabbits with renal and coarctational (stenosis of the abdominal aorta) hypertension demonstrated the same burst-like activity synchronous with the systolic contractions of the heart that was noted in normotensive animals. The threshold of the transit of the burst-like activity of the aortic nerve into the uniform one in cases of acutely elevated arterial pressure (induced by injections of noradrenalin and angiotensin) and the threshold of the disappearance of the mentioned activity after an acute reduction of the arterial pressure (induced by injections of acetylcholine, tetra-ethylammonium or by acute bleeding) in rabbits with renal and coarctational hypertension are shifted upwards, as compared to those in normotensive rabbits. It is the more true of the former threshold. The depressor reaction to the administration of the ganglionic blocker -- tetra-ethyl-ammonium -- in renal hypertension during the initial 2 months of the disease remains unchanged, with the exception of the 4th and 8th weeks, when it is elevated. It is concluded that the baroreceptors of the aortic arch percept the chronically elevated arterial pressure as a normal one reacting adequately to its acute changes in either direction. Thanks to this the barorecptors of the aortic arch strive to maintain a high level of the arterial pressure and provide for a stabilization of hypertension.

Adaptation, Physiological↗

PubMed2002

Subclinical doses of the nerve gas sarin impair T cell responses through the autonomic nervous system.

The nerve gas sarin is a potent cholinergic agent, and exposure to high doses may cause neurotoxicity and death. Subclinical exposures to sarin have been postulated to contribute to the Gulf War syndrome; however, the biological effects of subclinical exposure are largely unknown. In this communication, evidence shows that subclinical doses (0.2 and 0.4 mg/m(3)) of sarin administered by inhalation to F344 rats for 1 h/day for 5 or 10 days inhibited the anti-sheep red blood cell antibody-forming cell response of spleen cells without affecting the distribution of lymphocyte subpopulations in the spleen. Moreover, sarin suppressed T cell responses, including the concanavalin A (Con A) and the anti-alphabeta-T cell receptor (TCR) antibody-induced T cell proliferation and the rise in the intracellular calcium following TCR ligation. These concentrations of sarin altered regional but not total brain acetylcholinesterase activity. Interestingly, serum corticosterone levels of the sarin-treated animals were dramatically lower than the control animals, indicating that sarin-induced immunosuppression did not result from the activation of the hypothalamus-pituitary-adrenal (HPA) axis. Pretreatment of animals with the ganglionic blocker chlorisondamine abrogated the inhibitory effects of sarin on spleen cell proliferation in response to Con A and anti-TCR antibodies. These results suggest that the effects of sarin on T cell responsiveness are mediated via the autonomic nervous system and are independent of the HPA axis.

Animals↗

PubMed1992

Characterization of a kallidin receptor in the eel intestine.

Edman degradation of an eel bradykinin (BK) -like peptide isolated and detected by gel filtration and HPLC and RIA gave an amino acid sequence of Arg1-Pro-Pro-Gly-X-Ser-Pro-Leu-Arg9. Kallidin but not BK and des-Arg9-BK contracted eel intestine. The contractile effect of kallidin was not decreased by B1 and B2 receptor antagonists (up to 10(-6)M), nor by anticholinergics, antiadrenergics, ganglion blockers and an angiotensin II receptor antagonist but was attenuated by 10(-5)M indomethacin. Kallidin appears to interact with a receptor different from the BK B1 and B2 receptor types and prostaglandins may participate in the response.

Amino Acid Sequence↗