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At least 217 records · Page 12Linked to original sources
PubMed1980

Responsiveness to vasoactive agents of cerebral and mesenteric arteries isolated from control and reserpine-treated dogs.

1 Pretreatment of dogs for 20 to 24 h before the start of experiments with reserpine (0.5 mg/kg) depleted noradrenaline from cerebral and mesenteric arteries, the diminution being greater in the latter arteries. 2 Contractile responses of helically-cut strips of cerebral and mesenteric arteries to noradrenaline were unaffected by pretreatment with reserpine. Tyramine-induced contractions of mesenteric arteries were markedly attenuated by reserpine-pretreatment, whereas the contraction of cerebral arteries was not influenced. The contractile response of mesenteric arteries to transmural nerve stimulation or nicotine was abolished by reserpine-pretreatment, but the relaxation induced by nicotine of cerebral arteries contracted with prostaglandin F2 alpha was not affected. Pretreatment with reserpine attenuated the contractions of mesenteric arteries induced by angiotensin II, but did not alter the response of cerebral arteries to 5-hydroxytryptamine. 3 In prostaglandin-contracted cerebral and mesenteric arterial strips, relaxant effects of acetylcholine, isoprenaline and K+ were not significantly influenced by reserpine-pretreatment. 4 It appears that tyramine and nicotine do not release noradrenaline from dog cerebral arteries in amounts sufficient to cause significant contractions. Attenuation of the response to angiotensin II by pretreatment with reserpine is not the result of depletion of noradrenaline from the mesenteric arterial wall but may be due to interference with the mechanism specific to actions of angiotensin II.

Acetylcholine↗
PubMed1993

Comparison of cumulative and non-cumulative administration of vasoactive agents in arterial smooth muscle responses in vitro.

Two methods of determining concentration-response curves were compared in isolated endothelium-intact mesenteric arterial rings from Wistar rats: arterial contractile and relaxation responses were elicited by adding compounds cumulatively or introducing a single concentration at a time (non-cumulative method). The contractile responses induced by high concentrations of K+ (20-125 mM) were comparable between the two methods, whether or not the responses were elicited in the presence of phentolamine (10 microM) and atenolol (10 microM). Noradrenaline (1 nM-10 microM) likewise induced similar contractions regardless of method of administration, the only exception being the highest concentration (100 microM) which produced lower contractile force when added directly upon resting tension than after cumulative administration. This difference was abolished by atenolol (10 microM). Arterial smooth muscle relaxations induced by endothelium-dependent (acetylcholine 1 nM-10 microM) and -independent agents (nitroprusside 1 nM-1 microM, isoprenaline 10 nM-100 microM) were similar whether the relaxants were added in a cumulative fashion or in a single concentration introduced upon each precontraction. Thus, cumulative and non-cumulative administration of contractile and relaxing agents give quite comparable results. We conclude that the cumulative method is a reliable and time-saving way of studying vascular smooth muscle responses in vitro.

Acetylcholine↗
PubMedDate not supplied

Measurements of hindlimb blood flow recorded using Doppler ultrasound during administration of vasoactive agents in halothane-anesthetized horses.

The purpose of the study was to determine the ability of Doppler ultrasound to detect changes in femoral blood flow during pharmacologic manipulation of arterial blood pressure. Doppler ultrasonography was performed in the femoral vessels of six halothane-anesthetized horses before and during administration of phenylephrine HCI and sodium nitroprusside. The time-averaged mean velocity and volumetric flow were calculated. The contour of the velocity waveform was assessed, and the early diastolic deceleration slope (EDDS) and pulsatility index (PI) were calculated. Administration of phenylephrine HCI resulted in increased mean aortic blood pressure (MABP) by 40% (29.3-53.0%). This caused significant decrease in cardiac output (26.8 to 13.5 l/min), femoral arterial velocity (left artery 7.20 to 4.00 cm/s; right artery 5.01 to 3.39 cm/s) and volumetric flow (left artery 556 to 221 ml/min; right artery 397 to 193 ml/min) in the femoral vessels and significant increase in systemic vascular resistance (163 to 433 dyn-s/cm5), EDDS (1a: 285 to 468: ra: 250 to 481) and PI (1a: 9.38 to 20.4; ra 17.1 to 29.1). Administration of sodium nitroprusside resulted in a decreased MABP of 27.2% (22.5-33%). This increased cardiac output (20.8 to 32.4 L/min), however, no significant changes were observed in femoral blood flow. Despite obvious changes in the waveform contour, no significant change occurred in EDDS or PI. These results suggest that Doppler ultrasound may be useful for measuring femoral blood flow in anesthetized horses. However, waveform analysis appears to be limited when multiple changes occur in central and peripheral haemodynamics.

Anesthetics, Inhalation↗
PubMed1986

Contractile effects of various vasoactive agents in small rat portal veins and hepatic arteries and the influence of sympathetic denervation on the noradrenaline response.

Contractile responses were studied in isolated tubal segments of branches of the rat portal vein (luminal diameter approximately 300 microns) and hepatic artery (luminal diameter approximately 200 microns). Portal veins were approximately three times more sensitive to noradrenaline (NA) than hepatic arteries. 5-hydroxytryptamine contracted hepatic arteries concentration-dependently, whereas it produced only weak and inconsistent contractions in portal veins. Vasopressin effectively contracted hepatic arteries, whereas it had no effect on portal veins. Both vessel types responded to prostaglandin F2 alpha with contractions, although the drug potency was relatively low (EC50 greater than 10(-5) mol l-1). Histamine and carbachol failed to induce (hepatic arteries) or caused only weak (portal veins) contractions. Microsurgical hepatic hilar denervation reduced the catecholamine content of the parenchyma to less than or equal to 25% of controls. In both portal veins and hepatic arteries, the denervation procedure increased the NA sensitivity by factors of 3.1 and 2.0, respectively. In non-denervated livers, cocaine produced a similar increase of the NA sensitivity, whereas the drug had no significant effect in vessels from denervated animals. Thus, there was a marked difference between rat portal veins and hepatic arteries in their responsiveness to several contractile agents. Furthermore, the results of the present study indicate that the adrenergic nerves in both vessel types can be adequately removed by the microsurgical denervation procedure used.

Animals↗
PubMed1967

Renal erythropoietic factor: role of ions and vasoactive agents in erythropoietin formation.

Evidence is provided for the existence of a renal erythropoietic factor, devoid of vasopressor activity, which upon interaction in vitro with normal serum yields erythropoietin. When undialyzed serum is used, erythropoietin inactivation develops in the incubation mixtures, and this inactivation appears to be dependent on an enzymatic component in preparations of the factor and on ions in serum.

Animals↗
PubMed2004

Differential effects of sodium tungstate and vanadyl sulfate on vascular responsiveness to vasoactive agents and insulin sensitivity in fructose-fed rats.

High fructose feeding induces insulin resistance, impaired glucose tolerance, and hypertension in rats and mimics most of the features of the metabolic syndrome X. The effects of a 6-week treatment with the transition metals administered in drinking water, vanadium (VOSO4.5H2O, 0.75 mg/mL) or tungsten (Na2O4W, 2 g/mL), were investigated on the reactivity to norepinephrine (NEPI) or acetylcholine (ACh) of thoracic aorta rings isolated from fructose (60%) or standard chow fed rats. Maximal effect (Emax) and pD2 (-log EC50) values were determined in each case in the presence or absence of endothelium, while the degree of insulin resistance was determined using the euglycemic hyper insulinemic glucose clamp technique. Aortic segments isolated from 6-week fructose-fed animals were characterized by NEPI hyperresponsiveness (increase in Emax) and endothelium-dependent NEPI supersensitivity (increase in pD2) without any change in the reactivity to ACh. Vanadium or tungsten administered in fructose-fed animals prevented both hypertension and NEPI hyperresponsiveness, while vanadium, but not tungsten, reduced NEPI supersensitivity. Vanadium, but not tungsten, increased the relaxing activity of ACh, both in control and fructose-fed animals. Insulin resistance associated with high fructose feeding was reversed by vanadium but not by tungsten treatment. The differential effects of the two transition metals on vascular responsiveness to NEPI or ACh may be explained by their differential effects on insulin sensitivity.

Animals↗
PubMed2003

Role of endothelium-derived relaxing factors in the renal response to vasoactive agents in hypothyroid rats.

This study analyzed the role of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) in the abnormal renal vascular reactivity of hypothyroid rats. Renal responses to vasoconstrictors [VC: phenylephrine (PHE) and ANG II] and vasodilators [VD: ACh, sodium nitroprusside (SNP), and papaverine (PV)] were studied in kidneys from control and hypothyroid rats under normal conditions and after NO or EDHF blockade. NO was blocked by the administration of Nomega-nitro-l-arginine methyl ester (l-NAME) and EDHF by the administration of tetraethylammonium (TEA) or by an increased extracellular K+. The response to VC was also evaluated after endothelium removal. Hypothyroid kidneys showed reduced responsiveness to PHE and a normal response to ANG II. l-NAME and TEA administration produced an increased sensitivity to PHE and to ANG II in control preparations. l-NAME also increased the response to PHE in hypothyroid kidneys, but the differences between control and hypothyroid kidneys were maintained. TEA administration did not change the response to either VC in hypothyroid preparations. In endothelium-removed preparations, TEA was unable to increase pressor responsiveness to VC. Hypothyroid kidneys showed reduced responsiveness to ACh and SNP and normal response to PV. The differences between hypothyroid and control preparations in the responses to ACh and SNP were maintained after l-NAME or increased K+. In conclusion, this study shows that 1) the attenuated response to PHE in hypothyroidism is not related to an increased production of endothelium-derived relaxing factors NO and EDHF; 2) the response to VC in hypothyroid preparations is insensitive to EDHF blockade; and 3) hypothyroid preparations have a reduced reactivity to the NO donor, and NO-independent vasodilatation remains unaffected.

Angiotensin II↗