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PubMed1992

Effect of AWD 52-39 on vasoconstriction induced by noradrenaline and 5-hydroxytryptamine in vitro and in vivo in rats.

The vascular effect of the potential nootropic AWD 52-39 (1; N,N-diacetoxyethyl-9,10-dihydrolysergic acid amide) as well as its influence on noradrenaline- or 5-HT-induced vasoconstriction were studied in the isolated rat aorta and in anesthetized normotensive and pithed rats. Vasoconstriction was determined by measuring the increase in mean arterial pressure (MAP). Both in vitro and in pithed rats, 1 caused a slight vasoconstriction, whereas a dose-dependent short-lasting decrease in mean arterial pressure was found in normotensive rats. In vitro and in pithed rats, 1 exerted no influence on the noradrenaline-induced vasoconstriction, while the 5-HT-induced contractile response was significantly inhibited. These findings characterize 1 as a competitive antagonist at vascular 5-HT2 receptors without any alpha-adrenolytic effect.

Animals↗
PubMed2006

[The role of subtypes of voltage-gated K+ channels in pulmonary vasoconstriction induced by 15-hydroeicosatetraenoic acid].

AIM: To observe the effect of subtypes of Kv channels in rat pulmonary artery smooth muscle cells (PASMCs) on the process of pulmonary vasoconstriction induced by 15-HETE. METHODS: In the present study, ring of rabbit PA with specific Kv channel blockers were employed to functionally identify certain channel subtypes that took part in the process of 15-HETE induced pulmonary vasoconstriction; RT-PCR and Western blotting analysis were also used to measure the expression of subtypes of Kv in PASMCs exposed to 15-HETE,chronic hypoxia. RESULTS: Blocking of Kv1. 1, Kv1. 2, Kv1. 3 and Kv1. 6 channels did not affect 15-HETE induced vasoconstriction in normoxic rats; 15-HETE did not affect expression of Kv1. 1 and Kv1. 2 channels; 15-HETE significantly downregulated the expression of mRNA and protein of Kv1. 5 and Kv2. 1 in rat PASMCs. CONCLUSION: The results suggested that hypoxia may block Kv1. 5 and Kv2. 1 channels via 15-HETE mediated mechanism, leading to decrease numbers of functional Kv1. 5 and Kv2. 1 channels in PASMCs, leading to PA vasoconstriction.

Animals↗
PubMed1990

Attenuation of endothelin-induced regional vasoconstriction by isradipine: a nonspecific antivasoconstrictor effect.

The modification of endothelin effects by the calcium antagonist isradipine was investigated by infusion of 1.0 nM/kg endothelin, a dose known to cause profound vasoconstriction, into eight anesthetized rabbits, followed by an infusion of 10 micrograms/kg isradipine or its vehicle into four rabbits each. In a second series of experiments, only isradipine (same dose) or its vehicle was infused into six rabbits each. Endothelin increased blood pressure and caused systemic vasoconstriction, marked bradycardia, and cardiodepression (measured with a strain guage), yet decreased central venous pressure. The regional vascular effects (measured with microspheres) encompassed widespread vasoconstriction (especially to the kidneys, adrenals, stomach, cecum, and heart), but also a tendency for vasodilatation (hepatic artery). Isradipine decreased blood pressure in endothelin-treated and normal animals. It increased cardiac output more in the endothelin group. The interaction between endothelin and isradipine in the peripheral circulation was generally additive. Isradipine blunts many, but not all, endothelin effects, thus resembling the antivasoconstrictor effects of calcium antagonists against a variety of vasoconstrictor agents such as angiotensin II (Ang II) or vasopressin. Similar to these, endothelin appears to cause vasoconstriction by several mechanisms, one of which apparently involves L-channel activation. A specific interaction of endothelin with the L-channel appears unlikely.

Animals↗
PubMed1990

Increased plasma level of endothelin with vasoconstriction after dextran infusion.

Our previous study demonstrated that volume expansion with dextran produced blood pressure elevation due to vasoconstriction 3 hours after the cessation of infusion. To examine whether endogenous endothelin contributes to this vasoconstriction, we measured plasma level of endothelin before, immediately after, and 3 hours after the administration of dextran. Plasma level of endothelin decreased immediately after the administration (from 1.5 +/- 0.3 pg/ml to 1.1 +/- 0.2 pg/ml, P less than 0.05), and increased 3 hours after the administration (2.1 +/- 0.3 pg/ml, P less than 0.05). However, the changes in the plasma level of endothelin did not significantly correlated with those in blood pressure or total peripheral resistance. Thus, vasoconstriction after dextran infusion was accompanied by an increase in the plasma level of endothelin, but further evaluation is needed for the direct role of this peptide in the vasoconstrictive blood pressure elevation.

Animals↗
PubMed1990

[Cellular mechanisms of pulmonary vasoconstriction in an experimental model of protamine reversal of heparin].

The neutralisation of heparin by protamine can cause life-threatening pulmonary hypertension. We studied this reaction in animal experimental models (sheep and rat) to determine the cellular mechanisms of the pulmonary vasoconstriction. The heparin-protamine reaction (H-P) with pulmonary hypertension (peak of mean pulmonary artery pressure = 57.3 +/- 2.2 mmHg), decreased cardiac output (-20%), leukopenia (-30%) and plasma release of high concentrations of thromboxane B2 (6.03 +/- 0.03 ng/ml) was constantly observed in sheep. The reaction was identical in sheep with induced thrombocytopenia by administration of antiplatelet antibodies. On the other hand, the neutralisation of heparin by protamine in rats did not cause thromboxane release or pulmonary vasoconstriction although the leukopenia was identical to that observed in sheep. Therefore, the platelets and white blood cells did not seem to cause the pulmonary vasoconstriction induced by the H-P complexes. The inter-species difference observed suggests that pulmonary intravascular macrophages may be responsible for the liberation of eicosanoids and acute pulmonary vasoconstriction occurring during the neutralisation of heparin by protamine.

Animals↗
PubMed1990

Phorbol-12,13-dibutyrate-induced vasoconstriction in vivo: characterization of response in genetic hypertension.

To assess the role of protein kinase C (PKC) in the control of vessel tone in vivo in genetic hypertension, the vascular effects of phorbol-12,13-dibutyrate (PDBu), a PKC activator, was measured in the autoperfused hindlimb of reserpinized spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). PDBu infusion (1-3000 ng/kg/min) into the hindlimb elevated perfusion pressure in a dose-related manner. Vasoconstriction response characteristics (latency, T1/2 to peak effect, decay of effect) of PDBu were significantly longer (2- to 10-fold) than that produced by membrane receptor agonists; phenylephrine, SKF 89748, a lipophilic alpha-1 agonist, angiotensin II and 5-hydroxytryptamine. The tonic vasoconstriction induced by PDBu was not antagonized by prazosin, rauwolscine, cyproheptadine, [Sar1lle8]-angiotensin II but was inhibited reversibly by microbial PKC-inhibitors, K252a and staurosporine at concentrations (1.56-2.8 micrograms/kg/min) which did not block vasoconstriction by phenylephrine or 5-hydroxytryptamine. The EC50 for PDBu was identical in SHR and WKY. However, the maximal response to PDBu was significantly greater in SHR compared to WKY. Staurosporine lowered mean arterial pressure equally in SHR (20%) and WKY (17%) but reduced perfusion pressure in SHR (13%) to a slightly greater extent than in WKY (5%). Unlike the in vivo response, aortic rings removed from SHR were more sensitive to cumulative doses of PDBu than rings from WKY. It is concluded that PDBu-vasoconstriction in vivo is mediated largely through activation of PKC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Mechanism of cyclosporin potentiation of vasoconstriction of the isolated rat mesenteric arterial bed: role of extracellular calcium.

Hypertension is a serious side-effect of the clinical use of Cyclosporin A (CsA). One notion is that alterations of vascular reactivity contribute to this hypertension. In this study we used the isolated rat mesenteric vascular bed to test the specific hypothesis that CsA modifies vascular calcium regulation to potentiate vascular contractility. Mesenteric vessels from CsA-treated rats (10 mg/kg/day i.m. for 7 days) exhibited significantly greater vasoconstrictor responses to exogenous norepinephrine (NE) and potassium-induced depolarization than those of vehicle-treated animals. Similarly, in vitro CsA (8.3 X 10(-8) to 8.3 X 10(-6) M) augmented in a concentration-dependent manner both the sensitivity and the maximum response to NE and potassium. This effect of CsA on vasoconstriction was critically dependent on the presence of external calcium [( Ca++]o). The degree of vasoconstriction potentiation correlated significantly with the [Ca++]o which was used during exposure of the mesenteric bed to CsA. Reapplication of external calcium in the presence of CsA to "calcium-depleted" preparations increased significantly the amplitude of subsequent NE responses in a calcium-free medium. Thus, CsA-potentiated NE responses, once established, were not reversed by removing external calcium; however, attenuation occurred with the intracellular calcium antagonist dantrolene. Verapamil and nifedipine blocked potassium-elicited responses, but failed to prevent the CsA effect on NE-induced vasoconstriction. We conclude that CsA potentiation of vasoconstriction depends on extracellular calcium, and results from an enhanced transmembrane calcium transport. We speculate that CsA also increases the filling of intracellular stores of releasable calcium. These effects lead to greater calcium influx and greater intracellular calcium release upon stimulation.

Animals↗
PubMed1986

Sustained coronary vasoconstriction provoked by a peptidergic substance released from endothelial cells in culture.

Recent reports have shown that cultured endothelial cells release into the culture medium a substance (or substances) that contracts isolated preparations of arterial smooth muscle [endothelial-derived constrictor factor (EDCF)]. To evaluate the coronary and cardiac effects of EDCF, isolated rabbit hearts retroperfused in a nonrecirculating system with Krebs-Henseleit solution were challenged with bolus injections (100-600 microliter) of either serum-free minimum essential medium (vehicle) or aortic endothelial cell supernates concentrated in minimum essential medium (EDCF). EDCF, but not its vehicle, produced dose-dependent coronary vasoconstriction unaccompanied by changes in left ventricular contraction or heart rate. The constrictor responses were remarkably well sustained with little or no decrement in resistance occurring over a 15-min observation period. Nitroprusside inhibited the development of and reversed on-going vasoconstriction evoked by EDCF. Neither meclofenamate nor diethylcarbamazine influenced EDCF-induced pressor responses, thereby negating a role for arachidonic acid metabolites. Coronary vasoconstriction induced by EDCF also was unaffected by blockade of alpha-adrenergic, histaminergic or serotonergic receptors. Incubation of EDCF with trypsin attenuated the pressor effects markedly, suggesting that EDCF may be a peptide. Roles for angiotensin or substance P were ruled out, however, as saralasin failed to influence EDCF-induced constriction and since substance P was inactive in the perfused rabbit heart preparation. We conclude that a substance (or substances), probably a peptide, released from cultured endothelial cells provokes sustained coronary vasoconstriction by an unknown mechanism.

Animals↗
PubMed1987

Effects of K-351 on adrenergically induced renin release and renal vasoconstriction in anesthetized dogs.

Effect of 3-4-dihydro-8-(2-hydroxy-3-isopropylaminopropoxy)-3-nitroxy-2H-1-b enzopyran (K-351) infused into the renal artery on renin release during graded renal nerve stimulation (RNS) was investigated in pentobarbital-anesthetized dogs. K-351 (20 micrograms/min) produced significant suppression of the RNS-induced renin release; the renin secretion responses to RNS at lower frequencies (0.5 and 1 Hz) were almost abolished, and those at the highest frequency (3 Hz) were attenuated. K-351 also suppressed an increase in renal vascular resistance during RNS at 3 Hz. The same extent of inhibition in the renin secretion response to RNS was also obtained during infusion of DL-propranolol (100 micrograms/min). Inhibitory effect of K-351, prazosin, or phentolamine on the renal vasoconstriction induced by RNS and norepinephrine (NE) injected into the renal artery, an approximately 50% reduction in renal blood flow, was also assessed. K-351 and prazosin exerted a greater inhibitory effect on RNS-than on NE-induced vasoconstriction, and the opposite was true of phentolamine. The potency of K-351 in reducing the vasoconstriction due to RNS or NE was roughly estimated to be 10-30 times less than that of prazosin. These results suggest that K-351 shares beta- and alpha-adrenoceptor blocking properties, which effectively contribute to the suppression of adrenergically induced renin release and renal vasoconstriction.

Animals↗
PubMed1988

Effects of arotinolol on hemodynamics and adrenergically induced renin release and renal vasoconstriction.

Effects of 5-[2-[(3-tert-butylamino-2-hydroxypropylthio)-4-thiazolyl]-2- thiophenecarboxamide hydrochloride (arotinolol, S-596) on hemodynamic and adrenergically induced renin release and renal vasoconstriction were investigated in pentobarbital anesthetized dogs. Arotinolol (1 mg/kg i.v.) decreased systemic blood pressure (SBP), heart rate (HR) and renin secretion rate without change in renal blood flow. Degree of hypotension induced by arotinolol and basal plasma renin activity prior to the injection of the drug showed significant correlation. Arotinolol (20 micrograms/min) produced significant suppression of renal nerve stimulation (RNS)-induced renin release and attenuated an increase in renal vascular resistance during RNS at 3 Hz. The same extent of inhibition in the renin secretion response to RNS was also obtained during the infusion of dl-propranolol (100 micrograms/min). The renal vasoconstriction induced by RNS and norepinephrine (NE) was inhibited dose-dependently during the infusion of arotinolol (10, 30 and 100 micrograms/min), phentolamine (3, 10 and 30 micrograms/min) or prazosin (1, 3 and 10 micrograms/min). Arotinolol and prazosin exerted a greater inhibitory effect on RNS- than NE-induced vasoconstriction, and the opposite was true of phentolamine. Arotinolol dose-dependently decreased SBP and HR in a dose range of 0.01 to 3.0 mg/kg. The greater reduction in HR was observed with arotinolol at a lower dose range (0.01 to 0.1 mg/kg) than with propranolol. Arotinolol produced larger reduction of SBP, and less increase in carotid, vertebral, renal and external iliac vascular resistances than propranolol. These results suggest that arotinolol posesses a- and beta-adrenoceptor blocking properties, which effectively contribute to the suppression of the adrenergically induced renin release and renal vasoconstriction, and to the hypotensive effect.

Adrenergic beta-Antagonists↗
PubMed1988

The beta adrenoceptor blocker tertatolol causes vasodilatation in the isolated perfused vasoconstricted rat kidney.

The activity of the beta adrenoceptor antagonist tertatolol on renal vasoconstrictions was investigated. Infusion of increasing concentrations of tertatolol (10(-8) to 10(-5) M) progressively inhibited the constrictor responses to bolus injections of norepinephrine and to electrical stimulation in isolated perfused kidneys of both normotensive and spontaneously hypertensive rats. Also, in kidneys of normotensive rats the vasoconstrictions caused by serotonin and barium chloride were inhibited by tertatolol. During sustained vasoconstrictions induced by infusion of norepinephrine (6 X 10(-7) M) increasing doses of tertatolol (2.5 X 10(-7) g to 2 X 10(-5) g) caused rapid, reversible dilatations in the rat kidneys. The inhibitory responses caused by tertatolol were not antagonized by propranolol, atropine, hexamethonium, SCH23390, metoclopramide, mepyramine, cimetidine, naloxone, cocaine or indomethacin. During constrictions caused by norepinephrine, methylene blue significantly inhibited the renal vasodilatations caused by tertatolol, acetylcholine, papaverine and nitroglycerin but not those caused by atrial natriuretic factor. Unlike the other vasodilators, tertatolol did not inhibit the constrictions induced by prostaglandin F2 alpha (5 X 10(-6) M) in the rat kidneys. In canine renal arteries with endothelium, tertatolol (10(-9) to 10(-5) M) did not cause relaxations during contractions induced by norepinephrine, electrical stimulation or prostaglandin F2 alpha. Our data illustrate that tertatolol has potent vasodilator properties in the isolated perfused vasoconstricted rat kidney. The dilator response to the beta blocker cannot be inhibited by a variety of classical receptor blockers but ultimately seems to depend on the formation of cyclic GMP.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Effects of diethylcarbamazine and cromolyn sodium on hypoxic pulmonary vasoconstriction in dogs.

Evidence has recently been accumulated that leukotrienes might be involved in the still unknown biochemical mechanism of hypoxic pulmonary vasoconstriction. We therefore investigated the effects of i.v. cromolyn sodium, which prevents the release of leukotrienes from mast cells by a membrane stabilizing effect, and of i.v. diethylcarbamazine citrate (DEC), a leukotriene synthesis inhibitor, in 13 dogs challenged with the inhalation of 10% O2 in nitrogen (FIO2 0.1) during 10 min. The dogs were anaesthetized with pentobarbital, paralysed with pancuronium, ventilated with a FIO2 of 0.4 and equipped with catheters for the purpose of pulmonary and systemic vascular pressure measurements and thermodilution cardiac output determinations. Thirty minute infusions of DEC at respectively 100 mg, 400 mg, 2 g, 5 g, 10 g and 15 g (one dosage per dog) did not alter the hypoxic pulmonary pressor response. Dosages of 10 g and 15 g DEC were associated with systemic hypotension, and one additional dog given 20 g died in refractory shock. A continuous infusion of cromolyn sodium inhibited hypoxic pulmonary vasoconstriction, partially at 3 and 4.5 mg X kg-1 X min-1 (2 dogs) and completely at 6 mg X kg-1 X min-1 (3 dogs). A lower dosage of 1 mg X kg-1 X min-1 cromolyn sodium (one dog) had no circulatory effect. These results do not support the hypothesis that hypoxic pulmonary vasoconstriction is mediated by vasoconstricting leukotrienes in the dog. The mechanisms accounting for the inhibition of the pulmonary hypoxic pressor response by cromolyn sodium are uncertain.

Animals↗
PubMed1986

Hydrogen peroxide induced pulmonary vasoconstriction in isolated rat lungs is attenuated by U60,257, a leucotriene synthesis blocker.

Reactive oxygen metabolites cause pulmonary vasoconstriction and activate arachidonic acid metabolism. We proposed that hydrogen peroxide, generated enzymatically in an insolated rat lung model, would cause vasoconstriction which was independent of circulating cells, but dependent on activation of the arachidonic acid cascade. Although hydrogen peroxide caused an increase in lung effluent thromboxane B2 concentration, indomethacin did not inhibit hydrogen peroxide induced vasoconstriction. In order to test the hypothesis that hydrogen peroxide activates the 5-lipoxygenase pathway, lung effluents were analyzed for 5-hydroxy-eicosatetranoic acid (5-HETE) using a sensitive, highly specific mass spectrometer technique. Glucose oxidase increased the 5-HEFE effluent concentrations and this was prevented by U60,257. We therefore conclude that hydrogen peroxide stimulates the 5-lipoxygenase pathway and that substances derived from this pathway are at least in part responsible for the hydrogen peroxide induced vasoconstriction in isolated rat lungs.

Animals↗
PubMed1987

Stimulation of glycogenolysis and vasoconstriction in the perfused rat liver by the thromboxane A2 analogue U-46619.

Infusion of the thromboxane A2 analogue U-46619 into isolated perfused rat livers resulted in dose-dependent increases in glucose output and portal vein pressure, indicative of constriction of the hepatic vasculature. At low concentrations, e.g. less than or equal to 42 ng/ml, glucose output occurred only during agonist infusion; whereas at concentrations greater than or equal to 63 ng/ml, a peak of glucose output also was observed upon termination of agonist infusion coincident with relief of hepatic vasoconstriction. Effluent perfusate lactate/pyruvate and beta-hydroxybutyrate/acetoacetate ratios increased significantly in response to U-46619 infusion. Hepatic oxygen consumption increased at low U-46619 concentrations (less than or equal to 20 ng/ml) and became biphasic with a transient spike of increased consumption followed by a prolonged decrease in consumption at higher concentrations. Increased glucose output in response to 42 ng/ml U-46619 was associated with a rapid activation of glycogen phosphorylase, slight increases in tissue ADP levels, and no increase in cAMP. At 1000 ng/ml, U-46619 activation of glycogen phosphorylase was accompanied by significant increases in tissue levels of AMP and ADP, decreases in ATP, and slight increases in cAMP. In isolated hepatocytes, U-46619 did not stimulate glucose output or activate glycogen phosphorylase. Reducing the perfusate calcium concentration from 1.25 to 0.05 mM resulted in a marked reduction of the glycogenolytic response to U-46619 (42 ng/ml) with no efflux of calcium from the liver. U-46619-induced glucose output and vasoconstriction displayed a similar dose dependence upon the perfusate calcium concentration. Thus, U-46619 exerts a potent agonist effect on glycogenolysis and vasoconstriction in the perfused rat liver. The present findings support the concept that U-46619 stimulates hepatic glycogenolysis indirectly via vasoconstriction-induced hypoxia within the liver.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1985

Particle-induced coronary vasoconstriction during cardioplegic infusion. Characterization and possible mechanisms.

We have characterized an isolated rat heart preparation in which particles induce transient coronary vasoconstriction. Exploiting the fact that all commercially available intravenous solutions contain permissible levels of contaminant particles (usually 2 to 20 micron in diameter), we investigated whether these particles have any adverse effect upon coronary flow. A commercially available intravenous solution was modified to produce the St. Thomas' Hospital cardioplegic solution. Constant-pressure infusion of this solution over a 20 minute period caused a 46.2% +/- 5.1% reduction in coronary flow. This flow impairment could be limited to 13.3% +/- 3.5% by the incorporation of a 0.8 micron in-line filter. In hearts perfused with particle-containing solution followed by ultrafiltered solutions, the impairment of coronary flow was reversed within 1 minute. This quick reversal indicates that the particles were impairing flow not by physical occlusion of vessels but by triggering some form of transient vasoconstriction. In studies with filters of varying porosity (between 0.8 and 15.0 micron), the phenomenon was shown to be attributable to relatively small numbers of particles greater than 10.0 micron in diameter. In studies of myocardial protection, it was shown that the impairment of solution delivery and distribution caused by particles could severely reduce the protective properties of a chemical cardioplegic solution; hearts subjected to 180 minutes of hypothermic (20 degrees C) ischemic arrest with multidose (3 minutes every 30 minutes) cardioplegia recovered almost completely upon reperfusion if a filtered (0.8 micron) solution was used, but failed to recover when unfiltered, commercially prepared solutions were used. In an attempt to define the mechanisms underlying the particle-induced vasoconstriction, we conducted dose-response studies in which various vasoactive agents were used in an attempt to combat the effects of the particles. At their optimal concentrations, procaine (10.0 mmol/L), nifedipine (0.1 mumol/L), and adenosine triphosphate (1.0 mmol/L) completely prevented the problem; lidocaine and dipyridamole partially alleviated the effect; verapamil and isosorbide dinitrate were ineffective. These results indicate that several mechanisms acting at a small vessel level might contribute to the particle-induced vasoconstriction.

Adenosine Triphosphate↗
PubMed1984

Renal alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in dogs.

Clonidine (C) and guanabenz (G) are both alpha 2-agonists. Whereas C has been reported to cause anti-natriuresis proportional to renal vasoconstriction with acute infusion, G increases sodium and water excretion with little change in renal blood flow (RBF). C-mediated vasoconstriction may involve alpha 1-receptors. RBF in anaesthetized dogs was measured electromagnetically. Boluses of phenylephrine (P), C and G were injected into the renal artery via a perfusion cannula. Responses were expressed as delta RBF. Then prazosin or yohimbine were administered intra-arterially and dose-response curves repeated. The shift in dose ratio (delta ED50 after prazosin/yohimbine) for P was 52.9, for C was 4.7 and for G was 0.62. G was a 10-fold weaker vasoconstrictor than C, but G was still effective when alpha 1-receptors were blocked. Ten-fold differences were found between P, C and G for dependence upon alpha 1-adrenoceptors. Denervation did not significantly shift the curves. Thus, postsynaptic alpha 2-receptors can contribute to renal vasoconstriction, but the receptors are either less numerous or less efficiently coupled to contractile elements than in other beds. Verapamil markedly attenuated responses to C and G. Since tubular alpha 1-receptors have also been implicated in sodium transport, C may be more prone than G to cause anti-natriuresis both through stimulated tubular reabsorption and renal vasoconstriction.

Animals↗
PubMed1982

Calcium antagonists and alpha 2-adrenoceptors: possible role of extracellular calcium ions in alpha 2-adrenoceptor-mediated vasoconstriction.

A survey concerning the influence of calcium antagonists on the vasoconstriction induced by the selective stimulation of either postsynaptic alpha 1- or alpha 2-adrenoceptors in the resistance vessels of pithed rats and cats, as well as in ganglion-blocked rabbits, is presented. In every species studied, all calcium antagonists (organic: verapamil, D 600, diltiazem, nifedipine, nisoldipine, and a variety of new compounds; inorganic: Co2+, Ni2+, and Mn2+) significantly reduced the pressor response towards the stimulation of postsynaptic vascular alpha 2-adrenoceptors with B-HT 920 (and other agonists). However, the various calcium antagonists showed little influence on the vasoconstriction provoked by the excitation of vascular postsynaptic alpha 1-adrenoceptors. A correlation study revealed that there exists a close correlation between the depressant influence of the calcium-antagonistic drugs on the vasoconstriction due to alpha 2-adrenoceptor stimulation and the calcium-antagonistic potency in vitro. Accordingly, it is speculated that the vasoconstriction due to alpha 2-receptor stimulation requires the influx of calcium ions from the extracellular space across the membrane. This process is obviously sensitive to the influence of calcium-antagonistic drugs.

Animals↗
PubMed1984

Effect of verapamil on renal vasoconstriction induced by angiotensin II, norepinephrine or renal nerve stimulation in anesthetized dogs.

The effect of verapamil on the decrease in renal blood flow (RBF) induced by angiotensin II (Ang II), norepinephrine (NE) or renal nerve stimulation (RNS) was examined in pentobarbital-anesthetized dogs. The injection into the renal artery of Ang II (0.01-0.1 micrograms), or NE (0.1-1.0 micrograms), or RNS (1-10 Hz) decreased RBF in a dose- or frequency-dependent manner. The renal arterial infusion of verapamil (30 micrograms/min followed by 100 micrograms/min) brought about a sustained increase in RBF and inhibition of renal vasoconstriction induced by Ang II or NE, but not by RNS, when the extent of vasoconstriction was estimated in terms of absolute changes in RBF. We also observed that the inhibitory effect of verapamil on Ang II-induced vasoconstriction was greater than on NE-induced constriction, as estimated from the % change in RBF. These results indicate that in canine renal vasculature, verapamil exerts different inhibitory effects on the vasoconstriction induced by Ang II, NE or RNS.

Anesthesia↗