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At least 757 records · Page 42Linked to original sources
PubMed1989

Adrenergic and neuropeptide Y supersensitivity in denervated nasal mucosa vasculature of the pig.

The effects of sympathetic denervation for 2 weeks on vasoconstrictor reactivity to alpha-adrenoceptor agonists, neuropeptide Y (NPY) and alpha,beta-methylene adenosine triphosphate (mATP) were investigated in different vascular compartments of the nasal mucosa of pentobarbital-anesthetized pigs. Supersensitivity to the vasoconstrictor actions of noradrenaline (NA) was observed in the function of both resistance vessels (as revealed by a reduction in arterial blood flow) and capacitance vessels (reflected by a reduction in nasal mucosal volume). The NA supersensitivity was, to a large extent, of prejunctional type since inhibition of neuronal uptake by desipramine also markedly enhanced the NA response. Whereas the reduction in arterial blood flow and in mucosal volume induced by the alpha 1-agonist, phenylephrine, was not changed by denervation, the effects of the alpha 2-agonists UK 14.304 and oxymetazoline were enhanced and/or prolonged. Furthermore, the reduction in blood flow and volume induced by NPY was enhanced in both amplitude and duration. The effects of mATP on the amplitude of the volume response and the duration of the blood flow and volume changes were increased. The maximal reduction in superficial blood flow was larger, as revealed by the laser Doppler flowmetry signal, when NPY or adrenoceptor agonists were given to denervated animals. It is concluded that sympathetic denervation is associated with increased sensitivity and prolonged responses to a variety of vasoconstrictor agents in the pig nasal mucosa in vivo. However, alpha 2-adrenoceptor, NPY and mATP mechanisms seem to be influenced more by denervation than by alpha 1-adrenoceptor sensitivity.

Animals↗
PubMedDate not supplied

The comparative effect of administration of substances via the hepatic artery or portal vein on hepatic arterial resistance, liver blood volume and hepatic extraction in cats.

Compounds reaching the liver do so via either the hepatic artery or the portal vein. This paper reports on the effectiveness of administration of compounds into these alternate routes for their effects on the hepatic parenchymal cells, the hepatic arterial resistance vessels (blood flow) and hepatic capacitance (blood volume responses). All tests were done on cats under pentobarbital anesthesia. Perfusion of the parenchymal cell mass was assessed by comparing the hepatic elimination of indocyanine green (ICG) administered via the two vascular routes. The ICG uptake was assessed by measuring relative areas under the hepatic venous outflow curve obtained following bolus injections of ICG into the artery and portal vein. In a separate series, using different methods, the hepatic venous levels reached early (2 min) and later (5 min) during a constant infusion were compared during administration via the two routes and found to be equal. Parenchymal cell functions (ICG extraction, bile salt stimulation of bile flow) indicate that blood from the artery and portal vein supplies the hepatic parenchymal cells equally well. This suggests a well-mixed blood supply prior to exposure of either blood stream to parenchymal cells. Substances being processed by the liver are thus equally well handled if reaching the liver via either the arterial or portal blood stream. This has significance in validating the use of some isolated liver perfusion methods that perfuse only via the portal vein. Access of vasoactive compounds in the two blood streams to hepatic arterial resistance vessels was assessed using electromagnetic flow probes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1976

Hepatic venous compliance and role of liver as a blood reservoir.

Changes in hepatic blood volume in response to rapid elevations in hepatic venous pressure were examined in cats using hepatic plethysmography. The liver was intact and received blood from an intact portal vein and hepatic artery. The hepatic blood volume increased in response to elevated venous pressure. Compliance of the hepatic capacitance vessels became greater as the distending venous pressure was increased over the range of venous pressures studied (0-9.4 mmHg). When hepatic venous pressure was elevated to 9.4 MMHg, the hepatic blood volume more than doubled. The liver serves as an important buffer for rapid changes in blood volume, the importance increasing with greater infused volumes of fluid. While overall venous compliance decreased at distending pressures in excess of 5-6 mmHg, the compliance of the hepatic capacitance vessels shows marked increases at pressures above this level. Expansions of the blood volume results in elevations of central venous pressure. Within a few minutes the hepatic capacitance vessels sequester a significant proportion of the added volume. As long as central venous pressure is raised, the liver demonstrates a secondary fluid buffering role by filtering large volumes of fluid across the vascular bed into the peritoneum.

Animals↗
PubMed1995

Beta-adrenergic mechanisms in the nasal mucosa vascular bed.

In thiopentone-anesthetized mature pigs (n = 7), local intra-arterial infusion of the beta 2-adrenoceptor agonists terbutaline and salbutamol and the beta 3-agonist BRL 37344 induced dose-dependent increases in nasal arterial blood flow (BF) and volume of the nasal mucosa (reflecting capacitance vessel function). Increases were also found in the laser Doppler flowmeter signal, reflecting superficial mucosal BF. In contrast to terbutaline and salbutamol, BRL 37344 showed marked effects on volume. Pretreatment with the beta-adrenoceptor blocker propranolol significantly reduced the vasodilatory effects of terbutaline and salbutamol, whereas the BF increase evoked by BRL 37344 was not affected. Exogenous noradrenaline (NA) induced in vitro dose-dependent contractions of human nasal mucosa biopsies obtained from patients with non-allergic chronic rhinitis (n = 21) or non-allergic nasal polyposis (NANP, n = 16). On a molar basis, the contractile effect of NA was significantly greater in nasal mucosa samples without histological abnormalities when compared to biopsies with abundant inflammatory cells and edema within the submucosa. In the presence of propranolol, the vasoconstrictor effect of NA was significantly enhanced in biopsies with abundant inflammatory cells obtained from patients with NANP (P < 0.01). This observation suggests the possible occurrence of a beta 2 hyper-reactivity in the nasal mucosa of patients with NANP. After precontraction in a Krebs-Ringer solution with 50 nM K+, all nasal biopsies studied showed dose-dependent relaxation to terbutaline, salbutamol and BRL 37344. This relaxant effect was markedly reduced after pretreatment with propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1980

Effects of intravenous phentolamine on hemodynamics and resting pulmonary gas exchange in man.

The influence of intravenous phentolamine on hemodynamics, ventilation, and blood gases were studied in 22 patients with cardiac disease. Phentolamine produced a significant increase in the heart rate and cardiac index and a significant decrease in the mean arterial pressure, mean pulmonary artery pressure, left ventricular end diastolic pressure, peripheral vascular resistance, and pulmonary vascular resistance. There was no significant change in the arterial pH, PO2, PCO2, alveolar-arterial PO2, and the dead space-tidal volume ratio. The favorable hemodynamic responses are attributable to the fact that the vasodilator effect of phentolamine is predominately on the arteriolar resistance bed and much less on the venous capacitance bed. In addition, phentolamine has a positive inotropic action which is indirect and dependent on the release of norepinephrine.

Adolescent↗
PubMed2003

Identification of interstitial cells of Cajal in the rabbit portal vein.

Two layers of interstitial cells (ICs) of Cajal were detected by c-kit and methylene blue staining in the media of the rabbit portal vein in subendothelial intramuscular and deeper intramuscular positions, displaced radially from each other by about 40-70 microm. Two morphologically distinct types of ICs were found among enzymatically dispersed cells from this vessel: small multipolar cells with stellate-shaped bodies not exceeding 20 microm, and spindle-shaped cells from 40 to 300 microm in length with numerous branching processes. Relaxed smooth muscle cells (SMCs) had a more constant length (90-150 microm). The cell membrane capacitance was 46.5+/-2.2 pF in SMCs, 39.7+/-2.4 pF in spindle-shaped ICs and 27.8+/-0.7 pF in multipolar ICs. Although darker under phase contrast, after loading with fluo-4 AM, single isolated ICs of both types usually had brighter fluorescence than SMCs and displayed various spontaneous calcium events, including Ca(2+) sparks and Ca(2+) waves. Ca(2+) waves were usually followed by contraction of SMCs but no change in shape of ICs. In some ICs spontaneous [Ca(2+)](i) transients (lasting about 2s) which propagated towards the end of the processes were observed. Physical contacts between the processes of ICs and the body of one or more SMCs survived the isolation procedure. Application of noradrenaline (1-10 microM), caffeine (1-10 mM) or high-K(+) solution (60mM) led to a rise of [Ca(2+)](i) in both SMCs and ICs evoking contraction of SMCs but not ICs. No differences in electrophysiological characteristics between single enzymatically isolated IC and SMC were detected; thus, the resting membrane potential estimated under current-clamp conditions was -46.5+/-2.0 mV in spindle-shaped ICs and -45.6+/-2.7 mV in SMCs. Under voltage-clamp, both ICs and SMCs revealed a well-developed voltage-gated nifedipine-sensitive L-type Ca(2+) current, a set of K(+) currents, including spontaneous transient outward currents (STOCs) but no Na(+) current. This study for the first time directly demonstrated the presence in vascular tissue of ICs. Possible roles for ICs including their involvement in spontaneous activity of the vessel were discussed.

Aniline Compounds↗
PubMed2006

Stimulation of arachidonic acid release by vasopressin in A7r5 vascular smooth muscle cells mediated by Ca2+-stimulated phospholipase A2.

Arachidonic acid (AA) regulates many aspects of vascular smooth muscle behaviour, but the mechanisms linking receptors to AA release are unclear. In A7r5 vascular smooth muscle cells pre-labelled with (3)H-AA, vasopressin caused a concentration-dependent stimulation of 3H-AA release that required phospholipase C and an increase in cytosolic [Ca2+]. Ca2+ release from intracellular stores and Ca2+ entry via L-type channels or the capacitative Ca2+ entry pathway were each effective to varying degrees. Selective inhibitors of PLA2 inhibited the 3H-AA release evoked by vasopressin, though not the underlying Ca2+ signals, and established that cPLA2 mediates the release of AA. We conclude that in A7r5 cells vasopressin stimulates AA release via a Ca2+-dependent activation of cPLA2.

Animals↗
PubMed1985

Hemodynamic effects of angiotensin-converting enzyme inhibitors in essential hypertension: a review.

Angiotensin-converting enzyme inhibitors are vasodilators that exert their beneficial hemodynamic effects in hypertension primarily by withdrawal of the vasoconstricting action of endogenous angiotension II. Although the magnitude of the initial decrease in vascular resistance depends on renin activity, the long-term arterial blood pressure response does not appear to be influenced by initial renin levels. Cardiac output is not significantly altered by angiotensin-converting enzyme inhibition in patients with mild-to-moderate hypertension, but a rise toward normal levels often occurs in patients with severe hypertension or heart failure. Although right and left heart filling pressures are not significantly altered, other evidence suggests that these agents increase venous capacitance. Patients with severe hypertension, for example, have shown increased forearm venous distensibility in response to angiotensin-converting enzyme inhibitors, and a decrease in the ratio of cardiopulmonary blood volume to total blood volume has been demonstrated in normotensive patients with heart failure. Several studies have shown improved renal blood flow after angiotensin-converting enzyme inhibition, suggesting that renal vascular resistance is reduced more than systemic resistance. Reflex tachycardia and other neurohumoral counterregulatory responses occur less frequently than with other vasodilators, because neither the renin-angiotensin-aldosterone nor the autonomic nervous system is activated by angiotensin-converting enzyme inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

'Structural autoregulation'--the local adaptation of vascular beds to chronic changes in pressure.

Blood vessels readily adapt their design in response to sustained functional changes. If pressure (P) increases, the resulting thickening of the walls (w) of the resistance vessels, associated with a reduction in average inner radius (ri), keeps wall tension per unit wall layer (T) constant, because the increased w/ri ratio largely balances the raised pressure (Laplace's law: T = P X ri/w). The opposite occurs when there are sustained reductions in pressure. This locally elicited, mainly precapillary structural adaptation is a long-range equivalent to precapillary functional autoregulation and deserves to be called structural autoregulation. In primary hypertension there is an early 'structural resetting' of the systemic precapillary resistance, due to narrowing of ri and to vascular hyperreactivity ensuing from the increase in w/ri. These structural changes imply an increased resistance to flow at normal levels of vascular smooth muscle activity. Furthermore, even mild functional pressor influences will, if sustained, by a positive feedback interaction with the initially mild vascular hyperreactivity gradually accentuate the structural increase in w/ri. Marked rises in pressure may ensue from this interaction, implying that it is a major causative element in primary hypertension. As the renal preglomerular resistance vessels are similarly structurally autoregulated, this implies an early largely parallel resetting of the important renal 'long-term barostat function'. Further, as the walls of large arteries get thicker and stiffer, this helps to reset the baroreceptors. Finally, as the venous capacitance vessels adapt in a similar way the slight rise in average venous pressure in primary hypertension will reduce venous compliance, which helps to 'centralize' the usually slightly reduced blood volume.

Adaptation, Physiological↗
PubMed1996

Interdependence of calcium signaling and protein tyrosine phosphorylation in human endothelial cells.

The signal transduction cascade which initiates transmembraneous influx of Ca2+ into endothelial cells in response to the discharge of intracellular Ca2+ stores is thought to involve a step sensitive to tyrosine kinase inhibition. We investigated the interrelationship between Ca2+ signaling and protein tyrosine phosphorylation following cell stimulation with either the receptor-dependent agonist, bradykinin, or the protein-tyrosine phosphatase inhibitor, phenylarsine oxide. In cultured human endothelial cells phenylarsine oxide instigated a concentration-dependent increase in the intracellular concentration of free Ca2+ ([Ca2+]i). This increase in [Ca2+]i was not associated with the tyrosine phosphorylation of phospholipase C gamma, enhanced formation of inositol 1,4,5-trisphosphate, or the rapid depletion of intracellularly stored Ca2+ but was coincident with the enhanced and prolonged tyrosine phosphorylation of a number of cytoskeletal proteins. In bradykinin-stimulated cells the tyrosine phosphorylation of the same cytoskeletal proteins (most notably 85- and 100-kDa proteins) was transient when cells were stimulated in the presence of extracellular Ca2+, was maintained under Ca2+-free conditions, and was reversed following readdition of extracellular Ca2+. These data suggest that the tyrosine phosphorylation of 2 cytoskeletal proteins is determined by the level of Ca2+ present in intracellular stores thus indicating a critical role for tyrosine phosphorylation in the control of capacitative Ca2+ entry in endothelial cells.

Amino Acid Sequence↗
PubMed1996

Myogenic responses of isolated rat skeletal muscle venules: modulation by norepinephrine and endothelium.

The pressure-induced myogenic response of large venules of skeletal muscle and its possible interactions with adrenergic receptor activation and endothelial factors have not yet been elucidated. Therefore, first-order venules of rat gracilis muscle were isolated, cannulated, and placed in an organ chamber. Changes in internal diameter of the vessels as a function of perfusion pressure (PP) were obtained. In response to increases in PP (0.5-17.5 mmHg), the diameter of venules increased from 197.1 +/- 23.96 to 369 +/- 14.1 microns. In passive conditions (in Ca(2+)-free solution), the pressure-diameter curve of venules shifted significantly upward. In the presence of norepinephrine (NE; 10(-6) M) in the bath solution, the pressure-diameter curve of active venules shifted significantly downward, and in the pressure-normalized diameter curve, a negative slope developed (-6.1 +/- 4.6). In both the absence and presence of NE, removal of endothelium significantly reduced venular diameters in the pressure ranges of 3-5 and 2-5 mmHg, respectively, but did not change significantly the characteristics of the pressure-diameter curves. These findings indicate that the smooth muscle of venules actively responds to changes in intraluminal pressure. This response is greatly facilitated by NE and modulated by the endothelium. The myogenic response of skeletal muscle venules, especially in the presence of NE, could have a role in the regulation of the resistance and capacitance of venules and, consequently, blood flow and tissue exchange in skeletal muscle.

Animals↗
PubMed1987

Reflex control of nasal blood vessels.

The effect of stimulation of vagal afferent fibers on nasal blood vessels was studied in 36 cats. Volume change of the nasal capacitance vessels was measured by plethysmographic balloons inserted into the nose. Electrical stimulation of the vagus nerve produced a vasodilatation of nasal mucosa. Pulmonary stretch receptor stimulation by veratridine alkaloid and progressive lung inflation in open-chest cats also produced a vasodilatation of the nasal mucosa. These reflexes were abolished by sectioning the vagus nerves. These results suggest a reflex arc between the lung and nasal capacitance vessels which arises from pulmonary stretch receptors.

Airway Resistance↗
PubMedDate not supplied

[Presence of the regulatory peptide endothelin in the vascular endothelium of the human nasal mucosa].

Endothelin is a 21-amino acid peptide originally isolated from cultured endothelial cells. Besides being the most potent vasoconstrictor peptide. Endothelin is known to produce a wide range of biological effects: contraction of smooth airway muscle, stimulation of cell growth and modulation of hormone and neurotransmitter release. The aim of the present study was to use immunocytochemical techniques in investigating the possible occurrence of endothelin in normal human nasal mucosa. Endothelial cells of both capacitance and resistance blood vessels of the mucosa displayed endothelin-like immunoreactivity. It is reasonable to presume that endothelin, produced and released locally by endothelial cells, may play a role in controlling blood flow, in neuromodulation and in wound healing via a paracrine mechanism.

Endothelins↗
PubMed1982

Contrasting hemodynamic responses in severe heart failure: comparison of captopril and other vasodilator drugs.

Four studies were conducted in 36 patients with severe chronic heart failure to compare the central hemodynamic effects of captopril (CPT) to other vasodilator agents. While CPT produced less marked increases in cardiac output than did hydralazine (n = 14), nitroprusside (n = 15), or prazosin (n = 7), it produced decreases in left ventricular filling pressures similar to nitroprusside and prazosin but more than hydralazine. CPT and isosorbide dinitrate (n = 11) produced similar decreases in systemic vascular resistance and left ventricular filling pressure. However, cardiac output increased less with CPT than with nitrates, because heart rate slowed during CPT therapy. In addition, mean right atrial pressure decreased less with CPT than with nitrates, because CPT had minimal effects on limb venous capacitance and pulmonary arteriolar resistance. Alterations in left ventricular pressure-volume relationships likely contributed to the marked decreases in left ventricular filling pressures seen with CPT. In conclusion, the central hemodynamic effects of CPT differ significantly from other vasodilator drugs used in the treatment of heart failure patients. These effects cannot be characterized simply in terms of "balanced" peripheral arterial and venous vasodilation; CPT exerts highly complex effects on peripheral vessels as well as having actions independent of its peripheral vasodilator effects.

Adult↗