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At least 163 records · Page 9Linked to original sources
PubMed1987

Autocrine-paracrine mechanisms of vascular myocytes in systemic hypertension.

Recent data demonstrate that in addition to its conduit function, the blood vessel is an active synthetic and secretory organ containing several autocrine and paracrine systems that are involved with the local regulation of its own function. The endothelium plays a pivotal role in modulating the balance between thrombogenesis and thrombolysis. In addition, it secretes vasorelaxant and vasoconstrictive substances, growth factors and inflammatory mediators that exert paracrine influences on vascular myocyte function. The vascular myocyte also expresses autocrine substances which influence its own function. The autocrine systems include angiotensin, prostaglandins, platelet-derived growth factor, insulin-like growth factor and heparin. These local factors exert modulatory influences on myocyte contractility and growth. It is conceivable that genetic or acquired abnormalities of one or several of these check and balance systems can result in increased vascular tone, generalized vascular hypertrophy or hyperplasia, or a combination, and contribute to the pathogenesis of hypertension. These autocrine-paracrine systems may be important targets for antihypertensive drug development.

Blood Platelets↗
PubMed1994

Effects of bepridil on silent myocardial ischemia and eicosanoid metabolism in chronic stable angina pectoris after healing of myocardial infarction.

To investigate the effects of bepridil on silent myocardial ischemia and on eicosanoid metabolism, 10 patients with chronic stable angina underwent exercise treadmill testing and 48-hour ambulatory electrocardiographic monitoring both before and after 4 weeks of bepridil administration (150 mg/day). Fasting venous levels of thromboxane B2, 6-keto-prostaglandin F1 alpha, and leukotriene C4 were measured by radioimmunoassay. Bepridil decreased heart rate responses to daily activities during ambulatory monitoring, and significantly (p < 0.05) reduced the median frequency and duration of silent myocardial ischemic episodes (from 5.5 to 0 events/48 hours and from 86 to 0 minutes/48 hours respectively). Bepridil significantly decreased the blood pressure heart rate product at peak exercise and significantly prolonged the mean exercise tolerance time (from 456.6 to 527.0 second). Bepridil also significantly decreased the plasma levels of thromboxane B2 and leukotriene C4 at rest. These results suggest that bepridil may reduce silent myocardial ischemic episodes either by the reduction of cardiac oxygen demand during daily activities and exercise stress, or by controlling coronary and systemic vasomotor tone. The drug also has a salutary effect on eicosanoid metabolism, to which its efficacy on silent myocardial ischemic episodes may be related.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Inhibitory influence of sympathetic nerves on afferent nerve-induced extravasation in the rat incisor pulp upon direct electrical stimulation of the tooth.

Previous studies have shown that sympathetic nerve stimulation reduces afferent nerve-induced vasodilation by mechanisms unrelated to vasoconstriction in the rat incisor pulp. The present investigation concerned whether similar modulatory mechanisms might also influence neurogenic plasma extravasation in dental pulp. Rat mandibular incisors were electrically stimulated and blood flow reactions in the pulp were recorded by laser Doppler flowmetry. Plasma extravasation in the incisor pulp, gingiva and lip were indirectly assessed by the Evans-blue method. Stimulation of teeth with 50 microA (5 min) did not cause increased dye accumulation in the stimulated pulps whereas stimulation with 100 microA significantly increased the dye content in ipsilateral pulps by 32% as compared to controls; 100 microA stimulation was without effect in unilaterally denervated animals. Tooth stimulation with 50 microA (5 min), in the presence of either the alpha-adrenergic blocker phenoxybenzamine (3 mg/kg), or the alpha 1-adrenergic antagonist prazosin (50 micrograms/kg), as well as in chronically sympathectomized animals, significantly increased the Evans-blue content in the stimulated pulps by 47, 83 and 86%, respectively. Application of short trains of impulses (same number of impulses as for the continuous stimulation but producing minimal vasoconstriction) resulted in some dye accumulation, which was enhanced in the ipsilateral pulps in the presence of prazosin (100 micrograms/kg) or after acute resection of the superior cervical sympathetic ganglion by 70 and 64%, respectively. The Evans-blue content in the lip and gingiva was uninfluenced by the tooth stimulation. The results indicate that activation of sympathetic nerves inhibits the afferent nerve-induced plasma extravasation in rat incisor pulp and this effect is mediated by alpha-adrenoceptors not associated with vasoconstriction.

Animals↗
PubMed1984

Some effects of sympathetic stimulation and isoprenaline on fatigued tetanic contractions of skeletal muscle in the cat.

In anaesthetized cats, stimulation of the lumbar sympathetic trunk inconsistently elicited small increases in the contraction of fatigued Peroneus Longus muscles (Orbeli phenomenon). Facilitation of this anti-fatigue effect was regularly observed following close intra-arterial injection of isoprenaline, a beta-adrenergic agonist. Injection of the drug by itself exerted a marked anti-fatigue effect on muscle contraction.

Animals↗
PubMed1986

Effect of clonidine and gamma-aminobutyric acid on the discharges of medullo-spinal sympathoexcitatory neurons in the rat.

Single-unit recordings of 50 pressure-sensitive neurons with axonal projections to the thoracic spinal cord were obtained in the retrofacial portion of nucleus paragigantocellularis lateralis of halothane-anesthetized rats. Two types of cells were distinguished on the basis of their axonal conduction velocities: a slow-conducting (mean 0.6 m/s, group I) and a fast-conducting one (group II, mean 3.3 m/s). Both cell types were completely silenced by elevating mean arterial pressure above 160 mm Hg by means of aortic constriction and exhibited a plateau of high spontaneous activity below 70 mm Hg. Only group I neurons were significantly inhibited by the administration of clonidine in a dose producing 90% of its maximum hypotensive effect (11.5 micrograms/kg, i.v.). Hypotensive doses of clonidine administered into the fourth ventricle also produced a selective inhibition of group I neurons, while the others were unaffected. Iontophoretic applications of clonidine and norepinephrine produced an inhibition of the discharges of group I neurons qualitatively and quantitatively identical to that observed following administration of clonidine by the i.v. or i.c.v. route. Once more, group II cells were unaffected. In contrast, iontophoretically applied gamma-aminobutyric acid exerted a powerful inhibition of both cell types, an effect which was totally prevented or reversed by the gamma-aminobutyric acid antagonist bicuculline. Anatomical experiments were performed to uncover the potential source of catecholaminergic innervation of the area in which recordings were obtained. This area contains a large number of adrenaline-synthesizing neurons and receives a selective noradrenergic input from the A5 pontine group with no contribution from the A1, A2, A6 and A7 brainstem clusters of noradrenergic cells.

Animals↗
PubMed1986

Central impairment of renal nerve response to stimulation of medullary pressor area in rabbit endotoxic hypotension.

The present study was designed to determine if there is a central abnormality in the sympathetic efferent outflow through the brainstem in endotoxic hypotension. Mean blood pressure (MBP), heart rate (HR) and renal nerve activity (NA) were recorded simultaneously following intravenous injection of endotoxin (1 mg/kg). MBP fell significantly so that 30 min and 60 min after the injection, MBP were 76 +/- 11 mm Hg and 56 +/- 10 mm Hg respectively. Simultaneously with decreases in MBP, NA and HR also decreased significantly. Peak responses in MBP and NA to repetitive stimulation of medullary pressor area (MPA) were attenuated significantly after endotoxin. Onset and peak latencies of renal nerve discharges (RNDe) evoked by the electrical stimulation of the MPA at 5 min after endotoxin were significantly shorter than that before endotoxin, followed by a recovery to the pre-endotoxin level. Peak and total activities of RNDe were reduced significantly so that 30 min after endotoxin activities were 53 +/- 9% and 53 +/- 11% of pre-endotoxin levels respectively. However, responses in MBP, NA and RNDe to the stimulation of the thoracic sympathetic chain did not differ significantly between before and after injection of endotoxin. These data confirm the presence of a central neural abnormality in central sympathetic outflow in the hypotension induced by E. coli endotoxin.

Animals↗
PubMed1977

Dopamine receptors in the femoral vascular bed of the dog as mediators of a vasodilator and sympathoinhibitory effect.

ET 495 and apomorphine, injected in small doses (0.1--1 microng/kg) into the femoral artery, induced a dose-dependent increase in femoral blood flow. This dilator effect was abolished by section of the ipsilateral femoral nerve and sciatic nerve, transection of the spinal cord, alpha-adrenoceptor blockade, ganglionic blockade and guanethidine. In addition, the increase in blood flow was inhibited by intravenous administration of haloperiol (2 mg/kg i.v.) or pimozide (2 mg/kg i.v.) and by injection of small doses (10--50 microng/kg) of these drugs into the femoral artery. It was concluded that a dopaminergic component located in the femoral vascular bed of the dog may be involved in the local vasodilator and sympathoinhibitory effect of apomorphine and ET 495.

Animals↗
PubMed1995

Mechanisms of cortisol-induced hypertension in humans.

There is emerging evidence that cortisol plays a significantly greater role in human hypertension than previously thought. Apart from the well recognized role of cortisol in the hypertension of Cushing's syndrome, local cortisol excess has been recognized as responsible for rare forms of hypertension such as apparent mineralocorticoid excess and licorice abuse and more recently implicated in the hypertension of chronic renal failure, hypertension related to low birth weight and essential hypertension. Although cortisol-induced hypertension is characterized by sodium retention and volume expansion, studies with synthetic glucocorticoids or sodium restriction suggest that the hypertension is, to a substantial degree, independent of sodium and volume. Increase in cardiac output is not essential for cortisol-induced blood pressure rise but the precise role of increases in total or regional peripheral resistance as a primary mechanism has nto been determined. Increased pressor responsiveness, particularly to catechols, is a prominent feature but whether these changes are sufficient to account for the hypertension remains unclear. There is no evidence for increased sympathetic nervous activity as judged by measurements of plasma catcholamines, neuropeptide-Y, or resting noradrenaline spillover rate. Responses to mental stress or maximal hand-grip are unchanged and baroreflex sensitivity is increased. Octreotide profoundly reduced the elevated plasma insulin concentrations seen with cortisol administration but had no effect on the rise in blood pressure.

Hemodynamics↗
PubMed1995

Noradrenaline increases hyperalgesia to heat in skin sensitized by capsaicin.

Neurophysiological and behavioural observations in animals suggest that sympathetic neural activity and noradrenaline have an excitatory effect on nociceptor discharge in inflamed skin. To determine whether noradrenaline influences pain sensations in humans, heat hyperalgesia in forearm skin sensitized by topical application of 0.6% capsaicin was measured at sites of noradrenaline or saline ionophoresis in 10 healthy subjects. At control sites and sites of saline ionophoresis heat hyperalgesia decreased over the course of the experiment as inflammation subsided. In contrast, heat hyperalgesia persisted at sites of noradrenaline ionophoresis. These findings are consistent with neurophysiological observations that noradrenaline and sympathetic neural stimulation increase nociceptor discharge in inflamed skin, and suggest that sympathetic neural activity might increase pain associated with skin damage.

Adolescent↗
PubMed2005

Associated factors with urogenital score in natural and surgical menopause.

OBJECTIVE: To anticipate the factors associated with urogenital symptoms in both natural and surgical menopause. METHODS: A retrospective analysis was performed comprising 267 cases with spontaneous menopause and 87 surgical menopause cases without any use of hormone replacement therapy. Sociodemographic characteristics, reproductive and medical history, urogenital scale and psychological subscale of Greene Climacteric Scale were assessed and correlated with the age of menopause, time past since last menstrual period, parity, body mass index (BMI), mode of delivery among two groups. RESULTS: Mean age of women enrolled to the study were 46.8+/-0.3 years and 44.4+/-0.25 years, for natural and surgical menopause cases, respectively. Mean parity had no correlation with urogenital scale in two groups. However, a positive correlation was apparent between the time since last menstrual period, psychological subscore of Green Climacteric Scale and urogenital score in both women with natural and surgical menopause. BMI was negatively correlated with urogenital score among two groups (r(p)=-0.85, p=0.04). CONCLUSIONS: Intensity and frequency of urogenital symptoms and climacteric complaints as expressed in the Greene Climacteric Scale increase during menopausal transition. Care should be taken to ameliorate the quality of life (QOL) and to confront these problems in post-menopausal women.

Adult↗
PubMed2000

Migraine, but not subarachnoid hemorrhage, is associated with differentially increased NPY-like immunoreactivity in the CSF.

To test whether migraine and subarachnoid hemorrhage (SAH) are associated with increased sympathetic tone, we compared the neuropeptide Y-like (NPY-LI) and chromogranin A-like immunoreactivities (LI) of cerebrospinal fluid (CSF) from migraneurs and SAH patients with those from control subjects. Increased sympathetic tone was expected to produce higher co-release of these co-stored peptides and concordant changes in their CSF levels. In addition, we investigated a possible disturbed nitric oxide homeostasis by measuring CSF nitrites (NO). More than 70% of CSF NPY-LI corresponded to the chromatographic peak (HPLC) for the intact molecule in all three groups. Migraneurs had 64% higher CSF NPY-LI, but no significant difference in CSF chromogranin A-LI, as compared to controls. In contrast, SAH patients had 74% less CSF chromogranin A-LI and a trend to lower NPY-LI, as compared to controls. No differences in CSF NO were detected among groups. These results argue against an increased sympathetic tone in patients with either migraine or SAH, and suggest that the higher CSF NPY-LI of migraneurs probably originates from central neurons. Furthermore, our findings in SAH patients argue in favor of a decreased sympathetic tone; this could be a homeostatic response to counterbalance vasoconstriction mediated by other mechanisms.

Adult↗