Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYMPATHOLYTICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1990

Apparent vascular to cardiac sympatholytic selectivity of omega-conotoxin GVIA in the pithed rat.

The effects of omega-conotoxin GVIA (omega-CTX), a blocker of N-type voltage-operated calcium channels (VOCCs), were investigated in the pithed rat, omega-CTX (1.6 and 3.2 micrograms/kg i.v.) did not alter resting diastolic pressure or heart rate nor the pressor and chronotropic responses to noradrenaline injections (0.1-10 micrograms/kg). In contrast, the pressor responses to electrical stimulation of the whole spinal cord (0.2-6.4 Hz) were dose dependently reduced by omega-CTX whereas the concomitant tachycardia was less affected. When selective stimulation of the cardiac sympathetic outflow was applied, the resulting chronotropic response was more sensitive to omega-CTX. This result is discussed in the light of the possible interference of adrenal catecholamine release during whole spinal cord stimulation which is not sensitive to omega-CTX. These results provide in vivo evidence that omega-CTX is able to reduce sympathetic neurotransmission to the vasculature and the heart, presumably by blocking N-type VOCCs on pre- and post-ganglionic nerve terminals.

Animals↗
PubMed1995

Evidence against the involvement of the nucleus tractus solitarii in the sympatholytic effect of 8-hydroxy-2-(di-n-propylamino)tetralin in the cat.

In different animal species, microinjections of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) into the nucleus tractus solitarii failed to alter arterial blood pressure and sympathetic nerve activity; however, the cardiovascular effects (hypotension, bradycardia, reduction in sympathetic nerve activity) of intravenous administration of 8-OH-DPAT were significantly reduced after blockade of the nucleus tractus solitarii by kainic acid as well as after blockade of the lateral tegmental field by kainic acid. The aim of the present study was to clarify these conflicting results. In the anesthetized cat, inhibition of neurotransmission in the nucleus tractus solitarii by bilateral microinjections of either muscimol (1 nmol in 50 nl) or kynurenic acid (2.5 nmol in 50 nl) suppressed the baroreceptor reflex and abolished the synchronism between the renal sympathetic bursts; however, these procedures did not alter the dose-related hypotension, bradycardia and sympatho-inhibition elicited by cumulative doses of 8-OH-DPAT (1-30 micrograms/kg i.v.). Moreover complete electrolytic destruction of the nucleus tractus solitarii, assessed by a complete loss of the baroreceptor reflex and the cardiac-related bursts of the sympathetic nerves, failed to alter the inhibitory effects of i.v. 8-OH-DPAT. Bilateral microinjections of muscimol into the lateral tegmental field induced a decrease of mean arterial blood pressure, heart rate and renal nerve activity (by respectively -35 +/- 13 mm Hg, -30 +/- 16 beats/min and -53 +/- 14%) and greatly reduced the effects of subsequent i.v. administration of 8-OH-DPAT. The present data indicate that the nucleus tractus solitarii does not play a dominant role in the central action of 8-OH-DPAT whereas they confirm our previous results showing that the lateral tegmental field is involved in this action and in the mecanisms regulating sympathetic tone. The results also suggest that kainic acid lesions are not restricted to the region in which the neurotoxic agent is injected.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2002

Sympatholytic therapy in primary hypertension: a user friendly role for the future.

Effective therapy (Rx) in primary hypertension (PH) for 50 years, has featured sympathetic nervous system (SNS) mechanisms. Ganglionic blockers and reserpine were pre-eminent in the 1940s (mydriasis, ileus, impotence, peptic ulcer). Guanethidine, and in the 1960s clonidine and methyldopa, were step II agents to thiazide Rx in the 1950s. Reserpine depletes brain (depression) and peripheral (PPH) noradrenaline (NA) storage sites, guanethidine depleted NA storage via blockade of reuptake. Venomotor sympathoplegia resulted in postural hypertension. An analogue, metaiodobenzyguandine is used in diagnosis and Rx of pheochromocytoma. Clonidine lowers both central and PPH neuronal NA release via both stimulation of alpha agonist adrenoreceptors (sedation) and specific imadazoline binding sites (IBS). Methyldopa lowers pressure via PPH induced NA release (retrograde ejaculation) and via alphamethyl NA on central alpha-2 receptors (depression). The alpha-2 and alpha-2 receptor antagonists (alphaRA) cause reflex tachycardia and first-dose hypotension. Recently a two-fold incidence of congestive heart failure after alphaRA in treated primary hypertensives question their role in PH. The beta RA, with or absent alphaRA, remain premier since the 1970s due to mortality benefit in systolic dysfunction and post myocardial infarction, certifying the role of the SNS in the pathogenesis and sequelae and Rx of PH. The future includes beta RA, specific IBS agents, angiotensin (AII) RA with avid presynaptic AII affinity and vasopeptidase inhibitiors that raise peptides and suppress SNS.

Antihypertensive Agents↗
PubMed1997

Considerations in the treatment of insulin resistance and related disorders with a new sympatholytic agent.

BACKGROUND: Prospective studies have documented the importance of blood glucose control in diabetic patients for risks for cardiovascular diseases. At age 70 years, more than 30% of people are hypertensive and among these about one-third have diabetes or impaired glucose tolerance. It is urgent to treat hypertension in these patients with drugs that do not further impair glucose control. DRUG STUDIES: Prospective, randomized studies with antihypertensive drugs have demonstrated differences between different classes of drugs regarding effects on insulin sensitivity. Thus, treatment with beta-blockers or diuretics is associated with impaired insulin sensitivity, whereas most modern calcium channel blockers and angiotensin converting enzyme inhibitors are neutral. The most pronounced improvements have been obtained with alpha1-blockers. A new class of drugs, imidazoline I1-imidazoline receptor agonists, may be of interest in this context. Moxonidine, a drug in this class, inhibits sympathetic outflow and causes vasodilation. This effect together with other characteristics may lead to improved insulin resistance and glucose control. CONCLUSIONS: In populations at high risk for diabetes, it may be justified to select drugs that improve insulin sensitivity when treating insulin-resistant individuals for hypertension.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Peripheral sympatholytic effects of 1-alpha-acetylmethadol.

1-alpha-Acetylmethadol (LAAM), 1.4 mg/kg or greater, decreased the response of the cat nictitating membrane to pre- and postganglionic sympathetic nerve stimulation. LAAM had a greater effect on the low-frequency (0.5 Hz) than on the high-frequency (5-20 Hz) responses. No difference was observed between the effects of LAAM on the pre- as opposed to the postganglionic responses. The responses ot the nictitating membranes to intravenous epinephrine were not affected by LAAM. LAAM appears to act at the nerve terminal. The minimum dose of LAAM (1.4 mg/kg) which decreased the nictitating membrane responses also decreased blood pressure and heart rate. Naltrexone, 300 micrograms/kg, s.c., antagonized the effects of LAAM on the nictitating membrane responses and the cardiovascular actions of the drug. In anesthetized dogs, naltrexone completely blocked the blood pressure response to LAAM and partially blocked the effects of LAAM on heart rate and contractile force. The data suggest that LAAM may produce its cardiovascular effects, in part, by an action on the peripheral sympathetic nervous system which involves opiate binding sites. LAAM also appears to have direct actions on the heart to decrease heart rate and contractile force that do not involve opiate binding sites.

Animals↗