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PubMedDate not supplied

[Effect of the sympatholytic pirroxan on catecholamine excretion in experimental tetanus].

Excretion of catecholamines and vanilylmandelic acid was studied in rabbits with tetanic intoxication. It was found that catecholamine excretion increases up to 173% in the initial stages of the disease and falls to 51% at the height of the disease whereas excretion of vanilylmandelic acid progressively decreases down to 40% against normal. Pirroxan (10 mg/kg a day) reduces excretion of catecholamines and vanilylmandelic acid by three times, concurrently producing a definite cholinolytic effect.

Animals↗
PubMed1977

[Effect of adrenomimetics and sympatholytics on the adrenergic neural fibers and mast cells of the dura mater].

The effect of noradrenaline, dophamine and rausedyle on the adrenergic nervous apparatus and on the labrocytes of the dura mater in white rats was studied by means of Falk's and Glenner's methods and under light electron microscopy. The adrenergic nerve fibres and labrocytes are stated to respond to the injection of adrenomimetic and sympathomimetic drugs with increase or decrease of deposited monoamines on the background of corresponding clinical and vessel phenomena. The data obtained makes it possible to consider the adrenergic nerve fibres and labrocytes to be a single adrenergic apparatus of the dura mater.

Adrenergic Fibers↗
PubMed1997

Pharmacology and clinical use of moxonidine, a new centrally acting sympatholytic antihypertensive agent.

Moxonidine is a centrally acting antihypertensive. Its action is mediated by imidazoline I1 receptors located in the rostral ventro-lateral medulla (RVLM). Animal experiments show much smaller amounts are required to reduce blood pressure (BP) when it is given intracisternally, or injected directly into the RVLM, compared to intravenous dose. The antihypertensive action of microinjection of moxonidine into the RVLM in the spontaneously hypertensive rat (SHR) is abolished by pretreatment with imidazoline I1 blockade from efaroxan, but alpha(2) blockade from SKF 86466 has much less effect. Similarly the fall of BP in the SHR from intravenous moxonidine is reversed by the microinjection of efaroxan into the RVLM. Receptor binding studies demonstrate that moxonidine binds with an affinity for the imidazoline I1 receptor that is thirty-three times more effective than is alpha(2) receptor binding, while for clonidine the difference is only four times. Moxonidine reduces adrenaline, noradrenaline and renin levels in man, a finding consistent with central inhibition of sympathetic tone. Acute haemodynamic studies indicate that moxonidine results in a fall of BP due to a decline in systemic vascular resistance, while the heart rate, cardiac output, stroke volume and pulmonary artery pressures are not affected. Left ventricular end systolic and diastolic volumes are reduced. Left ventricular hypertrophy has been found to regress after 6 months treatment with moxonidine. After oral administration Tmax is about 1 h, bioavailability approaches 90%. Moxonidine is mostly excreted unchanged, biotransformation is unimportant. The T1/2 is 2.5 h, which is prolonged by renal insufficiency. However, suggesting possible retention in the central nervous system (CNS), the antihypertensive effect lasts longer than would be expected from the half-life, as moxonidine is suitable for once daily administration. Moxonidine is an effective antihypertensive agent. It has been compared with representatives from each important class of antihypertensive drugs, with clonidine, diuretics, both alpha- and beta-blocking drugs, calcium antagonists and ACE inhibitors. BP control has been similar with moxonidine and these other agents. The side effect profile of moxonidine is favourable, its lack of effect on central alpha(2) receptors is important in this regard.

Animals↗
PubMed2004

The evaluation of the N-type channel blocking properties of cilnidipine and other voltage-dependent calcium antagonists.

Sympathetic neurotransmission in tissues with intact sympathetic nerve arborization is extensively dependent on calcium influx via N-type calcium-channels. It was the objective of the present study to assess and compare the claimed sympatholytic effect of the 1,4-dihydropyridine compound cilnidipine with other voltage-dependent calcium-channel (VDCC) antagonists. We studied these compounds by means of three different models. In the rabbit isolated thoracic aorta, the alleged sympatholytic properties displayed by these compounds were evaluated in the noradrenaline spillover model. Additionally, the influence of cilnidipine on stimulation-induced constrictor responses was studied in the rat isolated tail artery (male Wistar rats, 250-300 g) in addition to its effect on noradrenaline-induced contractions. Finally, we studied the influence of cilnidipine and other calcium-channel blockers on stimulation-induced chronotropic responses, in order to address N- or L-type selectivity, in the pithed rat model (male Wistar rats, 260-320 g). Furthermore, we evaluated their effect on noradrenaline-induced tachycardia. In the isolated rabbit thoracic aorta preparation omega-conotoxin GVIA (0.1 microM) nearly abolished the sympathetic outflow caused by stimulation, whereas nifedipine (0.1 microM) and amlodipine (1 microM) did not influence the evoked noradrenaline release. Cilnidipine (1 microM) significantly attenuated the response by nearly 18% and mibefradil (1 microM) by c. 42%. The stimulation-induced constrictor response (prejunctional effect) in the rat isolated tail artery could be blocked by omega-conotoxin GVIA (0.5 and 1 microM). Cilnidipine (10 nm and 0.1 microM) significantly attenuated responses to stimulation by maximally 20%, whereas it did not influence the constrictor response to noradrenaline (postjunctional effect). The mean heart rate in the pithed rat model amounted to 309.3 +/- 3.6 beats/min (bpm). Electrical stimulation of the cardio-accelerator nerves (C7-Th1) resulted in an increase by 106.7 +/- 2.2 bpm. All antagonists studied, except for nifedipine, attenuated the chronotropic response to stimulation (P < 0.05). The rank order of sympatholytic efficacy was: omega-conotoxin GVIA (84.8%), mibefradil (75.1%), cilnidipine (43.0%) and amlodipine (34.8%). Noradrenaline (10 nmol/kg) increased the heart rate by 117.8 +/- 2.7 bpm. This chronotropic response was influenced equally well by the calcium-channels blockers as observed in the stimulation (prejunctional) experiment. In conclusion, the N-type channel blocking properties and thus sympatholytic effect of cilnidipine could be demonstrated in some (vascular) but not all (cardiac) models studied. At the level of the vasculature cilnidipine reduced the neurotransmitter release to electrical stimulation in both the noradrenaline spillover model and in the model of the rat isolated tail artery, respectively. For amlodipine and nifedipine no sympatholytic activity could be demonstrated. In the pithed rat model, we were unable to demonstrate a selective N-type blocking effect for the VDCC-antagonists.

Animals↗
PubMed1976

The effect of temperature on potassium chloride contracture in cat myocardium.

1. Contracture was induced in cat myocardium by exposure to 140 mM-KC1 In isotonic Tyrode solution. Force of contracture expressed as mg/mm2 (muscle cross-sectional area) falls with increasing cross-sectional area. 2. The effect of temperature on isometric force developed during contracture was evaluated both in normal (untreated) atrial and ventricular muscle and following treatment with sympatholytic drugs. 3. The force of contracture was not significantly affected by sympatholytic drugs at 36 degrees C. 4. In normal atrial and ventricular muscle, force of contracture decreased when the muscle was cooled from 36 to either 29 or 20 degrees C. 5. In atrial muscle, the effect of temperature was not changed by sympatholytic drugs. In contrast, exposure to sympatholytic drugs increased contracture force developed by ventricular muscle at 20 degrees C. Also, contracture force was significantly greater at 20 than at 36 degrees C in ventricular muscle from reserpine-pretreated cats. 6. It is suggested that ventricular muscle becomes more sensitive to the relaxing effects of endogenous catecholamines at temperature is lowered. 7. The differences shown between atrial and ventricular muscle with respect to the effect of temperature and sympatholytic drugs on contracture force may result from the differing amounts of sarcoplasmic reticulum found in these types of cardiac muscle and also from different mechanisms of "excitation-contracture" coupling in atrial and ventricular muscle.

Animals↗
PubMed1993

Lateral tegmental field involvement in the central sympathoinhibitory action of 8-OH-DPAT.

This study examined the effects of kainic acid and NMDA microinjections into the lateral tegmental field on the sympatholytic effect of the 5-HT1A agonist 8-OH-DPAT. Kainic acid has been reported to destroy cell bodies while leaving fibers of passage intact while NMDA excites the cell bodies but not the axons of neurons. Microinjection of kainic acid was found to block the usual sympatholytic effect of 8-OH-DPAT but not the sympathoinhibition produced by the alpha 2 agonist clonidine. Microinjection of NMDA elicited profound pressor responses related to an increase in sympathetic activity. Sympatholytic effects of 8-OH-DPAT and clonidine were transiently overridden by microinjections of NMDA, but not glutamate. A role for the lateral tegmental field in the generation of sympathetic tone and in the sympatholytic mechanism of 8-OH-DPAT is supported by the chemical lesion and stimulation studies.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

The effect of large-dose intrathecal opioids on the autonomic nervous system.

UNLABELLED: Decreases in blood pressure after the spinal injection of opioids suggest that intrathecal (IT) opioids may have a sympatholytic effect similar to that of local anesthetic drugs. We compared two groups of patients aged 10-16 yr (n = 10 in each group). Group One (IT group) received IT opioids. Group Two (Epidural group) received 0.5% bupivacaine epidurally. The sympathetic effects of IT opioids and epidural bupivacaine were monitored by the changes in toe relative to calf temperature and by the changes in pulse wave gradients with digital plethysmography. Changes in temperature gradients comparing calf to toe and increases in pulse amplitude indicate vasodilatation caused by sympathetic blockade in this model. Calf to toe temperature gradients (Deltacalf-Deltatoe) were evaluated by subtracting the two measurements. Pulse wave plethysmography was recorded before and after spinal and epidural injection at intervals of 10 min for 40 min. All patients demonstrated changes in their calf to toe gradients after IT and epidural injections (-3.2 +/- 1.6). Systolic blood pressure decreased from a mean of 70 +/- 15 mm Hg to 55 +/- 10 mm Hg. Pulse wave plethysmography amplitude increased after the intrathecal opioid and epidural bupivacaine injection similarly. We conclude that the increases in pulse wave amplitude and decreases in calf-toe gradients indicate a sympatholytic effect after IT opioids similar to that of local anesthetics. IMPLICATIONS: The sympatholytic effects of neuraxial opioids were compared with those of local anesthetics. Two groups of patients were assigned to receive a neuraxial opioid or bupivacaine. Our results demonstrate that opioids cause hypotension and peripheral vasodilatation similar to bupivacaine. This finding suggests that neuraxial opioids have a sympatholytic effect comparable to that of local anesthetic drugs.

Adolescent↗
PubMed1992

Influence of antihypertensive therapy on renal function.

Antihypertensive therapy influences kidney function by different mechanisms depending on the mode of action of the drug used. The GFR is improved by calcium entry blockers and ACE inhibitors, unaffected by vasodilators, alpha-blockers and centrally acting sympatholytics and impaired by beta-blockers. The same is true for renal blood flow and is due to changes of renal vascular resistance. Renal sodium excretion is impaired mostly by vasodilators, by alpha-blockers, sympatholytics and beta-blockers; in contrast, calcium entry blockers and ACE inhibitors acutely induce natriuresis. The RAAS is stimulated by vasodilators, unaffected by alpha-blockers and sympatholytics and suppressed by beta-blockers. Plasma catecholamines are stimulated by vasodilators and suppressed by centrally acting sympatholytics and unaffected by the others. Induction of acute renal functional impairment is reported for ACE inhibitors under conditions of compromised renal perfusion pressure such as in renal artery stenosis. These data from the literature reviewed are supported by our own experimental data on sodium balance under different drugs and micropuncture data in experimental renal artery stenosis. To achieve effective antihypertensive treatment with a low profile of side effects, careful monitoring of renal function seems to be mandatory.

Animals↗