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M J Crespo

Publications and source records attributed to M J Crespo.

At least 19 recordsLinked to original sources
PubMed2005

Angiotensin II-dependent vascular alterations in young cardiomyopathic hamsters: role for oxidative stress.

Recent studies indicate the presence of vascular alterations in 2-month-old Syrian cardiomyopathic hamsters (SCH). These alterations include enhanced angiotensin-converting enzyme (ACE) activity in the aorta, increased contractile response to angiotensin II and impaired vasorelaxation to acetylcholine in norepinephrine-precontracted aortic rings. The mechanisms leading to these vascular alterations are not known nor has their relationship to the cardiac abnormalities been established. We assessed the status of the cardiovascular system of 2-month-old hamsters first to establish if the observed vascular alterations are secondary to cardiac dysfunction, and second to examine the role of oxidative stress in the etiology of vascular dysfunction. Cardiac function parameters evaluated by echocardiography included stroke volume (SV), left ventricular end-diastolic volume (LVEDV), left ventricular fractional shortening (LVFS), ejection fraction (EF), cardiac output index (COI), heart rate (HR) and left ventricular posterior wall thickness (LVPWT). In addition, heart/body weight (heart/BW) ratios and systolic blood pressure were determined in normal hamsters and SCH. Our results indicated that systolic blood pressure increased 56% in SCH when compared to control animals (P<0.05). The increased blood pressure coexisted with normal COI, SV, LVEDV, LVPWT, LVFS, EF, HR and heart/BW ratios. NAD(P)H oxidase activity increased 77% in SCH compared to control animals (P<0.02). The increased oxidase activity was abolished by pre-treatment of animals with the angiotensin II type 1 receptor blocker losartan (25 mg/kg BW/day) for 10 days. Losartan also abolished the increased blood pressure observed at 2 months of age. The antioxidant N-acetylcysteine (NAC) abrogated the increased blood pressure when administered for 30 days to 1-month-old animals. Altogether, these findings suggest that the angiotensin II-dependent vascular abnormalities present in young cardiomyopathic hamsters are associated with oxidative stress and precede the echocardiographic abnormalities characteristic of heart failure.

Acetylcysteine↗
PubMed2003

Enalapril improves vascular and cardiac function in streptozotocin-diabetic rats.

Recent evidence points to the renin-angiotensin system (RAS) as one of the systems involved in the etiology of micro- and macrovascular disease in diabetic patients. To help elucidate this possibility, the effect of daily treatment with enalapril (25 mg/kg/d) was evaluated in streptozotocin (STZ)-diabetic rats at 2 weeks following the induction of diabetes. Untreated diabetic rats and non-diabetic rats that were age-matched were used for comparison. Vascular studies included the determination of aortic ring responses to norepinephrine (NE), angiotensin II (Ang II) and acetylcholine (Ach). Systolic blood pressure (SBP), cardiac output (CO) indices, plasmatic and vascular angiotensin-converting enzyme (ACE) activity and thickness of the aortic wall were also assessed. Enalapril improved Ach-induced relaxation by increasing the maximal relaxation from 54.3 +/- 4.3% in untreated diabetic rats to 89.8 +/- 6.2% (n=9, p<0.05) and by decreasing the EC50 value from 32.6 +/- 9.9 nmol/l in untreated diabetic animals to 17.9 +/- 5.1 nmol/l (n=8, p<0.05). In addition, enalapril normalized the high responses to NE found in diabetic rats without inducing changes in the EC50 value. A significant reduction in SBP (from 158 +/- 4 mm Hg to 123 +/- 1 mm Hg, p<0.05), combined with an improved CO index (from 40 +/- 2 ml/min x 100 g BW to 50 +/- 1 ml/min x 100 g BW), was observed in the enalapril-treated diabetic group. A significant regression of the media thickness was also observed in the aorta of diabetic rats after treatment. ACE activity in the aorta of diabetic rats, that was doubled compared to controls (p<0.05), decreased after enalapril treatment. These results point to the vascular RAS as one of the key systems in the etiology of vascular alterations at early stages of diabetes. Therefore, ACE inhibitors, as well as other pharmacological approaches targeting the vascular RAS, should be considered in the treatment of diabetic patients from the very early stages of the condition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Occurrence of Malassezia spp. in horses and domestic ruminants.

During a study on the occurrence of Malassezia spp. in 112 animals (50 horses, 25 goats, 25 sheep and 12 cows), Malassezia spp. were isolated from 60% of horses, 28% of sheep, 44% of goats and 58% of cows. In these animals, the occurrence of lipid-dependent species (42%) was much greater than the occurrence observed for M. pachydermatis (3%). Among the results obtained, we point out the first isolation of M. sympodialis, M. globosa and M. restricta from sheep, M. pachydermatis, M. furfur, M. sympodialis, M. obtusa, M. globosa and M. restricta from goats and M. furfur, M. slooffiae, M. obtusa, M. globosa and M. restricta from horses. To the authors' knowledge, this survey also states the first description of the presence of M. restricta in animals.

Animals↗
PubMed2002

Occurrence of Malassezia spp. in the external ear canals of dogs and cats with and without otitis externa.

We studied the lipophilic microbiota of the external ear canals of 332 animals (264 dogs and 68 cats), with and without otitis externa, over an 11-year period from 1988 to 1999. Malassezia pachydermatis was isolated from 62.2% and 50% of dogs with and without otitis externa, respectively, and from 41.2% and 17.6% of cats with and without otitis externa, respectively. In the group of animals studied for lipid-dependent species, these yeasts were isolated from 4.5% of dogs with otitis externa and from 23.1% and 8.9% of cats with and without otitis externa, respectively. M. sympodialis and M. furfur were isolated from cats and M. furfur and M. obtusa from dogs. Our findings show that lipid-dependent Malassezia species may contribute to the etiology of otitis externa in dogs and cats.

Animals↗
PubMed2001

Chronic administration of losartan plus hydrochlorothiazide improves vascular status in young cardiomyopathic hamsters.

The combination of an angiotensin II receptor antagonist and a thiazide has been used extensively in the treatment of patients with overt heart failure. The effect of this combination on the vascular wall early in the disease, however, has not been investigated. To evaluate this effect, the vascular status of 3-month-old cardiomyopathic hamsters was assessed after daily administration of a combination of losartan (25 mg/kg, p.o.) and hydrochlorothiazide (6.5 mg/kg, p.o.) over an 8-week period. Age-matched golden hamsters were used as healthy controls. The contractile response of aortic rings to endothelin-1 was significantly higher in cardiomyopathic hamsters than in control animals. Concentration-response curves for the endothelin-1-induced contraction were displaced to the right after hydrochlorothiazide+losartan treatment (toward the curves for healthy controls); however, E(max) from treated hamsters was significantly reduced when compared to E(max) from untreated cardiomyopathic animals (1.016+/-0.073 vs. 1.346+/-0.153 g, P<0.05, n=6). No significant differences in the EC50 values from these curves were observed between hydrochlorothiazide+losartan treated and untreated cardiomyopathic animals (2.90+/-0.95 vs. 1.10+/-0.85 nM, P>0.05). The acetylcholine-induced relaxation observed in cardiomyopathic animals was not improved after treatment with hydrochlorothiazide+losartan or hydrochlorothiazide alone, but the combination of these drugs increased significantly the basal production of nitric oxide (NO). Angiotensin-converting enzyme activity increased in plasma (from 29.9+/-1.23 to 41.16+/-1.82 nmol x mg(-1) x min(-1), n=8, P<0.05) but decreased in the aorta (from 0.33+/-0.02 to 0.25+/-0.017 nmol x mg(-1) x min(-1), n=6, P<0.05) after treatment with hydrochlorothiazide+losartan. In addition, the combination of these drugs reduced the heart-to-body mass ratio (3.96+/-0.07 for treated vs. 5.01+/-0.20 mg/g for untreated animals, n=7, P<0.05), and the thickness of the aortic media (0.076+/-0.003 for treated vs. 0.149+/-0.009 mm for untreated animals, n=8, P<0.05). Although hydrochlorothiazide alone lowered systolic blood pressure to the same level achieved with both drugs in combination (from 166+/-10 for untreated cardiomyopathic animals to 84+/-1 mm Hg for hydrochlorothiazide+losartan, and 80+/-5 mm Hg for hydrochlorothiazide alone, P<0.05), no significant reduction in heart-to-body mass ratio was observed in animals treated with the diuretic alone (P>0.05). In conclusion, in this model of heart failure, chronic hydrochlorothiazide+losartan administration normalizes the vascular responses to endothelin-1, improves basal vascular tone, and prevents the development of cardiac and vascular hypertrophy.

Acetylcholine↗
PubMed2000

Interaction between AT1 and alpha1-adrenergic receptors in cardiomyopathic hamsters.

BACKGROUND: Cross talk between angiotensin AT1 and alpha1-adrenergic receptors has been reported previously and points to the existence of physiologic regulation between the renin-angiotensin system and the sympathetic nervous system at the receptor level. This regulation may play an important role in the control of blood pressure and may be modified in different cardiovascular pathologies. Nevertheless, neither the physiologic actions nor the clinical relevance of the interaction between these 2 receptors has yet been established. To reveal these aspects in relation to heart failure, the interaction between vascular AT1 and alpha1-adrenergic receptors was evaluated in the Syrian cardiomyopathic hamster model. METHODS AND RESULTS: The vascular response of each individual receptor to vasoactive agonist was assessed in the presence and absence of antagonists of the other receptor using aortic rings from 11-month-old Syrian cardiomyopathic hamsters. Age-matched golden hamsters were used as controls. In control hamsters, concentration-response curves for the norepinephrine (NE)-induced contraction were significantly displaced to the left after 100 mmol/L losartan incubation. The maximal tension achieved (Emax) values increased by 26+/-4.3% after incubation (P < .05). Similar results were obtained when 20 micromol/L enalapril was used to block angiotensin II (Ang II) synthesis. NE concentration-response curves were also displaced to the left and Emax increased by 27%+/-8.0% (P < .05). The concentrations that induce 50% of the maximal contraction (EC50) were 22.2+/-0.2 nmol/L for untreated and 27.1+/-2.0 nmol/L for losartan-treated aortic rings (n = 8, P > .05). However, EC50 values were significantly reduced in aortic rings treated with enalapril (7.51+/-0.16 nmol/L, n = 8, P < .05). Blockade of alpha1 receptor with 10 micromol/L prazosin increased the response to Ang II by 32% (n = 6, P < .05). In contrast, when these experiments were repeated in aortic rings from cardiomyopathic animals, no interaction between the 2 receptors was observed. NE concentration-response curves, Emax (9.6%+/-2.8% increase after enalapril. and 5.8%+/-6.5% increase after losartan, P > .05) and EC50 values (14.7+/-0.7 nmol/L without treatment, 17.5+/-1.5 nmol/L with enalapril and 11.1+/-0.8 with losartan, n = 8, P > .05) were similar. Furthermore, in cardiomyopathic animals, prazosin did not modify the vascular response to Ang II. CONCLUSIONS: An interaction exists between vascular AT1 and alpha1-adrenergic receptors in control hamsters but not in cardiomyopathic animals. This interaction seems to be bidirectional and counterregulatory. The lack of this regulation may promote a state of enhanced vascular wall activity, which could contribute to the increased vasoconstriction and total peripheral resistance characteristic of heart failure.

Angiotensin I↗
PubMed2000

Evaluation of different preservation and storage methods for Malassezia spp.

Freezing at -80 degrees C, lyophilization, preservation in distilled water, and storage in different culture media were performed in order to find a suitable method that allowed a prolonged storage of Malassezia spp. Freezing at -80 degrees C was the only method successful at maintaining all species.

Animals↗
PubMed2000

Otitis externa associated with Malassezia sympodialis in two cats.

The lipid-dependent species Malassezia sympodialis was isolated from two cats with otitis externa. To our knowledge, this is the first report of the isolation of lipid-dependent species of the genus Malassezia associated with skin disease in domestic animals.

Animals↗
PubMed2000

Atypical lipid-dependent Malassezia species isolated from dogs with otitis externa.

During a survey of the occurrence of Malassezia species in the external ear canals of dogs with chronic otitis externa, lipid-dependent Malassezia species were isolated in three dogs. These species were identified as Malassezia furfur and M. obtusa but showed atypical assimilation patterns. To our knowledge, this is the first report of the isolation of lipid-dependent species of the genus Malassezia in association with canine otitis.

Animals↗
PubMed1999

Correlation between changes in morphology, electrical properties, and angiotensin-converting enzyme activity in the failing heart.

Evidence is available that morphologic and electrophysiologic abnormalities are present in the failing heart. In the present work, the progressive changes in electrical properties and morphology of the failing heart of Syrian cardiomyopathic hamsters (TO2) were investigated at different stages of the pathological process, and the possible role of the renin-angiotensin system was studied. Cardiomyopathic hamsters 2 and 11 months of age were used. Age-matched normal hamsters (F1B) were utilized as controls. Measurements of membrane potential, conduction velocity and refractoriness were made with conventional intracellular electrodes connected to a high impedance DC amplifier. Serum and cardiac angiotensin-converting enzyme (ACE) activities were measured in controls and cardiomyopathic animals. The results indicated that interstitial fibrosis and calcification were present in the heart of 2-month old Syrian cardiomyopathic hamsters. Measurements of the resting potential performed in the isolated right ventricle of 2-month old Syrian cardiomyopathic hamsters indicated an average value of -66.7 +/- 0.96 mV (n = 25); in the controls of the same age was -78.5 +/- 1 mV (n = 25, P < 0.05); and in 11-month old cardiomyopathic hamsters was -67.8 +/- 0.83 mV (n = 10). The duration of the action potential measured at 50 and 90% of repolarization in 2-month old hamsters was well above the controls. The conduction velocity measured in the isolated right ventricle of 2-month old Syrian cardiomyopathic hamsters (44.2 +/- 1.6 cm/s, n = 12) was not different from the control (43.7 +/- 1.1 cm/s, n = 7, P > 0.05) but was significantly larger than that recorded from the ventricle of 11-month old animals (37.8 +/- 2.9 cm/s, n = 11, P < 0.05). ACE activity was 0.26 +/- 0.01 nmol/mg x min in the heart of controls at 2 months of age and did not change with age. Although in the 2-month old cardiomyopathic hamsters the enzyme activity (0.28 +/- 0.04 nmol/mg x min) was not different from the controls (P > 0.05), in myopathic animals at 11 months of age, the enzyme activity (0.56 +/- 0.027 nmol/mg x min) was greater than controls (P < 0.05). The ACE activity in plasma followed the same pattern. The conclusion from these experiments is, that some parameters like resting potential, action potential duration, and morphological abnormalities appeared quite early in the failing process. The decline in conduction velocity, however, appeared later on, concurrently with the activation of plasma and cardiac renin-angiotensin systems.

Age Factors↗
PubMed1999

Vascular alterations during the development and progression of experimental heart failure.

BACKGROUND: Congestive heart failure (HF) is a multifactorial and progressive condition associated with multiple systemic and vascular alterations. The onset and progression of these alterations and the cause of the condition remain undefined. The main purpose of the present study was to help understand the temporal evolution of vascular alterations and their contribution to the pathogenesis of HF. Vascular reactivity to angiotensin II (Ang II) and norepinephrine (NE), as well as circulating and local angiotensin-converting enzyme (ACE) activity, were assessed in the Syrian cardiomyopathic hamster (SCH) model. METHODS AND RESULTS: We have shown previously that in 2-month-old SCH animals that had not yet developed the clinical manifestations of HF, the contractile response of aortic rings to Ang II was markedly enhanced compared with normal animals. In addition, SCHs showed increased ACE activity in aortic tissue. To assess the relevance of these findings to the development and progression of HF, the temporal evolution of the contractile response of aortic rings to Ang II and NE was evaluated in hamsters at 2, 6, and 11 months of age. Age-matched normal hamsters were used as controls. Within the SCH group, the maximal contraction induced to 10 mumol/L of NE in 2- and 11-month-old animals was similar, but significantly greater than in the age-matched controls (for 2-month-old animals; 1.43 +/- 0.21 g in SCHs v 1.04 +/- 0.15 g in controls; P < .05 and for 11-month-old animals; 1.41 +/- 0.14 g in SCHs v 1.06 +/- 0.07 g in controls; P < .05). The drug concentrations necessary to obtain 50% of the maximal response from the NE concentration-response curves were similar for SCHs and controls at all ages tested. In contrast, the contractility induced by 0.1 mumol/L of Ang II increased progressively in cardiomyopathic animals from 2 to 11 months of age (from 1.3 +/- 0.1 to 1.8 +/- 0.2 g; n = 9; P < .05). In age-matched normal hamsters, the contractile response to Ang II (0.9 +/- 0.1 g) did not vary with age. These findings were observed concomitantly with an increased ACE activity in plasma (18.65 +/- 1.77 nmol/mg x min in controls v 26.5 +/- 1.79 nmol/mg x min in SCHs; P < .05; n = 7) and in heart tissue (0.244 +/- 0.016 nmol/mg x min in controls v 0.563 +/- 0.027 nmol/mg x min in SCHs; P < .05; n = 20) of 11-month-old SCHs. CONCLUSIONS: These results suggest that, in young animals, increased vascular response to elevated levels of NE and hyperreactivity to Ang II could be critical factors in the development and progression of HF. Indeed, Ang II-induced contractility, as well as plasma and heart ACE activity, are good predictors of the progression and severity of HF.

Angiotensin II↗
PubMed1999

Isolation of Malassezia furfur from a cat.

During a survey of the occurrence of Malassezia species in the external ear canals of cats without otitis externa, Malassezia furfur was isolated. This is the first report of the isolation of M. furfur from cats.

Animals↗
PubMed1997

Altered vascular function in early stages of heart failure in hamsters.

BACKGROUND: Congestive heart failure is a clinical condition associated with alterations in the normal balance of neurohumoral agents and factors acting on the vascular wall. The etiology of this condition, however, remains largely undefined. To help elucidate the pathophysiology of this disease, vascular function and angiotensin-converting enzyme activity were evaluated in 2-month-old Syrian cardiomyopathic hamsters (SCHs) that had not yet developed heart failure. Age-matched normal hamsters were used as control hamsters. METHODS AND RESULTS: Vascular function studies included determinations of contractile responses of aortic rings to 0.1 microM angiotensin II and 0.1 microM norepinephrine. In addition, endothelial function was evaluated by the vasorelaxant action of acetylcholine on norepinephrine-precontracted aortic rings. The results indicate that the pressor effect of angiotensin II (0.1 microM) was 35% greater in aortic rings from SCRs than that observed in control animals. This effect is specific for angiotensin II because the contraction induced by NE (0.1 microM) was similar in both of these strains. Angiotensin-converting enzyme activity was three-fold higher in aorta homogenates from SCHs but normal in plasma and heart tissue when compared with control hamsters. Aortic ring preparations from SCHs also exhibited endothelial dysfunction because the maximal relaxation elicited by 10 microM acetylcholine was reduced 53%. Concentration-response curves with acetylcholine yielded EC50 values that were threefold lower in SCHs (97.2 +/- 0.1 nM) than in control animals (286 +/- 7 nM). Indomethacin (1 microM) increased the vasorelaxant effect of acetylcholine 28% in SCHs and shifted to the left the concentration-response curve of this agonist, suggesting an increased relaxation with the cyclooxygenase inhibitor. No effect of indomethacin on acetylcholine-induced relaxation was observed in control animals. Sodium nitroprusside induced similar relaxations in both control animals and SCHs, suggesting that the vascular smooth muscle response is normal in SCR. CONCLUSIONS: Altogether these results point to a state of enhanced vascular contractility in young SCHs that could predispose these animals to develop heart failure, the enhanced vascular contractility could result from increased activity of the local renin-angiotensin system, augmented vascular response to angiotensin II, reduced nitric oxide synthesis, and enhanced production of prostaglandins.

Animals↗
PubMed1996

Endothelial dysfunction in the San Juan hypertensive rat: possible role of the nitric oxide synthase.

Endothelial dysfunction is recognized as a critical event in the etiology of cardiovascular diseases, but its possible role during aging in arterial hypertension remains poorly defined. We evaluated the response of aortic rings precontracted with 0.1 microM norepinephrine (NE) to acetylcholine (ACh) in the San Juan hypertensive rats (SJH-Rs) (F19, F20) and Munich Wistar rats (MW). SJH-Rs is a model of inbred salt-sensitive hypertension, whereas similarly treated inbred MW rats are their normotensive counterpart. These experiments were performed with adult (6-7 months) and aged (11-13 months) rats to assess the effects of age and hypertension on endothelium-dependent relaxation. We generated dose-response curves by adding cumulative doses of ACh from 1.0 nM to 10.0 microM. In addition, we evaluated the Ca(2+)-dependent nitric oxide synthase (NOS) activity by increasing cell calcium with the ionophore A23187. The results indicate that hypertension induces a displacement to the right of the dose-response curve to ACh in both adults and aged SJH-Rs; IC50 for adult rats was 0.72 +/- 0.3 microM for SJH-Rs and 0.059 +/- 0.03 microM for MW (p < 0.05). Aged animals showed similar results: IC50 of 0.78 +/- 0.03 microM for SJH-Rs and of 0.043 +/- 0.01 microM in age-matched MW rats (p < 0.025). However, no difference was observed between hypertensive (SJH-Rs) adult and aged animals. Similarly, no difference was observed between adult and aged MW control animals. The displacement of the dose-response curve to ACh in SJH-Rs appears to be associated with a reduced activation of NOS since in precontracted aortas from aged animals 1 microM A23187 induced a relaxation of 51.2 +/- 12% in MW as compared with 34.4 +/- 7% in SJH-Rs (n = 5, p < 0.05). These results indicate that endothelial dysfunction exists in SJH-Rs. The data suggest that an alteration of the endothelial NOS may be the cause of this abnormality. Finally, the magnitude of the endothelial dysfunction is not age dependent within the range evaluated.

Acetylcholine↗
PubMed1996

Inhibition of smooth muscle cell calcium mobilization and aortic ring contraction by lactone vastatins.

OBJECTIVE: To determine the effects of vastatins on the contraction of rat aortic rings and to assess their effects on calcium mobilization using cultured smooth muscle cells from rat aorta. METHODS: Aortic rings from Sprague-Dawley rats were mounted on stainless steel wires to determine the generation of tension using force-displacement transducers. The tension (g) developed by angiotensin II (100 nmol/l) was measured under basal conditions and after 45 min incubation with 20 micromol/l simvastatin. The effect of 20 mol/l simvastatin, lovastatin, mevastatin and pravastatin on noradrenaline concentration-response curves and the angiotensin II-induced calcium mobilization was also evaluated. RESULTS: Addition of angiotensin II to aortic rings incubated in Krebs' Ringer bicarbonate medium produced tension generation (0.9 +/- 0.12 g = 100%). Treatment of aortic rings with simvastatin inhibited the angiotensin II-induced contraction 58 +/- 0.06%. To evaluate this effect further, dose-response curves with noradrenaline were measured in the presence and absence of 20 micromol/l simvastatin, lovastatin, mevastatin and pravastatin. The results indicate that simvastatin, lovastatin and mevastatin inhibited the contraction induced by noradrenaline (10 micromol/l) by about 50%. Pravastatin did not inhibit aortic ring contraction. Furthermore, the concentration required for 50% of the maximal contraction (EC50) by noradrenaline (6.2 +/- 0.1 nmol/l) was significantly increased by simvastatin, lovastatin, mevastatin and pravastatin. The inhibition of vascular contraction by vastatins appears to involve inhibition of 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase activity because the inhibitory effect of simvastatin was reduced 50% by 10 mmol/l mevalonic acid. To determine whether the depression of vascular contraction by these agents was correlated with cell calcium changes, the angiotensin II-induced calcium mobilization was determined in Fura-2 loaded cells, before and after treatment with these inhibitors. Simvastatin, lovastatin and mevastatin significantly reduced the angiotensin II-induced calcium mobilization. The concentration that induced 50% inhibition was 3.3 micromol/l for simvastatin, 17.4 micromol/l for mevastatin and 21.7 micromol/l for lovastatin. No effect of pravastatin on calcium mobilization was observed. CONCLUSIONS: These findings suggest that lactone vastatins depress vascular contraction by reducing cytosolic calcium release in vascular smooth muscle cells. These agents also appear to exert competitive and non-competitive type antagonisms on noradrenaline action.

Angiogenesis Inhibitors↗
PubMed1995

Cardiac refractoriness in rats is reduced by angiotensin II.

We investigated the effect of angiotensin II (AII) on cardiac refractoriness in muscle trabeculae isolated from adult rat ventricle. Strength-interval curves were initially obtained under control conditions and after exposure of the muscle to Tyrode's solution containing 10(-9) M AII. AII displaced the strength-interval curves to the left. The minimal current intensity needed to elicit a propagated response was reduced by AII for all intervals used. The effect of AII was not influenced by propranolol 10(-6) M or phentolamine 10(-7) M but was blocked by 250 microM DuP 753. No change in resting potential was observed with 10(-9) M AII, but action potential duration at 50% APD50 of its amplitude was reduced by 25% and conduction velocity was appreciably decreased (41%). The effect of the peptide on APD was blocked by DuP 753. Spontaneous discharges of APs were elicited by a single stimulus in fibers exposed to 10(-9) M AII, supporting the view that AII has an arrhythmogenic action.

Action Potentials↗
PubMed1993

Effect of enalapril on intracellular resistance and conduction velocity in rat ventricular muscle.

The effect of enalapril on the intracellular resistance (ri) and conduction velocity was investigated in isolated rat trabeculae. The results indicated a decline in the internal resistance of 35.5% (SE +/- 3.3) and an increase in conduction velocity of 58.7% (SE +/- 6.6). The action potential duration was not altered, but the resting potential was increased by 10.5 mV (SE +/- 4.4). Enalaprilat had no effect on ri probably because the molecule is a diacid and does not cross the cell membrane. These findings indicate that the renin-angiotensin system is involved in the modulation of cell communication in cardiac muscle and that the beneficial effect of the drug in patients with congestive heart failure is, in part, related to an improvement of electrical synchronization of heart cells.

Action Potentials↗