On the modification of the acute lethality in mice following whole body x-irradiation by several vasoconstrictor agents.
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Animals↗
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Role of endothelium and nitric oxide in the in vitro response of equine colonic venous rings to vasoconstrictor agents.
OBJECTIVE: To determine in vitro contractile responses of equine colonic veins to various vasoconstrictor agents. ANIMALS: Colonic veins collected from 8 adult horses. PROCEDURE: Veins were cut into 4-mm-wide rings, placed in organ baths at 37 C, and attached to a force-transducer interfaced with a polygraph; 2 g of tension was applied, and rings were allowed to equilibrate for 45 minutes. Bath solution was replaced, and tension was reapplied at 15-minute intervals. Cumulative concentration responses (10(-8) to 10(-4) M) were determined for each agent, using separate rings (n = 8). Three vein groups were evaluated: endothelium-intact, endothelium-denuded, and N omega-nitro-L-arginine methyl ester (L-NAME, 10(-5) M)-treated. Maximal responses by each vein to each agent were considered 100%; responses to lower concentrations were calculated as percentage of maximum. RESULTS: Considering all vein groups, comparison of the doses that caused 50% of the maximal contraction revealed relative sensitivity of colonic veins to be: angiotensin II (ANG) > thromboxane B2 analogue (TXB) > 5-hydoxytryptamine (5HT) > norepinephrine (NE) > histamine (HST) > prostaglandin F2 alpha (PGF) > vasopressin (VP). Compared with ANG, PGF, TXB, and VP, treatment with HST, 5HT, and NE evoked significantly greater responses. Endothelium-denuded and L-NAME-treated colonic veins had significantly greater maximal contractile responses than did endothelium-intact veins. CONCLUSIONS: Response of colonic veins to vasoconstrictor agents was differential; sensitivity was not altered by endothelium removal or L-NAME treatment; maximal responses of endothelium-intact veins were greater than those of endothelium-denuded and L-NAME-treated veins; and responses of endothelium-denuded and L-NAME-treated veins were not different. CLINICAL RELEVANCE: Alterations in colonic veins that mimic conditions associated with large-colon volvulus may contribute to blood flow alterations, edema formation, and vascular responses to hypovolemic and endotoxic shock.
Analysis of Variance↗
Contribution of prostaglandins to the renal vascular supersensitivity to vasoconstrictor agents exhibited by New Zealand genetic hypertensive rats.
1. Studies were made of the effects on responses to vasoconstrictor agents of prostaglandins released from Krebs perfused isolated kidneys of genetic hypertensive and normotensive rats. 2. Prostaglandin E-like activity, detected by bioassay, was released from kidneys of both groups of rats during the vasoconstriction produced by noradrenaline, angiotensin or prostaglandin F2alpha. 3. In preparations obtained from hypertensive rats, responses to higher doses of noradrenaline or angiotensin were initially greater than those from normotensive rats and these were then reduced to a greater extent by infusion of indomethacin, which abolished release of prostaglandin E-like activity. Thereafter, in kidneys of either group, vasoconstriction to noradrenaline was potentiated by infusion of prostaglandin E2. 4. We conclude that, in rats, renal prostaglandins released in response to vasoconstrictor agents could augment the effect of such agents and in genetic hypertensive rats release of renal prostaglandins could contribute to the disease.
Animals↗
Chloride anion concentration as a determinant of renal vascular responsiveness to vasoconstrictor agents.
1. The role of chloride concentration in modulating vasoconstrictor responses of the rat isolated kidney, perfused with Krebs-Henseleit solution, to angiotensin II (AII), arginine vasopressin (AVP) and phenylephrine (PE) was investigated. 2. Reduction of perfusate chloride from a high (117 mM) to low (87 mM) concentration, by substitution of sodium chloride with a mixture of sodium salts of propionate, acetate and methanesulphonate, reduced responsiveness to all three vasoconstrictors, the change for AII being most pronounced. 3. For AII, reduced vasoactivity with low chloride was evident both in terms of the threshold dose and on the linear part of the dose-response curve but not for the maximum response. This attenuating effect of low chloride on the vasoconstrictor response to AII was reversed when perfusion with high chloride was reinstituted. Continuous perfusion with high chloride progressively increased the vasoconstrictor effect of low doses of AII for successive dose-response curves. 4. In addition to reducing responses on the linear part of the dose-response curve for both AVP and PE, low chloride also reduced the maximum vasoconstrictor response to PE, whereas the threshold dose for the two agonists was unchanged. In contrast to the enhanced pressor response to AII, during continuous perfusion with high chloride, tachyphylaxis occurred with AVP and PE. 5. The ability of chloride to modify renal responsiveness to vasoconstrictor agents may contribute to the increase in renal vascular resistance and decrease in glomerular filtration rate (GFR) which occurs during infusion of hyperchloremic solutions into the renal artery and explain the need for chloride as the anion accompanying sodium in salt-sensitive hypertensive models.
Angiotensin II↗
Regional differences in the response to vasoconstrictor agents of dog and monkey isolated coronary arteries.
Contractile responses to vasoconstrictor agents were compared in helical strips of dog and monkey epicardial coronary arteries of different sizes. Contractions of large, medium and small arteries induced by KCl ( 30mM ) were virtually identical. Contractions induced by 5-hydroxytryptamine (5-HT) (10(-9) - 2 X 10(-6) M) were in the order of large greater than medium greater than small arteries in dogs, and large = medium greater than small arteries in monkeys. Cinanserin suppressed these responses. In contrast, contractions produced by angiotensin II (AII) (10(-7) M) were in the order of small greater than medium greater than large arteries in dogs, and small greater than medium = large arteries in monkeys. Sar1-Ala8-angiotensin II markedly attenuated the peptide-induced contractions. Contractions induced by prostaglandin F2 alpha (PGF2 alpha) were significantly greater in large and medium sized arteries than in small arteries in dogs, while those of the arteries of different sizes isolated from monkeys did not differ. Contractions induced by carbocyclic thromboxane A2 (c-TXA2), in arteries of different sizes in dogs and monkeys, did not differ. These results suggest that the sensitivity and/or the population of 5-HT receptors are greater in proximal coronary arteries than in distal arteries, while, in contrast, the sensitivity and/or population of AII receptors are greater in distal coronary arteries. Receptors for PGF2 alpha and c-TXA2 appear to react to a similar degree in monkey arteries of different sizes, although receptors for PGF2 alpha appear to be fewer in distal coronary arteries in dogs.
Angiotensin II↗
Regional autoregulatory responses during infusion of vasoconstrictor agents in conscious dogs.
We investigated pressure-dependent autoregulatory responses in mesenteric, iliac, and renal vascular beds of conscious dogs during intravenous infusion of angiotensin II, phenylephrine, or arginine vasopressin at rates which increased arterial pressure by 20-40 mmHg. The arteries supplying these beds were instrumented with an electromagnetic flow probe, a nonoccluding catheter, and an electromagnetic flow probe, a nonoccluding catheter, and an occluder cuff connected with a servo-amplifier, which enabled us to return perfusion pressure to control levels during infusion of the vasoconstrictor agents. We attempted to differentiate between the increase in vascular resistance due to the direct effect of the vasoconstrictor agent and the increase induced by an autoregulatory response induced by elevations of aortic perfusion pressure. We measured a strong degree of autoregulation in the renal vascular bed with a fractional compensation value close to 1. Moderate autoregulation occurred in the mesenteric vascular bed, where the compensation was 0.4-0.5 with angiotensin II and phenylephrine and between 0.74 and 0.94 with vasopressin. No autoregulatory capacity could be demonstrated in the hindlimb. The findings indicate that, under conditions of increased systemic blood pressure, both the renal and the mesenteric vascular beds contribute to the increase in total peripheral resistance by pressure-dependent vasoconstrictor responses.
Angiotensin II↗
Medical management of purulent rhinitis. A double-blind comparison of vasoconstrictor agent alone with a combination of vasoconstrictor and antimicrobial drugs.
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Child↗
Vascular reactivity to various vasoconstrictor agents and endothelium-dependent relaxations of rat thoracic aorta in the long-term period of pinealectomy.
In this study, the effects of reduced melatonin concentrations in the long-term period of pinealectomy on mean arterial blood pressure (BP) and vascular responses in isolated rat thoracic aorta were investigated. Rats were pinealectomized (Px) two months before the beginning of the studies. Rings of endothelium-intact and -denuded rat arteries were mounted in isolated tissue baths for the measurements of isometric contractile force. No significant difference was determined between the arterial BP of Px (88.1 +/- 1.9 mmHg) and control (83.8 +/- 1.2 mmHg) rats. All arteries isolated from control and Px rats showed essentially identical contractions in response to phenylephrine, serotonin, calcium, clonidine, vasopressin, and angiotensin-II. Only endothelin-1 (ET-1)-induced contractions in the endothelium-denuded vessels isolated from Px rats were found to be increased to some extent. Pinealectomy did not affect acetylcholine or sodium nitroprusside-induced relaxation in the rat aorta either. These data suggest that reduced melatonin levels two months after pinealectomy did not modify either the vascular reactivity to various vasoconstrictor agents except the partially increased contractile responses to ET-1 in the endothelium-denuded thoracic aortas of Px rats or the endothelium-dependent and -independent relaxations in rat thoracic aorta. Restoration of the increased vascular responses to some vasoconstrictor agents, which were reported previously, may be the reason of why the hypertension is temporary following pinealectomy.
Acetylcholine↗
Amplification by serotonin of responses to other vasoconstrictor agents in the rat tail artery.
1. A low concentration of serotonin (3 nmol/L), which did not exert a direct vasoconstrictor action, amplified the responses to certain other vasoconstrictor agents (alpha 1-adrenoceptor agonists, KCl, ATP and vasopressin) in isolated perfused segments of the rat tail artery. 2. Low concentrations of serotonin (0.3 and 1 nmol/L) amplified vasoconstrictor responses to sympathetic nerve stimulation, but higher concentrations of serotonin (10 and 30 nmol/L) produced vasoconstriction and reduced responses to sympathetic nerve stimulation. 3. The calcium channel blocking drug diltiazem (1 and 10 mumol/L) produced concentration-dependent reductions of vasoconstrictor responses to phenylephrine. The amplifying effect of serotonin on responses to phenylephrine was attenuated by 1 mumol/L and abolished by 10 mumol/L diltiazem, and was also abolished in a Ca2+-free medium. 4. Ketanserin (10 nmol/L) antagonized the vasoconstrictor action of serotonin and, to a lesser extent, the vasoconstrictor actions of phenylephrine and noradrenaline. It abolished the amplifying effect of a low concentration of serotonin on responses to noradrenaline and phenylephrine. 5. The amplification of vasoconstrictor response in the rat tail artery by serotonin appears to be due to activation of receptors of the 5-HT2 subtype which are coupled to an increase in Ca2+ influx into the vascular smooth muscle cells.
Animals↗
The role of nitric oxide in the responses of equine digital veins to vasodilator and vasoconstrictor agents.
Isolated equine digital veins were examined in vitro to study the importance of the endothelium in the responses to both vasodilator and vasoconstrictor agents and to characterise the endothelial-derived mediators involved. Carbachol (Cch; 1 microM) and bradykinin (Bk; 1 nM) caused relaxation of U44069-induced tone by 79.5 +/- 0.35% and 73.7 +/- 4.0% respectively. Mechanical removal of the endothelium completely prevented relaxant responses to Cch and to Bk showing they were mediated by the endothelium. Treatment of veins with NG-nitro-L-arginine methyl ester (L-NAME; 30 and 300 microM) inhibited vasorelaxant responses to both Cch and Bk whereas the cyclooxygenase inhibitor, ibuprofen (10 microM) had no inhibitory effect. The inhibitory action of L-NAME on the relaxations produced by Cch was partly reversed by L-arginine (3 and 10 mM). Cch-relaxations were potentiated in the presence of super oxide dismutase (15 units/ml) and inhibited by methylene blue (10 microM). The vasorelaxant effects of ATP (0.01 microM to 0.1 mM) were not dependent on the presence of the endothelium and the selective P2y receptor agonist, 2-methylthio-ATP proved to be ineffective as a vasodilator. Removal of the endothelium did not enhance the vasoconstrictor effects of the alpha 1 adrenoceptor agonist phenylephrine (0.01 microM to 0.1 mM) and treatment with L-NAME (300 microM) did not change the vasoconstrictor responses to 5-HT (1 nM to 10 microM) or the alpha 2 adrenoceptor agonist BHT-920 (1 nM to 1 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗
Influence of inhibition of endothelium-derived nitric oxide formation to effects of vasoconstrictor agents neuropeptide Y, clonidine, and ergonovine on coronary vascular resistance.
To determine whether inhibition of endothelium-derived nitric oxide (EDNO) synthesis enhances the effects of exogenous vasoconstrictor agents on the coronary vasculature, we examined the effects of neuropeptide Y (NPY), clonidine, and ergonovine on coronary vascular resistance (CVR) with and without EDNO inhibitor and compared the results. In 15 anesthetized mongrel dogs, the left circumflex coronary artery (LCX) was perfused with arterial blood from the left common carotid artery through an extracorporeal bypass tube and LCX blood flow was measured with an electromagnetic flowmeter. Nine of the dogs were pretreated with intracoronary NG-nitro-L-arginine methyl ester (L-NAME 300 microM in LCX blood) (L-NAME group) and the other 6 were treated with normal saline (vehicle group). Three doses of NPY (4.3, 43, 430 ng/kg), two doses of clonidine (30 and 300 ng/kg), and one dose of ergonovine (20 micrograms/kg) were infused into LCX. NPY decreased LCX flow and increased CVR dose dependently in both groups, and there was no significant difference in the dose-response relation between the two groups. Clonidine decreased LCX flow and increased CVR in both groups, and there was no difference in the effect between the groups. In contrast, ergonovine decreased LCX flow and increased CVR to a greater degree in the L-NAME group than in the vehicle group (p < 0.01). Thus, inhibition of EDNO synthesis by L-NAME did not result in enhancement of the vasoconstrictor effects of NPY and clonidine, whereas it significantly enhanced the effect of ergonovine, possibly through inhibition of ergonovine-induced EDNO release.
Animals↗
Enhanced vascular reactivity to various vasoconstrictor agents following pinealectomy in the rat: role of melatonin.
The mesenteric vascular bed preparation of control and pinealectomized (PX) male Wistar rats was used to examine vascular reactivity to two concentrations each of norepinephrine, serotonin, angiotensin, and potassium. Vasoconstrictor responses to 50- and 100-ng injections of norepinephrine and 0.5- and 1.0-microgram injections of serotonin were 30-40% higher in preparations from PX rats. Reponses to 100 ng but not to 50 ng of angiotensin were also significantly higher in preparations from PX rats. Responses to 1.5- and to 3.0-mg injections of potassium did not differ significantly in either case. In vivo injection of 20 microgram of melatonin 3 h prior to dissection of the preparation, or in vivo perfusion of 20 ng melatonin per millilitre of buffer completely reversed the increased vascular response to all vasoconstrictor agents tested in the PX preparations, but had little effect in control preparations. Also observed in PX rats was a significant increase in blood pressure, serum sodium, and increased body and heart weight. Arterial wall sodium was also elevated in PX rats. These changes may be relevant to the increased vascular reactivity of PX rats. The increased vascular responsiveness of PX rats may be specific for agents that stimulate calcium release from intracellular stores (norepinephrine, angiotensin) rather than those that stimulate calcium influx from extracellular fluid (potassium). Melatonin lack may be the cause of the vascular changes in the PX rats as both in vivo and in vitro it lowered the vasoconstrictor effects of the agents tested, but only in PX rats; it had no significant effect in the control rats.
Angiotensin II↗
Effects of alpha,beta-methylene ATP on resistance and capacitance blood vessels of the cat intestinal circulation; a comparison with other vasoconstrictor agents and sympathetic nerve stimulation.
The autoperfused intestinal circulation of pentobarbitone anaesthetized cats was used to study the effects of alpha,beta-methylene ATP (1-100 micrograms i.a.) on pre-capillary resistance vessels and post-capillary capacitance (venous) blood vessels in comparison with other vasoconstrictor agents (also given i.a.) and the effects of sympathetic nerve stimulation (0.25-16 Hz). All cats were treated with atropine and propranolol. alpha,beta-Methylene ATP, noradrenaline and sympathetic nerve stimulation all caused dose- or frequency-dependent constriction of both resistance and capacitance vessels. alpha,beta-Methylene ATP was particularly active on capacitance vessels causing a greater constriction than either noradrenaline or sympathetic nerve stimulation. In comparison, angiotensin II and vasopressin caused a selective constriction of resistance vessels and prostaglandin F2 alpha a selective constriction of capacitance vessels. The results demonstrate that functional P2x purinoceptors are present on both arterial and venous blood vessels of the cat intestinal circulation.
Adenosine Triphosphate↗
Inhibition of the adrenalectomy-induced increase in plasma renin concentration by vasoconstrictor agents in rats.
Plasma renin concentrations in rats increase after bilateral adrenalectomy without sodium substitution. The effects of i.v. infused (asp1-beta-amid, val5)-angiotensin II (1 mug/kg min), felypressin (phen2, lys8-vasopressin) (40 mU/kg min) and phenylephrine (30 mug/kg min) were investigated on the increase in plasma renin concentration. These effects of the agents were compared with their actions on blood pressure, heart rate and renal hemodynamics. In rats with destroyed macula densa cells the effect of bilateral adrenalectomy without sodium substitution was also studied. Adrenalectomy still increased the plasma renin concentration. Angiotensin II and felypressin, also depressed under these conditions the elevation of plasma renin concentration caused by adrenalectomy. The mechanism of the adrenalectomy-induced renin release and its suppression by vasoconstrictor agents is discussed.
Adrenalectomy↗
Amplifying effects of several vasoconstrictor agents of alpha 1-adrenoceptor-mediated contraction of isolated thoracic aortae of the guinea pig.
In guinea-pig aorta phenylephrine and noradrenaline induced concentration-dependent contractions when beta-adrenoceptors were blocked. The contractile response to phenylephrine was amplified by previous application of subthreshold concentrations of 5-hydroxytryptamine, ouabain, B-HT 920, Bay K 8644, phorbol-12-myristate-13-acetate and arachidonic acid. Bay K 8644 also enhanced the contractile response to noradrenaline. The amplification was not substantially altered by removing the endothelium of the aorta. The increase in cytosolic calcium availability induced by the vasoconstrictor agents investigated may be responsible for the enhancement of the alpha 1-adrenoceptor-mediated contractions.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
[New evaluation of vasoconstrictor agents with local anesthetics].
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Anesthetics, Local↗
Potentiation of responses to sympathetic nerve stimulation and vasoconstrictor agents by SK&F 103829 in the feline mesenteric circulation.
1. The amplification of vasoconstrictor effects of several agonists and sympathetic nerve stimulation, caused by 5-HT2 receptor activation, was studied in the autoperfused mesenteric circulation of anaesthetized cats. To produce long lasting and selective 5-HT2 receptor stimulation we used SK&F 103829 (2,3,4,5 tetrahydro-8[methyl-sulphonyl]-1H3-benzazepin-7-ol methensulphonate). We assessed that SK&F 103829 was a strong contractile partial agonist in isolated preparations of rat tail artery and calf pulmonary artery. 2. The intrinsic activity of SK&F 103829 with respect to 5-hydroxytryptamine (5-HT) was 0.8 in rat tail artery and 0.6 in calf pulmonary artery. SK&F 103829-induced contractile responses were surmountably antagonized by ketanserin with a potency expected from its affinity for 5-HT2 receptors. SK&F 103829 surmountably antagonized the effects of 5-HT in rat tail artery with a pKp of 5.8. 3. Concentrations of SK&F 103829 causing greater than threshold constrictions enhanced vasoconstrictor responses of sympathetic nerve stimulation, noradrenaline, angiotensin II, methoxamine and alpha, beta-methylene ATP in the mesenteric arterial bed. Increases in mesenteric arterial pressure by noradrenaline, observed in the presence of prazosin, were also potentiated by SK&F 103829. 4. Ketanserin prevented both the constrictor effect of SK&F 103829 and the SK&F 103829-evoked potentiation of the responses to noradrenaline and angiotensin II in the mesenteric arterial bed. Ketanserin, however, failed to abolish (once established) the SK&F 103829-evoked potentiation of the constrictor effects caused by both noradrenaline and angiotensin II. 5. Short lasting constrictor effects of 5-HT were reversed to dilator effects by SK&F 103829 in both the mesenteric arterial and venous bed, thereby revealing the existence of vasodilator 5-HT receptors.6. The main finding is consistent with a sensitization of the mesenteric arterial bed to vasoconstrictor responses mediated through alpha 1- and alpha2-adrenoceptors, angiotensin II receptors and purinoceptors by SK&F 103829-evoked activation of 5-HT2 receptors. This property, together with the direct constrictor effect of the mesenteric arterial bed suggest that SK&F 103829 can reduce portal venous flow thereby being a useful therapeutic principle for the treatment of portal hypertension.
Animals↗
TERMINATION OF MIGRAINE HEADACHE BY A NEW ANTI-INFLAMMATORY VASOCONSTRICTOR AGENT.
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Analgesics↗