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M Pfaffendorf

Publications and source records attributed to M Pfaffendorf.

At least 37 records · Page 2Linked to original sources

Probing the selectivity of allosteric modulators of muscarinic receptors at other G-protein-coupled receptors.

1. The aim of the present investigation was to analyse whether three prototype allosteric modulators of ligand binding to muscarinic receptors, i.e. alcuronium, gallamine, and the alkane-bis-ammonium compound W84 (hexane-1,6-bis[dimethyl-3'-phthalimidopropylammonium bromide]), may have allosteric effects on radioligand-binding characteristics at other G-protein-coupled receptors, such as cerebral A1 adenosine receptors (Gi-coupled), cardiac left ventricular alpha1-adrenoceptors (Gq), and beta-adrenoceptors (Gs). 2. The modulators were applied at concentrations known to be high with regard to the allosteric delay of the dissociation of the antagonist [3H]-N-methylscopolamine (NMS) from muscarinic M2-receptors: 30 micromol l(-1) W84, 30 micromol l(-1) alcuronium, 1000 micromol l(-1) gallamine. As radioligands, we used the adenosine A1-receptor ligand [3H]-cyclopentyl-dipropylxanthine (CPX), the alpha1-adrenoceptor ligand [3H]-prazosin (PRAZ), and the beta-adrenoceptor ligand (-)-[125I]-iodocyanopindolol (ICYP). Allosteric actions on ligand dissociation and the equilibrium binding were measured in the membrane fractions of rat whole forebrain (CPX) and of rat cardiac left ventricle (PRAZ, ICYP, NMS), respectively. 3. CPX and PRAZ showed a monophasic dissociation with half-lives of 5.88+/-0.15 and 12.27+/-0.46 min, respectively. In the case of CPX, neither the binding at equilibrium nor the dissociation characteristics were influenced by the allosteric agents. With PRAZ, the binding at equilibrium remained almost unaltered in the presence of W84, whereas it was reduced to 36+/-2% of the control value with alcuronium and to 42+/-2% with gallamine. The dissociation of PRAZ was not affected by W84, whereas it was moderately accelerated by alcuronium and gallamine. In the case of ICYP, the binding at equilibrium was not affected by the allosteric modulators. The dissociation of ICYP was slow, and after 3 h, more than 50% of the radioligand was still bound, so that a reliable half-life could not be calculated. ICYP dissociation was not affected by W84. In the presence of alcuronium and gallamine, the dissociation curve of ICYP revealed an initial drop from the starting level, followed by the major phase of dissociation being parallel to the control curve. 4. In summary, the allosteric action of the applied agents is not a common feature of G-protein-coupled receptors and appears to be specific for muscarinic receptors.

Adrenergic alpha-Antagonists↗

Evidence for a sympatholytic effect of mibefradil in the pithed rat preparation.

OBJECTIVE: The T-type prevalent calcium channel blocker mibefradil (MIB) was shown to possess N-type calcium channel blocking properties. As this particular type of calcium channel is known to be crucially involved in the neuronal release of noradrenaline, we have investigated whether MIB could be a sympatholytic drug. METHODS: To evaluate the sympathoinhibitory action, the effects of 3 and 10 micromol/kg MIB on the tachycardic effect of electrical stimulation of the preganglionic cardioaccelerator nerves in the pithed rat were investigated. The effect of MIB on the dose-response curve of externally applied noradrenaline was also studied. To compare the results with a classic L-type calcium channel blocker, the experiments were repeated with 3 and 10 micromol/kg verapamil (VER). RESULTS: The maximal increase in heart rate in response to electrical nerve stimulation was 96 +/- 7 bpm (control, n = 6), 70 +/- 6 bpm (3 micromol/kg MIB, n = 8), 57 +/- 6 bpm (10 micromol/kg MIB, n = 5), 93 +/- 5 bpm (3 micromol/kg VER, n = 6) and 46 +/- 7 bpm (10 micromol/kg VER, n = 5). The tachycardic response to electrical stimulation at 1, 5 and 10 Hz was completely blocked by 5 mg/kg intravenous guanethidine. The maximal increase in heart rate in response to noradrenaline was 96 +/- 4 bpm (control, n = 6), 103 +/- 6 (3 micromol/kg MIB, n = 6), 42 +/- 9 bpm (10 micromol/kg MIB, n = 5), 73 +/- 5 bpm (3 micromol/kg VER, n = 5) and 40 +/- 7 bpm (10 micromol/kg VER, n = 6). Under control conditions and in the presence of 3 micromol/kg MIB and VER the maximal effect of noradrenaline was reached at 0.1 micromol/kg whereas in the presence of 10 micromol/kg MIB and VER it was reached at a dose of 1 micromol/kg. MIB at a dose of 3 micromol/kg was significantly more effective in reducing the chronotropic response to electrical stimulation compared with externally applied noradrenaline. For VER the opposite holds true. These differences were not observed with doses of 10 micromol/kg MIB and VER. CONCLUSION: Mibefradil, besides its direct effect on cardiac T- and L-type calcium channels, reduces the release of noradrenaline from sympathetic nerve endings, most probably by inhibition of presynaptic N-type calcium channels. In the model used this effect is only observable at relatively low concentrations, most probably because of the direct cardiodepressant action of MIB provoked by L-type channel blockade.

Animals↗

The differential time courses of the vasodilator effects of various 1,4-dihydropyridines in isolated human small arteries are correlated to their lipophilicity.

OBJECTIVES: To investigate a possible relationship between the time courses of action of various calcium antagonists and their lipophilicity, characterized as log P-values. METHODS: The functional experiments were performed in vitro in human small subcutaneous arteries (internal diameter 591 +/- 51 microm, n = 7 for each concentration), obtained from cosmetic surgery (mamma reduction and abdominoplasty). The vessels were investigated in an isometric wire myograph. The vasodilator effect of the calcium antagonists was quantified by means of log IC50-values, and the onset of the vasodilator effect for each concentration studied was expressed as time to Eeq90-values (time to reach 90% of the maximal effect). RESULTS: Log IC50-values were -8.46 +/- 0.09, -8.33 +/- 0.25 and -8.72 +/- 0.16 for nifedipine, felodipine and (S)-lercanidipine, respectively (not significant). On average, nifedipine reached time to Eeq90 in 11 +/- 1 min. For felodipine and (S)-lercanidipine the corresponding values were 60 +/- 11 min and 99 +/- 9 min, respectively. The differences between these values were statistically significant (P< 0.01). In spite of these differences in the in-vitro human vascular model, the three calcium antagonists are equipotent with regard to their vasodilator effects. Linear regression analysis of the correlation between the logarithm of the membrane partition coefficient (log P-values) of the calcium antagonists tested [2.50, 4.46 and 6.88 for nifedipine, felodipine and (S)-lercanidipine, respectively] and their respective values found for time to Eeq90 was highly significant. CONCLUSIONS: It appears that a higher log P-value is correlated with a slower onset of action.

Adipose Tissue↗

Intracoronary-administered urapidil does not influence myocardial contractility, metabolic activity, or coronary sinus blood flow in humans.

OBJECTIVE: To compare the acute effect of intracoronary administration of urapidil and saline on myocardial contractility and metabolic activity. DESIGN: Prospective, controlled, open-label study. SETTING: University teaching hospital. PARTICIPANTS AND INTERVENTIONS: Eight patients with stable coronary artery disease (CAD) undergoing elective percutaneous transluminal coronary angioplasty (PTCA) received normal saline followed by urapidil, 4 mg, injected directly into the left main coronary artery. MEASUREMENTS AND MAIN RESULTS: Because local intracoronary administration is a non-steady-state condition, an in vitro model was used before the clinical experiments to establish the kinetic effects of acute administration of urapidil. The clinical experiments were performed in eight patients with CAD after PTCA. Measurements included a complete hemodynamic profile, coronary sinus blood flow (continuous thermodilution), left ventricular (LV) peak (+) dP/dt, LV peak (-) dP/dt, LV dP/dt/P(D)40, and LV end-diastolic pressures. Arterial and coronary venous blood samples were also obtained for the calculation of myocardial oxygen consumption. Baseline measurements I were first obtained, followed by intracoronary injection of 2 mL of saline. Additional measurements were obtained 1, 5, and 10 minutes after administration of saline. After a resting period (15 minutes), baseline measurements II, and intracoronary injection of urapidil, 4 mg (dissolved in 2 mL saline), additional measurements were obtained 1, 5, and 10 minutes later. Heart rate decreased 2.7+/-3.5 beats/min after injection of saline, whereas heart rate increased 2.0+/-1.8 beats/min after intracoronary urapidil, resulting in a significant difference in treatment effect (p = 0.003). There were no additional differences in treatment effect for any of the other measured or calculated parameters reflecting systemic hemodynamics, LV contractility, coronary dynamics, and myocardial metabolic activity. CONCLUSION: The results suggest that intracoronary bolus administration of preservative-free urapidil, 4 mg, is not associated with any detectable effect on myocardial contractility or coronary smooth muscle in awake nonsurgical patients with CAD, after PTCA.

Adrenergic alpha-Antagonists↗

Effects of sodium depletion on the role of AT1- and alpha-adrenergic receptors in the regulation of forearm vascular tone in humans.

OBJECTIVE: Sodium depletion stimulates the renin-angiotensin and sympathetic nervous systems, which may affect the role of each of these systems in the regulation of vascular tone. We investigated the influence of sodium depletion on the roles of the angiotensin II type 1 receptor and the alpha1- and alpha2-adrenergic receptors, and on nitric oxide generation, in the regulation of human forearm vascular tone. SUBJECTS AND METHODS: We studied the effects of the angiotensin II type 1 receptor antagonist losartan (0.1-3 microg/kg per min), angiotensin II (0.01-10 ng/kg per min), the alpha1- and alpha2-adrenoceptor antagonists doxazosin (3-100 ng/kg per min) and yohimbine (0.5-4 microg/kg per min) and the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA; 7.5-60 microg/kg per min) on forearm blood flow in control subjects (n = 12) and sodium-depleted subjects (n = 11). Sodium depletion was achieved by 3 days of pretreatment with 40 mg furosemide twice a day and a sodium-restricted diet. Forearm blood flow was measured by venous occlusion plethysmography. RESULTS: Sodium depletion resulted in activation of the renin-angiotensin and sympathetic nervous systems, as indicated by increased levels of plasma renin, aldosterone and heart rate (P < 0.05). Blood pressure remained unchanged. Losartan at the highest dose increased forearm blood flow in the sodium-depleted group by 42 +/- 9%, but had no effect in controls (P < 0.05). Both doxazosin and yohimbine caused an increased vasodilatory effect in the sodium-depleted versus the control group (228 +/- 42 versus 83 +/- 13% and 192 +/- 24 versus 95 +/- 8%, respectively; P < 0.05). The constrictor effects by angiotensin II and L-NMMA of -65 +/- 6% and -79 +/- 4%, respectively, in controls were unchanged by sodium depletion. CONCLUSIONS: In sodium-depleted subjects, endogenous angiotensin II appears to play a role in the regulation of forearm vascular tone, in contrast to sodium-replete conditions. Furthermore, in these subjects the role of alpha1- and alpha2-adrenoceptors in the regulation of forearm vascular tone was enhanced compared with control conditions. Neither the forearm vascular effects of exogenously infused angiotensin II nor those of baseline nitric oxide production were influenced by sodium depletion.

Adrenergic alpha-Antagonists↗

Influence of losartan and nicardipine on the contractile responses of human subcutaneous arteries and veins to angiotensin II.

In the human forearm vascular bed, the arterial constrictor effects of angiotensin II were found to be caused by an AT1-receptor mediated calcium influx, while the venous constrictor effects appeared to be independent of L-type calcium channels. In this study, we investigated the influences of the AT1-receptor antagonist losartan and the calcium channel blocker nicardipine on the angiotensin II-induced constriction of small isolated subcutaneous arteries and veins obtained from human mammary tissue. Subcutaneous arteries and veins were isolated from mammary tissue from 9 healthy women who underwent breast reduction surgery. Effects of angiotensin II (0.3 nM to 1 mM), losartan (0.1 mM) and nicardipine (0.1 mM) were investigated in a myograph set up. Identification of arteries and veins was confirmed histologically after the experiments. Drug effects were expressed relatively to the potassium-induced contraction. Angiotensin II concentration-dependently contracted arteries and veins by maximally 1.66 +/- 0.31 N/m and 0.43 +/- 0.08 N/m, respectively (P < 0.05). In arteries the angiotensin II were subject to a mild degree of tachyphylaxis: the Emax of the repetitive concentration-response curve (CRC) was reduced from 105 +/- 4% of the potassium-induced contraction to 84 +/- 6% (P < 0.05); the EC50 value was unchanged (P > 0.05). In veins no tachyphylaxis was observed. Losartan caused a rightward shift of the CRC of angiotensin II in arteries and veins (P < 0.05), and reduced the Emax in arteries from 105 +/- 4 to 85 +/- 9% (P < 0.05), but did not change the Emax in veins. Nicardipine significantly decreased the Emax in arteries and veins (to residual values of 10 +/- 2 and 20 +/- 4%, respectively, of the control values). In conclusion, the angiotensin II-induced constriction of human arteries and veins isolated from mammary tissue are AT1-receptor mediated and inhibited by losartan. The nearly complete inhibition by nicardipine indicates that the constrictor effects in both types of vessels are dependent on L-type calcium channels.

Acetylcholine↗

Comparative effects of mibefradil and other calcium antagonists on resistance arteries of different end organs.

The biphasic contractile responses of rat isolated mesenteric, renal, coronary and basilar small arteries to potassium-induced depolarization were investigated. The tonic phase is assumed to be exclusively the result of L-type calcium channel (LCC) activation, whereas in the generation of the phasic phase T-type calcium channels (TCC) may be involved. In order to evaluate whether TCC blockade has any influence on depolarization-induced contractions the effects of the LCC antagonists nifedipine, diltiazem and verapamil were compared with those of the combined L- and TCC antagonist mibefradil. Small arteries (size 393.6 +/- 4.8 microns, n = 104) were dissected from the respective organs of male Wistar rats (300-350 g) and studied in an isometric wire myograph. The effects of increasing concentrations of the calcium antagonists on repetitive potassium-induced contractions were quantified by means of cumulative concentration-response curves. A comparison was made with mesenteric vessels of SHR and WKY for nifedipine and mibefradil. Nifedipine was the most potent compound in blocking both the phasic phase (reduction 66-77%) and the tonic phase (IC50 = 1.1-5.4 nM). The effect of mibefradil on the phasic response was comparable to that of verapamil and diltiazem. With respect to the tonic response mibefradil was comparable to verapamil (IC50 = 19.6-178.9 nM). These findings indicate that the TCC blockade does not contribute to the vasodilator effect of mibefradil under the conditions investigated.

Animals↗

Morphologic and functional consequences of intimal hyperplasia in the rat carotid artery.

The influence of neointima formation on functional characteristics was investigated in rat carotid artery preparations. The process of intimal hyperplasia development in the injured carotid arteries was followed in time both morphologically and morphometrically. Simultaneously with the loss of endothelial cells due to the balloon injury procedure, the vasodilator responses to methacholine were abolished. The sensitivity for the alpha1-adrenoceptor agonist phenylephrine appeared to be increased only immediately after injury. The balloon injury method led to significant neointima formation in the rat left common carotid artery 14 days after the intervention. Eight weeks after balloon injury, the neointimal mass reached its maximum. Parallel to the development of intimal hyperplasia, the alpha1-mediated vasoconstrictor responses to phenylephrine were significantly impaired. After 12 weeks of observation, reoccurrence of mature endothelial cells on the luminal surface of the neointima could be observed. Simultaneously, the vascular responses to phenylephrine and methacholine recovered. The vasoconstrictor responses to high potassium concentrations (100 mM) as well as the vasodilator effects of sodium nitroprusside appeared to be uninfluenced by balloon injury throughout the period of observation. From this study we conclude that both the receptor-mediated contractile responses to alpha1-adrenoceptor stimulation and the endothelium-dependent vasodilator responses to methacholine become severely impaired as a consequence of balloon catheter injury followed by intimal hyperplasia. However, these pharmacological responses may fully recover upon a prolonged period of endothelial regeneration.

Adrenergic alpha-1 Receptor Agonists↗

Possible mechanism of the negative inotropic effect of alpha1-adrenoceptor agonists in rat isolated left atria after exposure to free radicals.

1. This study was designed to investigate the mechanism(s) of the negative inotropic effects of alpha1-adrenoceptor agonists observed in rat isolated left atria after exposure to free radicals. 2. Ouabain and calphostin C were used in contraction experiments to block the sodium pump and protein kinase C. Methoxamine-induced phospholipase C and Na+/K+ ATPase activities were measured. 3. Methoxamine (300 microM) increased contractile force by 1.6 +/- 0.2 mN in control atria but decreased contractile force in electrolysis-treated atria by 2.0 +/- 0.1 mN (P < 0.05), as determined 10 min after methoxamine addition. In contrast, the positive inotropic effects of endothelin-1 (30 nM) and isoprenaline (10 microM) were reduced from 2.6 +/- 0.3 to 1.3 +/- 0.1 mN and from 2.6 +/- 0.3 to 1.7 +/- 0.2 mN, respectively, by electrolysis treatment (P < 0.05), but not converted into a negative inotropic action. 4. In an inositol phosphate assay we observed that the stimulation of phospholipase C by methoxamine was attenuated by electrolysis when the (electrolyzed) medium from the organ bath was used, but the phospholipase C responses were restored by the use of fresh medium. However, fresh medium did not counteract the negative inotropic effect of methoxamine. Accordingly, the negative inotropic effect of methoxamine is not directly related to the impaired phospholipase C responses seen in atria subjected to electrolysis. 5. Ouabain (10 microM) and the protein kinase C inhibitor calphostin C (50 nM), completely prevented the negative inotropic effect of 300 microM methoxamine in electrolysis-treated atria. 6. Measurement of the Na+/K+ ATPase activity, revealed that in control atria, alpha1-adrenoceptor stimulation with 300 microM methoxamine, decreased the Na+/K+ ATPase activity by 14.4 +/- 7.7%. In contrast, methoxamine increased the Na+/K+ ATPase activity by 48.8 +/- 8.9% (P < 0.05) in electrolysis-treated atria. Interestingly, this increase in Na+/K+ ATPase activity was completely counteracted by calphostin C (1.4 +/- 0.1% over basal). 7. These results indicate that the negative inotropic effects of alpha1-adrenoceptor agonists, observed in rat isolated left atria exposed to free radicals, are likely to be caused by protein kinase C-mediated phosphorylation and subsequent activation of the Na+/K+ ATPase.

Adrenergic alpha-1 Receptor Agonists↗

Thyroid status affects the rat cardiac beta-adrenoceptor system transiently and time-dependently.

1. The aim of this study was to investigate the time-dependency of the influence of dysthyroid states on the beta-adrenoceptor system in rat heart left ventricle. Therefore, the influence of acute and chronic hyper- and hypothyroidism on beta-adrenoceptor-induced left ventricular responses, beta-adrenoceptor density, cardiac noradrenaline tissue concentrations, Gs alpha-proteins, and basal and stimulated adenylate cyclase activities was determined. 2. Hyperthyroid rats were obtained by feeding with thyroxine (T4)-containing rat-chow for 1, 4 and 8 weeks. Hypothyroidism was induced by adding 0.05% propylthiouracil (PTU) to the drinking water. Rats of varying ages were used in order to compensate for the differences in the duration of the treatments. Rats were aged 3 and 5 months at the end of the experiments. 3. Thyroxine treatment for 4 and 8 weeks increased the cardiac sensitivity to isoprenaline, but maximal induced inotropic responses were decreased. Cardiac ventricular beta-adrenoceptor density was increased only in rats treated with T4 for 1 week. This transient effect of hyperthyroidism on cardiac beta-adrenoceptor density was not observed in older rats. The PTU treatment resulted in a stable decrease of cardiac beta-adrenoceptor density. 4. Left ventricular tissue noradrenaline concentrations were unaffected by hyperthyroidism, where a decrease was observed in hypothyroid rats. Density of Gs alpha proteins was increased in hearts from chronic hyperthyroid rats. 5. These results indicate that the increased sensitivity to beta-adrenoceptor-mediated stimulation in chronic hyperthyroidism cannot be attributed to changes in cardiac beta-adrenoceptor density, but is probably caused by an enhanced content of Gs alpha. Accordingly, in hyperthyroidism, the beta-adrenoceptor system is influenced time-dependently, whereas hypothyroidism affects the beta-adrenoceptor system independent of time.

Adenylyl Cyclases↗

Effects of angiotensin II and losartan in the forearm of patients with essential hypertension.

OBJECTIVE: Angiotensin II type 1 receptor-mediated constrictor effects may be modulated by hypertension-related vascular changes, changes in receptor function and in neurohumoral activity. DESIGN: The forearm blood flow (FBF) effects of angiotensin II, methoxamine, and losartan were investigated in essential hypertensive patients. Minimal forearm vascular resistance was measured to determine structural vascular changes. METHODS: Seven hypertensive patients were selected, and seven matched normotensives. Angiotensin II (0.01-10 ng/kg per min) was infused during predilatation by sodium nitroprusside (6.1 +/- 0.6 ng/kg per min) before and during losartan infusion (0.3-3 microg/kg per min). Methoxamine (0.2-2 microg/kg per min) was co-infused with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine. FBF, measured by venous occlusion plethysmography, was expressed as the change in FBF ratio (FBFinfused arm/FBFnon-infused arm). RESULTS: Baseline FBF (infused arm) was increased by sodium nitroprusside from 2.56 +/- 0.80 to 5.46 +/- 0.92 (P<0.05) and from 2.66 +/- 0.25 to 5.42 +/- 0.40 ml/100 ml per min (P<0.05) in the hypertensive and normotensive group, respectively. Baseline forearm vascular resistance (FVR) was higher in the hypertensive than in the normotensive group [51 +/- 8 versus 33 +/- 3 mmHg/ (ml/100 ml per min); P<0.05]. Angiotensin II caused a maximal change in FBF ratio (Emax) by -70 +/- 3 and -72 +/- 6% in the hypertensive and normotensive group, respectively (NS). Tachyphylaxis did not occur. Infusions of losartan at 0.3, 1 and 3 microg/kg per min reduced the Emax values from -70 +/- 3 to -50 +/- 5, -45 +/- 5 and -15 +/- 2%, respectively, in the hypertensive group, and from -72 +/- 6 to -62 +/- 4, -45 +/- 2 and -32 +/- 2%, respectively, in the normotensive group (NS). Infusion of methoxamine significantly reduced the FBF ratio by -58 +/- 6 and -69 +/- 5% in the hypertensive and normotensive groups, respectively (NS). Minimal FVR, after forearm ischemia, was the same in hypertensives and normotensives, namely 3.2 +/- 0.7 and 3.2 +/- 0.4 mmHg/(ml per 100 ml per min), respectively (NS). CONCLUSIONS: Angiotensin II type 1- and alpha1-mediated vascular effects were unchanged by essential hypertension. Baseline FVR was greater in the hypertensives than in the normotensives, while minimal FVR was the same. These results indicate that the forearm vascular bed of the patient group studied does not show important structural and renin-angiotensin system-related functional changes as a result of hypertension.

Adult↗

Venoconstriction by angiotensin II in the human forearm is inhibited by losartan but not by nicardipine.

Arterial constriction by angiotensin II (Ang II) in the human forearm is inhibited by the infusion of the AT1-receptor antagonist losartan. We investigated venous constriction by Ang II in the forearm of 19 healthy subjects (23 +/- 1 years) and the inhibitory effects of losartan. Furthermore, we investigated, in both the arterial and venous systems, whether the constrictor effects of Ang II are calcium influx dependent by determining the influence of nicardipine. Arterial forearm blood flow (FBF) and maximal venous outflow (MVO) were measured by venous-occlusion plethysmography. Sodium nitroprusside (5-12.5 ng/kg/min) was infused to predilate the forearm vasculature. Ang II (0.1, 1, and 10 ng/kg/min) was infused before and during losartan (0.3 and 3 microg/kg/min) or nicardipine (0.05 and 0.15 microg/kg/min), respectively. Ang II decreased FBF (Emax-FBF) by 79 +/- 4% and MVO (Emax-MVO) by 28 +/- 3% (p < 0.05). Nicardipine at 0.05 and 0.15 microg/kg/min reduced Emax-FBF from -79 +/- 4% to -48 +/- 4% and -6 +/- 2%, respectively (p < 0.05). Losartan in both doses completely inhibited Emax-MVO (p < 0.05), whereas nicardipine did not influence the venoconstriction by Ang II (p > 0.05). In conclusion, Ang II causes a constriction of both arteries and veins in the human forearm, which may be inhibited by losartan. The arterial constriction appears to be caused by an AT1-receptor-mediated calcium influx via L-type calcium channels. In contrast, the venoconstrictor effect of Ang II proved insensitive to the calcium antagonist nicardipine.

Adult↗

Bradykinin B2-receptor-mediated positive chronotropic effect of bradykinin in isolated rat atria.

The positive chronotropic effect of bradykinin was investigated in isolated spontaneously beating atria of the rat. Cumulative additions of bradykinin (0.3-100 nM) caused a concentration-dependent increase in the beating rate of the atria by maximally 35+/-4 beats/min, approximately 25% of the 1 microM isoprenaline-induced maximal responses. In contrast, the active metabolite of bradykinin and selective bradykinin B1-receptor agonist, Des-Arg9-bradykinin, did not influence the spontaneous frequency of beating. Propranolol (1 microM) combined with prazosin (1 microM) did not affect the positive chronotropic effect of bradykinin. A selective bradykinin B2-receptor antagonist, Hoe 140, concentration-dependently shifted the response curves for bradykinin to the right, whereas the bradykinin B1-receptor antagonist, Lys-[Leu8]Des-Arg9-bradykinin had no effect. The tachycardic responses to bradykinin were potentiated by ramipril, an angiotensin-converting enzyme/kininase II inhibitor, but not affected by Nomega-nitro-L-arginine methyl ester hydrochloride, a nitric oxide synthesis inhibitor. Indomethacin and meclofenamate, two cyclooxygenase inhibitors, abolished the bradykinin-induced chronotropic effect. These results indicate that exogenous bradykinin induces a positive chronotropic effect that occurs independent of adrenoceptors. The bradykinin-induced chronotropic effect is mediated by bradykinin B2 receptors, whereas B1 receptors do not play a role in mediating this effect. Prostaglandins but not nitric oxide appear to be involved in bradykinin-induced positive chronotropic effect.

Animals↗

Positive chronotropic activity of bradykinin in the pithed normotensive rat.

The positive chronotropic effect of bradykinin was investigated in the pithed rat preparation. Cumulative treatment with bradykinin (0.20 nmol/kg-6.59 mumol/kg, intravenous [i.v.]) caused a dose-dependent increase in heart rate (HR) by a maximum of 80 +/- 3.3 beats min-1. In contrast, the active metabolite of bradykinin and selective bradykinin B1-receptor agonist, [des-Arg9]-bradykinin did not influence the spontaneous frequency of beating. Propranolol alone reduced the bradykinin-induced increase in HR and a combination of propranolol with prazosin abolished the chronotropic effect of bradykinin. The selective bradykinin B2 receptor antagonist. Hoe 140, dose-dependently shifted the dose-response curves of bradykinin to the right, whereas the bradykinin B1 receptor antagonist, des-Arg10-[Leu9]-kallidin proved ineffective. From our experiments it may be concluded that bradykinin induces tachycardia in the pithed rat primarily by stimulating the sympathetic ganglia leading to the release of noradrenaline, which subsequently activates cardiac beta 1-adrenoceptors. The bradykinin-induced chronotropic effect is mediated by bradykinin B2-receptors, whereas B1-receptors appear not to be involved.

Adrenalectomy↗

Differential time course of the vasodilator action of various calcium antagonists.

It is rather the rate of the vasodilator effect than its magnitude which determines the triggering of reflex tachycardia associated with dihydropyridine calcium antagonists (DHP-CA). We therefore compared the rate of the vasodilator effects of a series of CA (both DHP and non-DHP) in rat isolated mesenteric artery preparations (size 256 +/- 3 microns, length 2 mm) from male Wistar rats (weighing 300-350 g) in an isolated wire myograph according to Mulvany and Halpern [12]. The mean force of the KCl-induced contraction amounted to 2.3 +/- 0.1 mN/mm. Potency (given as IC50-values), differential time course of action and recovery of the contractile response of the vessels after wash-out were established. These three parameters adhere to the following sequences: (1. potency) barnidipine [corrected] > (S)-lercanidipine > barnidipine racemate [corrected]> amlodipine > nifedipine, lacidipine > (R)-lercanidipine > verapamil, mibefradil; (2. differential time course) lacidipine, amlodipine > (S)- and (R)-lercanidipine, barnidipine [corrected], barnidipine racemate [corrected] > mibefradil, verapamil, nifedipine; (3. recovery) nifedipine > verapamil, barnidipine [corrected], amlodipine > barnidipine, lacidipine > mibefradil, (R)-lercanidipine > (S)-lercanidipine. In conclusion, barnidipine [corrected] proved to be the most potent vasodilator agent; interestingly, barnidipine was 20 times less potent when applied as a racemic mixture. A slow onset of action in DHP is a very important mechanism in preventing reflex tachycardia. For non-DHP (verapamil, mibefradil) reflex tachycardia probably is prevented by a direct effect on the conductive tissue in the myocardium.

Amlodipine↗

Contribution of ATP-sensitive potassium channels to beta-adrenoceptor-mediated responses.

In isolated hearts the inotropic response to the beta-adrenoceptor agonist isoproterenol is known to be abolished after ischaemia and reperfusion. The aim of this study was to investigate whether at decreased glucose levels the beta-adrenoceptor-mediated responses in vascular smooth muscle would be depressed, since low glucose conditions mimic the influence of ischaemia. Accordingly, we investigated the influence of low glucose levels in the extracellular space on the vasorelaxation induced by isoproterenol and salbutamol in rat isolated thoracic aortic ring preparations with an intact endothelium and we attempted to further analyze the underlying mechanisms. Therefore, forskolin, dibutyryl-cAMP and glibenclamide (an ATP-sensitive K(+)-channel blocker) were studied as well. In a glucose-free medium the concentration-response curve for isoproterenol was shifted to the left compared to that obtained under normal glucose conditions. The maximal relaxation induced by isoproterenol was not affected by the absence of glucose. In contrast, the maximal relaxation induced by salbutamol in glucose-free medium decreased by 50% compared to that obtained under normal glucose conditions. Glibenclamide caused a concentration-dependent decrease of the maximum relaxation by isoproterenol in a glucose-free medium, but had no effect under normal glucose conditions. Glibenclamide did not influence the concentration-response curves for salbutamol, neither in the presence nor in the absence of glucose in the medium. The relaxation caused by forskolin and dibutyryl-cAMP was not influenced by glibenclamide in a medium devoid of glucose. In endothelium-denuded preparations glibenclamide did not affect isoproterenol-induced responses neither in the presence nor in the absence of glucose. It is concluded that beta-adrenoceptor stimulation opens ATP-sensitive potassium channels under conditions of impaired ATP-metabolism by a cAMP-independent pathway, which needs an intact endothelium.

Adenosine Triphosphate↗

The influence of oxidative stress on various inotropic responses in isolated rat left atria.

The effects of free radicals, generated by electrolysis of a physiological salt solution, on various inotropic responses to drugs in isolated rat left atria were studied. Evidence for the generation of hydroxyl radicals was obtained from an appropriate fluorimetric assay. The amount of free radicals produced by electrolysis of the medium proved current-dependent. Exposure of isolated rat left atria to the medium which had been subjected to electrolysis caused a current-dependent decrease in contractile force. Oxidative stress, as a result of the electrolysis of the medium, caused altered inotropic responses to extra cellular Ca2+ (pD2 control group: 2.62 +/- 0.06 vs. 2.44 +/- 0.07 electrolysis group), sodium withdrawal (rise in contractile force control group: 1.73 +/- 0.19 mN vs. 0.48 +/- 0.21 mN electrolysis group) and lowering of stimulation frequency. The response to isoprenaline was diminished in atria subjected to oxidative stress and led to a rightward shift of the concentration response curves (pD2 control group: 7.56 +/- 0.10 vs. 6.77 +/- 0.11 electrolysis group). In addition, the inotropic responses to forskolin (pD2 control group: 6.17 +/- 0.12 vs. < 4.5 electrolysis group) and dibutyryl cAMP (rise in contractile force caused by 1 x 10(-5) M db-cAMP in control group: 2.15 +/- 0.01 mN vs. 1.21 +/- 0.10 mN electrolysis group) proved blunted as well. Measurement of the adenylyl cyclase activity revealed that free radicals attenuated the basal (by 11.1%) and forskolin stimulated (155.0 +/- 5.1 vs. 48.0 +/- 1.8 pmol cAMP/mg prot./min for control and electrolysis group respectively) activity of the adenylyl cyclase. DMSO, a well known hydroxyl radical scavenger, was able to abolish the free radical-induced decrease in the response to isoprenaline. Surprisingly, addition of alpha-adrenoceptor agonists to atria subjected to electrolysis-generated free radicals led to a rapid decrease in contractile force. DMSO was unable to counteract the negative intropic effect of methoxamine in atria subjected to oxidative stress. This negative inotropic response to alpha-adrenoceptor agonists in atria subjected to electrolysed medium is unlikely to be the direct result of phospholipase C or protein kinase C activation. Angiotensin II (which stimulates PLC, as well) did not reduce contractile force and chelerythrine (a PKC inhibitor) was unable to counteract the negative inotropic effect of the adrenoceptor agonists. In addition, the negative inotropic effect of methoxamine proved insensitive to 10(-6) M phentolamine and 10(-5) M doxazosin, which indicates an alpha-adrenoceptor independent mechanism. From this study we conclude that free radicals alter responses to various inotropic stimuli. These alterations may be the result of injured contractile elements, transporter molecules and molecules involved in signal transduction. Addition of alpha-adrenoceptor agonists after oxidative stress leads to a alpha-adrenoceptor. PLC and PKC independent decrease in contractile force.

Adenylyl Cyclases↗

Morphology and function of preserved microvascular arterial grafts: an experimental study in rats.

The aim of this study is to examine the morphology and function and small-caliber, arterial grafts after preservation in the University of Wisconsin solution (UW). Rat carotid arteries were stored in UW (n = 10) or in phosphate-buffered saline (PBS) (n = 10) for 1, 3, 7, and 14 days and were examined with light microscopy (LM) and scanning electron microscopy (SEM). Rat aortic preparations were stored in UW or PBS for 1 hour, 24 hours, 72 hours, 7 days, and 14 days and assessed for functional responses (stimulated contraction and endothelium-dependent relaxation). Segments (5 mm) of rat carotid arteries were stored in UW or PBS for 3 days, 7 days, and 14 days and orthotopically implanted as autografts and allografts. No immunosuppressive or anticoagulant agents were used. After 28 days of implantation, the grafts were assessed for patency and excised for LM and SEM. In UW, the endothelial layer remained intact up to 9 days of storage. In PBS, the endothelial layer showed deterioration after 1 day and was completely lost after 3 days. Functional responses were demonstrated to exist for as long as 7 days storage in UW. In PBS, no responses could be evoked after 24 hours storage. Autografts preserved in UW for 3 days (n = 6), 7 days (n = 6), and 14 days (n = 6) showed patency rates of 83.3%, 66.6%, and 66.6%, respectively, whereas patency rates of allografts were 66.6%, 33.3%, and 33.3%, respectively. Autografts stored in PBS for 3 days (n = 6), 7 days (n = 6), and 14 days (n = 6) showed patency rates of 33.3%, 33.3%, and 50%, respectively, whereas patency rates of allografts were 16.7%, 0%, and 33.3%, respectively. The UW preserved autografts showed normal morphology. All other groups showed vessel wall degeneration which in the allograft groups, were accompanied by lymphocellular infiltration. In conclusion, the endothelial layer and vessel wall of arteries are adequately preserved in UW. Functional responses are retained up to 14 days storage in UW, but, are lost after 24 hours storage in PBS. Autograft implantation studies accordingly show good performance of arterial segments preserved in UW, whereas allografts are subject to degradation as a result of rejection.

Adenosine↗