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 631 records · Page 35Linked to original sources
PubMed1987

Chronic effects of direct vasodilation (pinacidil), alpha-adrenergic blockade (prazosin) and angiotensin-converting enzyme inhibition (captopril) in systemic hypertension.

Chronic responses of systemic hemodynamics and blood pressure counterregulatory ("pseudo-tolerance") mechanisms were investigated in matched groups of patients with essential hypertension after 1 month of vasodilator therapy with pinacidil (a direct arterial dilator), prazosin (an alpha 1-adrenergic blocking drug) or captopril (an angiotensin-converting enzyme inhibitor). For equivalent decreases in mean arterial pressure compared with placebo baseline (approximately 8 mm Hg supine and 12 mm Hg upright), prazosin and captopril did not increase cardiac index or heart rate. In contrast, marked decreases in systemic vascular resistance with pinacidil (approximately 25%, p less than 0.05) were accompanied by reflex increases in cardiac index (approximately 20%, p less than 0.05). Activity of the sympathetic nervous system, measured by supine and upright plasma norepinephrine (NE), increased approximately 50% with pinacidil and prazosin (p less than 0.001 each), whereas captopril decreased supine plasma NE by 12% (p less than 0.05) and did not change upright plasma NE. All 3 drugs caused an expansion of height-adjusted blood volume (approximately 14%). Pinacidil and prazosin caused reversible weight gains of 0.9 and 0.7 kg, respectively, whereas captopril reversibly decreased body weight by 0.8 kg (p less than 0.05), suggesting differential effects of the 3 drugs on interstitial fluid volume. During chronic therapy, all 3 drugs may require concomitant diuretic therapy, whereas concomitant sympatholytic therapy may be required with the potent vasodilator pinacidil. Captopril may be associated with the lowest cardiac risk because of its lack of stimulatory effects on the sympathetic nervous system and cardiac index.

Adrenergic alpha-Antagonists↗
PubMed1988

Cardiac involvement in hypertension.

Despite improved patient detection and pharmacologic therapy, the effect of treatment of hypertension on mortality from coronary artery-related events remains unresolved. Left ventricular (LV) hypertrophy, a known consequence of hypertension, is associated with an excess mortality independent of other known cardiovascular risk factors. Recently, LV hypertrophy accompanying hypertension has been associated with ominous ventricular arrhythmias. However, it does not necessarily follow that regression of LV hypertrophy will reduce this increased mortality. Diastolic dysfunction, manifested by reduced ventricular distensibility of the hypertrophying left ventricle, appears to be an early characteristic of the hypertensive heart since echocardiographic techniques have demonstrated diastolic filling abnormalities in untreated essential hypertensives even before significant LV hypertrophy appears. Not all antihypertensive agents diminish LV mass and improve diastolic dysfunction. Certain sympatholytic agents, calcium antagonists, beta-adrenergic blockers, and the angiotensin-converting enzyme inhibitors appear to diminish LV hypertrophy. However, future studies are needed to determine if these agents that appear to reverse findings of LV hypertrophy and improve diastolic dysfunction will also reduce risk of coronary artery disease and related events.

Cardiomegaly↗
PubMed1989

Hypertension in the aged: a pathophysiologic basis for treatment.

According to major surveys, hypertension is found in over half the population aged 65 years or over. In this age group, systolic blood pressure is at least as important as diastolic blood pressure as a predictor of cardiovascular morbidity and mortality. Overall, the presence of hypertension is associated with approximately a threefold increase in the likelihood of major events. Differing factors contribute to the hypertension. Loss of proximal arterial compliance, affecting the larger conduit vessels, occurs often with aging and explains the tendency for systolic pressure to increase while diastolic pressure remains constant or even decreases. A loss of baroreceptor sensitivity also may contribute to hypertension. There is an increase in responsiveness of the sympathetic nervous system and an enhanced sensitivity to its effects in the elderly, perhaps reflecting a decline in the buffering activity of peripheral vascular beta receptors. It is possible, too, that sodium retention may contribute to hypertension in some older patients. Although diuretics traditionally have been the mainstay of treatment in these patients, it is now recognized that other classes of antihypertensive agents may be equally as effective yet less prone to metabolic or symptomatic adverse events. Sympatholytic drugs, calcium channel blockers and angiotensin-converting enzyme inhibitors, either as monotherapy or in combination with low-dose diuretics, have been shown to be efficacious in the elderly. These agents also can produce regression of left ventricular hypertrophy, an additional property that may contribute to a reduction in serious cardiac complications.

Age Factors↗
PubMed1983

Time course of regression of left ventricular hypertrophy in treated hypertensive patients.

In a prospective study, 32 hypertensive patients with echocardiographic evidence of left ventricular hypertrophy were treated with methyldopa, hydrochlorothiazide, or methyldopa and hydrochlorothiazide combined. Echocardiograms and electrocardiograms were obtained in each of the 32 patients before treatment, at the point of initial blood pressure control, and then one, three, and six months thereafter; in 27 patients these studies were also obtained after 12 and 18 months. Left ventricular end-diastolic posterior wall thickness decreased in seven patients whose blood pressure was controlled with methyldopa alone (p less than 0.01) and in 17 patients whose blood pressure was controlled with methyldopa and hydrochlorothiazide combined (p less than 0.01); in both groups, the reduction in left ventricular posterior wall thickness at end-diastole was apparent one month after blood pressure control was established (p less than 0.05). In contrast, no significant reduction in left ventricular posterior wall thickness at end-diastole was observed in eight patients who had equivalent control of blood pressure with hydrochlorothiazide alone (p = 0.34). During the 18-month follow-up period, ventricular septal thickness at end-diastole decreased in the group treated with methyldopa and hydrochlorothiazide combined (p = 0.03); whereas, ventricular septal thickness at end-diastole appeared to increase in the group treated with hydrochlorothiazide alone (p less than 0.01). These results suggest that evidence of regression of left ventricular hypertrophy may be detected as early as one month after blood pressure is controlled with methyldopa or methyldopa and hydrochlorothiazide combined; whereas, long-term control of hypertension with hydrochlorothiazide alone was not associated with evidence of regression of left ventricular hypertrophy. Although the patient number are small, these data suggest that there are differences in the long-term effects of diuretics and sympatholytic drugs on left ventricular anatomy, which may, in part, relate to divergent effects on the sympathetic nervous system.

Adult↗
PubMed1983

Effect of long-term antihypertensive therapy on cardiac anatomy in patients with essential hypertension.

M-mode echocardiography was used in 12 patients with essential hypertension to study changes in cardiac anatomy during long-term therapy with hydrochlorothiazide (50 to 100 mg) and alpha-methyldopa (500 to 1,750 mg). Echocardiographic examination was performed after six weeks of treatment with hydrochlorothiazide alone and after four to six weeks, six months, and nine months of treatment with both hydrochlorothiazide and alpha-methyldopa. Hydrochlorothiazide alone induced a small, and not significant, change in blood pressure (from 157 +/- 16 (SD)/105 +/- 9 to 150 +/- 14/101 +/- 5 mm Hg). Changes in echocardiographic parameters of cardiac anatomy were not observed during short-term diuretic therapy. Addition of alpha-methyldopa further reduced blood pressure (to 133 +/- 11/90 +/- 6 mm Hg, p less than 0.001), which was maintained throughout the study. Gradual decreases in diastolic septal thickness (from 10.9 +/- 1.1 to 9.5 +/- 1.0 mm, p less than 0.01), relative wall thickness (from 0.40 +/- 0.06 to 0.36 +/- 0.06, p less than 0.05) and left ventricular cross-sectional area (from 18.9 +/- 2.9 to 17.3 +/- 2.6 cm2, p less than 0.05) were observed. Posterior wall thickness did not change significantly during the study. The results provide evidence for regression of echocardiographic parameters of cardiac muscle mass during long-term antihypertensive treatment with a diuretic and a centrally-acting sympatholytic drug. Regression of left ventricular mass was not clearly related to changes in casual blood pressure. However, patients who showed a decrease in septal thickness tended to have a greater decrease in systolic blood pressure than those in whom septal thickness did not change during therapy. Moreover, patients in whom a decrease in left ventricular transverse dimension was observed, had a greater decrease in both systolic and diastolic blood pressure than those in whom left ventricular diastolic dimension did not change.

Adult↗
PubMed1986

Historical perspective on the management of hypertension.

Remarkable progress has been made during the past 30 years in the management of hypertension, a disease that affects approximately one out of every four adults in the United States. In the 1960s, at least half of the individuals with hypertension were unaware of their disease, and the blood pressures of fewer than 20 percent were controlled at normotensive levels. In contrast, in the 1980s, only a small percentage, perhaps as few as 10 or 15 percent of hypertensive patients, are unaware of their disease and, in many parts of the country, more than 60 percent are being treated to goal blood pressure levels. More effective treatment of hypertension is probably a major reason for the 45 percent decrease in stroke mortality rates in the last 12 years alone and for the dramatic decrease in the number of hypertensive patients in whom renal failure or congestive heart failure develops. In addition, at least a portion of the 25 to 30 percent decrease in coronary mortality rates can probably be attributed to better management of patients with hypertension. The availability of antihypertensive drugs in the 1950s (rauwolfia preparations, veratrum derivatives, thiocyanates, hydralazine, and the ganglion blockers) and the discovery of more effective agents in the period from the 1960s to the present have dramatically improved the prognosis of hypertensive patients. Thiazide diuretics, centrally acting sympatholytic agents, beta-adrenergic inhibitors, and, more recently, selective alpha-adrenergic inhibitors, converting-enzyme inhibitors, and calcium entry blockers are examples of these medications. All of these agents have some side effects, with varying patient acceptability. The search continues for newer drugs that are well tolerated, that lower blood pressure by reducing peripheral resistance, and that produce few metabolic changes. A detailed review of the physiologic effects of antihypertensive medications, as well as a critique of the clinical trials and some of the problems noted in the pharmacologic management of hypertension, is presented.

Adrenergic alpha-Antagonists↗
PubMed1986

Pharmacology of terazosin.

Terazosin is a quinazoline antihypertensive agent that is chemically similar to prazosin. The saturated furan ring of terazosin distinguishes these two compounds. Terazosin (0.1 to 3.0 mg/kg) lowered blood pressure without increasing heart rate when given orally to spontaneously hypertensive rats. No tolerance was observed during five days of repeated oral administration. Although equally efficacious in spontaneously hypertensive rats as its congener prazosin, terazosin exhibited a more gradual onset of action than prazosin, a more uniform and linear dose-response curve, and a less variable duration of action. When administered intravenously to dogs, terazosin lowered blood pressure primarily by decreasing peripheral vascular resistance. Pretreatment with phenoxybenzamine but not with atropine or propranolol resulted in a greatly reduced hypotensive response to terazosin, demonstrating that this effect of terazosin is mediated by a sympatholytic mechanism of the alpha type. The nature of the alpha-blocking properties of terazosin was evaluated in vitro using both radioligand binding studies and functional tests in rabbit aorta and pulmonary artery. These studies demonstrated that terazosin is highly selective for alpha1 receptors. The affinity for alpha1 receptors was approximately one-third that of prazosin. Like prazosin, terazosin displayed minimal interaction with alpha2 receptors. Median lethal dose values in rats ranged from 0.255 to 0.270 g/kg for intravenous administration and from 5.5 to 6.0 g/kg, for oral administration. Oral administration of high doses of the compound to rats did not produce any gastrointestinal irritation and/or apparent abnormal behavioral effects. Comparison of the oral activity of terazosin in spontaneously hypertensive rats with the oral toxicity values in normal rats revealed a high efficacy/safety ratio. Terazosin given intravenously to rats and mice was 2.6 to 5.0 times less toxic than prazosin. The absorption of terazosin appeared to be slower than that of prazosin in rats. However, from eight to 16 hours after dosing, terazosin concentrations in plasma exceeded those of prazosin, suggesting the possibility of once-daily dosing with terazosin. In addition, terazosin exhibited statistically significant cholesterol lowering effects in gerbils.

Administration, Oral↗
PubMed1991

Effects of guanethidine on sensitization to natural stimuli and self-mutilating behaviour in rats with a peripheral neuropathy.

In the present study we have used a recent rat model for neuropathic pain to investigate the effect of the sympatholytic drug guanethidine on changes in behavioural responses evoked by mechanical, heat and cold stimuli and on self-mutilating behaviour. After a unilateral peripheral mononeuropathy induced by ligatures around the right common sciatic nerve, the left side receiving just a sham wound, lesioned and non-operated control animals were treated with saline or guanethidine (30 mg/kg) for 4 consecutive days commencing 5 days before or 10 days after surgery. Behavioural parameters were followed for 4 weeks after drug treatment. Lesioned rats were found to be sensitized to the otherwise innocuous cold stimulus and showed decreased response thresholds to noxious heat and mechanical stimuli. Some lesioned animals self-mutilated. Treatment with guanethidine diminished heat and cold sensitization considerably, but had less effect on mechanical sensitization and, if administered before surgery, rather increased the severity of self-mutilating behaviour. While these results are in agreement with clinical observations on the prominence of sensitization to evoked stimuli, especially cold, and the effectiveness of guanethidine in sympathetically maintained neuropathic pain, they indicate that the mechanisms involved in sensitization to different stimuli and self mutilating behaviour differ.

Animals↗
PubMed1988

Studies on the mechanism of prazosin induced sympatho-inhibition.

Intravenous administration of the alpha 1-adrenoceptor antagonist, prazosin (3-300 micrograms/kg), produced a depression of sympathetic-cholinergic electrodermal responses evoked by electrical stimulation of the posterior hypothalamus in pentobarbital anesthetized cats. Pretreatment with the alpha 2-adrenoceptor antagonists yohimbine (0.5 mg/kg) or idazoxan (0.1 mg/kg) significantly blocked the depressant effects of prazosin but had no effect on hypothalamic evoked electrodermal responses when given alone. Electrodermal responses were readily elicited in animals depleted of CNS monoamines. Monoamine depletion, however, totally abolished prazosin's depression of centrally evoked electrodermal responses. Prazosin also depressed the amplitude of electrodermal responses evoked by electrical stimulation of the cervical spinal cord in spinalized cats. In contrast to hypothalamic stimulation, yohimbine when given alone potentiated spinally evoked electrodermal responses which suggests that both excitatory and inhibitory mechanisms were being activated. Taken together these results suggest that prazosin produces its CNS sympatholytic effect by enhancing inhibition mediated by alpha 2-adrenoceptor mechanisms and not directly by blockade of excitatory alpha 1-adrenergic receptors in the central nervous system. A spinal cord site of action for prazosin is also implicated.

Adrenergic Fibers↗
PubMed1991

Mechanism of ketanserin-induced sympatho-inhibition.

Experiments were undertaken to determine if sympatho-inhibition produced by ketanserin is due to antagonism of central nervous system alpha 1-adrenoceptors rather than central 5-HT2 receptors and if (like prazosin) it produces sympatho-inhibition indirectly via a central (presynaptic) alpha 2-adrenoceptor mechanism. Administration of ketanserin (0.03-3.0 mg/kg i.v.) caused a dose-related depression of sympathetic-cholinergic electrodermal responses evoked by electrical stimulation of the hypothalamus in pentobarbital anesthetized cats. No effect of ketanserin was observed on electrodermal responses evoked by preganglionic sympathetic nerve stimulation nor did the more specific 5-HT2 receptor antagonist, cinanserin, produce a central sympatholytic effect at dosages up to 3 mg/kg i.v. Pretreatment with alpha 2-adrenoceptor blockers yohimbine, idazoxan, or rauwolscine significantly antagonized ketanserin-induced sympatho-inhibition. Depletion of central nervous system (CNS) monoamines totally prevented ketanserin-induced sympatho-inhibition although clonidine (30 micrograms/kg i.v.) continued to be effective. These results suggest that ketanserin acts in the CNS to reduce sympathetic reactivity by blocking alpha 1-adrenoceptors and not 5-HT2 receptors. In this regard, ketanserin appears to act in a manner similar to other alpha 1-adrenoceptor antagonists (e.g. prazosin and indoramin) by an apparent presynaptic facilitation of alpha 2-adrenoceptor mediated tonic inhibition descending from the lower brainstem.

Adrenergic alpha-Antagonists↗
PubMed1991

The effects of 8-OH-DPAT on medullary 5-HT neurons and sympathetic activity in baroreceptor-denervated animals.

The effects of the 5HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) on medullary 5-hydroxy-tryptamine (5-HT) neuronal firing and inferior cardiac sympathetic nerve activity were simultaneously determined in baroreceptor-denervated cats. 5-HT neuronal firing was inhibited by 50% at a 1 microgram/kg i.v. dose of 8-OH-DPAT in the baroreceptor-denervated animal. Unit firing was completely inhibited by a 3 microgram/kg dose. In contrast, 8-OH-DPAT inhibited inferior cardiac nerve activity between 10 and 100 micrograms/kg i.v. A similar relationship between the 8-OH-DPAT-induced inhibition of 5-HT unit activity and sympathetic nerve activity was observed in sham-operated control animals. These data suggest that the sympatholytic effects of 8-OH-DPAT cannot be explained on the basis of an autoreceptor effect of the drug.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

8-OH-DPAT-induced inhibition of renal sympathetic nerve activity and serotonin neuronal firing.

The effects of the 5-HT1A receptor 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) administered i.v. on medullary 5-HT neuronal firing and renal sympathetic nerve activity were determined in spontaneously breathing anaesthetized cats. Low doses of 8-OH-DPAT (1-3 micrograms/kg) caused a similar reduction in 5-HT neuronal firing and renal nerve activity while high doses (10-30 micrograms/kg) completely inhibited neuronal firing but caused only 80% inhibition of renal nerve activity. These data are discussed in relationship to the mechanism of sympatholytic action of 8-OH-DPAT and the serotonergic regulation of sympathetic nerve activity.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1985

Nonneural vascular smooth muscle tone in arterioles of the hamster cheek pouch.

The object of the present study was to employ specific pharmacological agents and the chemical sympatholytic drug 6-hydroxydopamine (6-OHDA) to characterize the neural and adrenergic control of vascular smooth muscle tone in arterioles of the hamster cheek pouch. Arteriolar diameters were measured in the superfused cheek pouch of anesthetized male golden hamsters. All orders of arterioles constricted in response to norepinephrine (10(-7) g/ml) and increased superfusion solution PO2, and dilated in response to isoproterenol (10(-7) g/ml) and adenosine (10(-4) M). Tetrodotoxin (10(-6) g/ml), phentolamine (10(-6) g/ml), and propranolol (10(-6) g/ml) had no effect upon arteriolar diameters under resting conditions. However, phentolamine and propranolol completely blocked vessel responses to norepinephrine and isoproterenol, respectively. Arterioles dilated during superfusion with either 6-OHDA (300 micrograms/ml) or its acidic vehicle. However, vessel diameters returned toward control values during the subsequent 2-hr washout period and exhibited no net dilation following recovery from 6-OHDA or its vehicle. This study suggests that neural and adrenergic mechanisms are not the primary determinants of arteriolar tone in the hamster cheek pouch.

Adenosine↗
PubMed1984

Positive inotropic and toxic effects of brevetoxin-B on rat and guinea pig heart.

Brevetoxin-B (GbTX-B), a cyclic polyether purified from the marine dinoflagellate Gymnodinium breve, produced positive inotropic and arrhythmogenic effects on isolated rat and guinea pig cardiac preparations at concentrations between 1.25 X 10(-8) and 1.87 X 10(-7) M. The toxin (10(-7) M) transiently increased left ventricular +dP/dt, hydraulic work, and oxygen consumption of paced working rat hearts, then reduced these variables during continuous exposure. Brevetoxin-B exerted a much smaller positive inotropic effect on working guinea pig hearts, but produced a marked and sustained inotropic effect on guinea pig left atria. The toxin also produced arrhythmias in rat and guinea pig hearts, characterized by ventricular tachycardia and A-V blockade. Sympatholytic procedures (beta blockade or reserpine pretreatment) partially blocked the positive inotropic effects, and eliminated the ventricular tachycardia, but not the A-V blockade. Tetrodotoxin markedly inhibited the positive inotropic effect of GbTX-B. Brevetoxin-B did not inhibit guinea pig cardiac Na,K-ATPase activities. The results show that GbTX-B is a potent cardiotoxin and suggest that GbTX-B exerts positive inotropic and arrhythmogenic effects by increasing sarcolemmal sodium permeability, and by releasing catecholamines from sympathetic nerve endings.

Animals↗
PubMed1987

Mechanism of anestrus in rats treated with an antihypertensive agent, losulazine hydrochloride.

The mechanism of anestrus in rats treated with losulazine, a peripheral sympatholytic antihypertensive agent, was investigated by determining its effect on hypothalamic catecholamines and serum sex hormones and by evaluating the influence of bromocriptine on the reproductive functions of rats treated with losulazine. Groups of six female Upjohn Sprague-Dawley rats were treated orally with 10 mg/kg/day of losulazine and/or 18.75 mg/kg/day of bromocriptine for 15 or 27 days. Six rats were treated with losulazine plus 6.25 mg/kg/day of bromocriptine for 16 days followed by losulazine alone for 11 days. Rats treated with losulazine only were depleted of hypothalamic catecholamines, were hyperprolactinemic, and had interrupted estrous cycles and attenuated vaginal mucosa. Treatment with bromocriptine, a dopamine receptor agonist, resulted in suppression of serum prolactin and normal estrous cycles. Rats reverted back to hyperprolactinemia and anestrus shortly after bromocriptine withdrawal. These results suggest that hyperprolactinemia mediated through hypothalamic dopamine depletion is the mechanism of anestrus in rats treated with losulazine.

Anestrus↗
PubMed1981

Evidence for a central depressor action of postsynaptic alpha 1-adrenergic receptor antagonists.

The effects of alpha-adrenergic receptor antagonists on sympathetic nervous discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor intact and denervated cats. Prazosin (50 microgram/kg, i.v.) produced a rapid fall in mean arterial pressure (MAP) and no significant change in heart rate (HR) in baroreceptor denervated cats. Prazosin administration was also associated with a prolonged inhibition of SND. Nerve activity was significantly reduced within 5 min of prazosin administration remained depressed throughout the 2 h observation period. Like prazosin, WB-4101 (0.5 mg/kg, i.v.) also produced significant reductions in MAP and SND. In addition, WB-4104 produced a transient bradycardia. The decreases in MAP and SND were reversed by piperoxane (0.5 mg/kg, i.v.). Both prazosin and WB-4101 inhibited the pressor response to i.v. norepinephrine. In baroreceptor intact cats, prazosin decreased MAP and SND, but did not affect HR. In contrast, phentolamine (1 mg/kg, i.v.) decreased MAP but increased SND and HR. These data indicate that the sympatholytic action of WB-4101 and prazosin results from a centrally mediated reduction in SND as well as a peripheral blockade of alpha-adrenergic receptors. These data further suggest that noradrenergic neurons normally facilitate the outflow of sympathetic nerve activity from the central nervous system.

Adrenergic alpha-Antagonists↗
PubMed1996

Contralateral temperature changes of the finger surface during video endoscopic sympathectomy for palmar hyperhidrosis.

One hundred and eight consecutive patients with primary palmar hyperhidrosis were surgically managed by coagulation of bilateral T2 sympathetic ganglia using video thoracoscopic techniques. Patients were divided into two groups. In the first group (N = 46), finger surface temperature of the ipsilateral index finger was recorded before and after T2 ganglionectomy. The average increase of post-operative temperature was 2.74 +/- 0.27 degrees C (mean +/- SE) on the right side and 2.67 +/- 0.33 degrees C on the left (P < 0.05). The significant rise of temperature resulting from sympatholytic vasodilatation was only noted in cases of exact ablation of the T2 ganglion. In the second group (N = 62), surface temperatures of both index fingers were monitored and recorded simultaneously. These patients were arbitrarily subdivided into Group 2-A (N = 29) when right side ganglionectomy was performed first and Group 2-B (N = 33) when left side ganglionectomy was done initially. After the first ganglionectomy was completed, an ipsilateral increase with a contralateral decrease of temperature was observed; the average increase of temperature was 1.92 +/- 0.35 degrees C and 2.19 +/- 0.30 degrees C, and the average decrease was 1.50 +/- 0.51 degrees C and 1.67 +/- 0.39 degrees C for Group 2-A and 2-B respectively (P < 0.05). The authors postulate that a cross-inhibitory effect by the post-ganglionic neurons innervating blood vessels of the upper extremities may exists in humans and this effect is released after ganglionectomy, resulting in contralateral vasoconstriction and decrease of finger surface temperature.

Adolescent↗
PubMedDate not supplied

Mechanism of the pressor response to intraperitoneal injection of bradykinin in guinea pigs.

Single intraperitoneal (IP) injection of bradykinin (BK) in anesthetized guinea pigs caused concentration-related pressor effects and slight, not significant tachycardia. Intravenous injections of BK in the same animal model evoked hypotension and a marked tachycardia. IP injection of des-Arg9-BK, a selective B1 receptor agonist, caused no changes of blood pressure or heart rate. The pressor response to IP BK was reduced by concomitant IP injection of lidocaine or of D-Arg[Hyp3,D-Phe7,Leu8]BK, a B2 receptor antagonist. It was also inhibited by acute animal pretreatment with sympatholytic drugs, by chronic animal exposure to capsaicin, or acute spinalization, but it was not affected by atropine, propranolol, indomethacin, [Leu8]des-Arg9-BK, a B1 receptor antagonist, or by acute cervical vagotomy. These results suggest that pressor responses to IP BK in anesthetized guinea pigs are reflex in nature, involving abdominal, capsaicin-sensitive, nonvagal visceral afferents, efferent components of the sympathetic nervous system and possibly supraspinal centers, and likely to be mediated by B2 receptors of kinins presumably located on abdominal visceral afferents.

Animals↗