Involvement of K(ATP) channels in diethylstilbestrol-induced relaxation in rat aorta.

The estrogens prevent cardiovascular diseases that among other effects could be related to the modulation of the vascular tone via modifying ionic channel permeability. ATP-sensitive K(+) (K(ATP)) channels seem to be involved in diethylstilbestrol-induced relaxation in isolated rat aorta precontracted by noradrenaline (30 nM), since the effect is inhibited by glibenclamide (1--10 microM), and 1 mM tetraethylammonium, but not by 30 mM tetraethylammonium or paxilline. The antiestrogen tamoxifen, the inhibitor of protein kinase A, Rp-cAMPS, and the inhibitor of ornithine decarboxylase, difluoromethylornithine, antagonized diethylstilbestrol-induced relaxation. The association of glibenclamide with these compounds separately did not modify the effect of glibenclamide alone on diethylstilbestrol-induced relaxation. Functional K(ATP) channels are present in rat aorta, since diazoxide induced relaxation sensitive to glibenclamide. Papaverine, dibutyryl cyclic AMP and spermine relaxed isolated rat aorta although this was not sensitive to glibenclamide. The relaxation to forskolin was antagonized by glibenclamide. We conclude that diethylstilbestrol-induced relaxation in rat aorta is related to the modulation of K(ATP) channels. Cyclic AMP-dependent mechanisms and polyamine synthesis may mediate this modulation.

Mechanisms involved in UTP-induced contraction in isolated rat aorta.

The mechanisms of UTP-induced contractions in the rat aorta strips were studied. These were only partially inhibited in a Ca(2+)-free medium or by incubation with verapamil or nifedipine. Successive challenges did not decrease the magnitude of the contraction in the absence of external Ca(2+). Quin 2(acetoxymethyl) ester (Quin 2AM), 8-(N,N-diethylamino)octyl 3,4,5-trimetoxybenzoate (TMB-8), thapsigargin and ryanodine inhibited these contractions. The participation of protein kinase C is also very likely, since downregulation by the phorbol 12,13 dibutyrate (PDB) decreased UTP-induced contraction, and staurosporine and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) antagonized UTP-induced contractions and relaxed UTP-induced tonic contractions. Therefore, different pools of intracellular Ca(2+) and protein kinase C seem to participate in UTP-induced contraction and in the mechanisms of maintenance in a Ca(2+)-free medium.

Role of genomic mechanisms on cAMP-dependent positive inotropism in isolated left atrium of rat.

It is well known that beta-adrenoceptor stimulation induces positive inotropism by cAMP-dependent phosphorylation of cardiac calcium channels. Furthermore, hypertrophy of different tissues including the heart have been related to the stimulation of these adrenoceptors via mechanisms coupled to activation of transcription and protein synthesis. Early effects of isoproterenol mediated via this pathway has also been associated to the stimulation of beta-adrenoceptors. However, the effects on the inotropism through genomic mechanisms have not yet been described. Isoproterenol (3 nM to 3 microM) induced a concentration-dependent positive inotropism, in isolated left atrium of male Wistar rats electrically stimulated (0.5 Hz, 5 ms, 30-50% above the threshold voltage), which was antagonized by atenolol (1 microM) and inhibited by a protein kinase A inhibitor, (R)p-cAMPS (10 microM). The inhibitor of transcription, actinomycin D (4 microM), and the protein synthesis inhibitor, cycloheximide (35.5 microM), significantly decreased the positive inotropism induced by isoproterenol. Forskolin (0.1 to 3 microM), an activator of adenylyl cyclase, induced a concentration-dependent positive inotropism which was also inhibited by (R)p-cAMPS, actinomycin D and cycloheximide. In the left atrium of rat, isoproterenol induced a positive inotropism which seems, at least in part, dependent upon intact transcription and protein synthesis, as suggested by the fact that the response was inhibited by the incubation with actinomycin D and cycloheximide. In addition, this genomic effect seems to be mediated by a cAMP-dependent mechanism. As it was inhibited by a protein kinase A inhibitor ((R)p-cAMPS) and similarly to isoproterenol, the positive inotropism induced by forskolin, which increases cytosolic cAMP, was also inhibited by actinomycin D and cycloheximide.

Pharmacological evidence for a receptor mediating sustained nucleotide-evoked contractions of rat aorta in the presence of UTP.

The contractile effect of ATP given alone or in the presence of other nucleotides was studied in rat aortic strips. A sustained contraction in response to ATP (30 microM to 10 mM) was observed during UTP exposure instead of the fast transient contraction produced via P2x purinoceptor activation in the absence of UTP, and contrary to the relaxation elicited when the tone had been raised by noradrenaline and KCl. This sustained ATP effect was produced in the smooth muscle and not via the same mechanism through which UTP elicited contraction, since the contractions in response to UTP and ATP were additive. They were also coupled to different transduction pathways: the effect of UTP but not that of ATP was pertussis toxin-sensitive. In contrast to the fast transient ATP contraction during basal tone, the sustained response was not desensitized by alpha,beta-methylene ATP exposure (30 microM), but was inhibited by reactive blue 2 (10 and 30 microM). Among the nucleotides assayed, UDP and ATPgammaS also enabled ATP to elicit a sustained contraction. ADP, AMP, dATP, 2-methylthio ATP, alpha,beta-methylene ATP, GTP, GDP, GMP, CTP and ITP also induced a sustained contraction in the presence of UTP. However, adenosine (1 mM) and adenine (0.3 to 3 mM) induced relaxation when the tone had been raised by UTP. According to these results a non-selective nucleotide receptor, different from the P2 purinoceptors functionally characterized so far, seems to mediate sustained contractions in rat aortic strips in the presence of UTP, UDP or ATPgammaS.

Severe uremia depresses the ability of perifused rat pituitary cells to secrete growth hormone in response to growth hormone releasing hormone.

To examine whether growth hormone (GH) secretion is impaired by chronic renal failure (CRF) and to gain some insight into the influence of uremia itself and associated malnutrition, the GH secretory response of dispersed anterior pituitary cells perifused with GH-releasing hormone (GHRH) was investigated in 5/6 nephrectomized (UREM, N = 15) and three groups (N = 15 each) of normal renal function, sham-operated rats under three different nutritional conditions: fed "ad libitum" (SAL), pair-fed with a diet similar to the UREM group (SPF), and pair-fed with a diet similar to the UREM group in terms of protein ingestion but calorically supplemented up to intake of SAL group (SPF+). Ten days after nephrectomy, UREM rats had severe CRF, as shown by much higher (P < 0.0001) serum urea nitrogen concentrations (X +/- mean +/- SE) than sham groups (59 +/- 6 versus 8 +/- 0, 9 +/- 0, and 5 +/- 0 mmol/L, respectively), and they were growth retarded, as shown by lower gains (P < 0.0001) in weight (13.5 +/- 2.5 versus 62 +/- 2.1, 20.5 +/- 1.9, and 50.4 +/- 1.0 g) and length (2.9 +/- 0.2 versus 5.8 +/- 0.1, 3.6 +/- 0.1, and 5.6 +/- 0.1 cm). Perifusion studies showed similar basal GH secretory rate (ng/min/10(7) cells) in the four groups. A fixed sequence of progressively increasing GHRH doses resulted in a lower overall mean GH secretion in UREM rats (15.8 +/- 1.6 ng/min/10(7) cells), as compared with SAL (50.8 +/- 9.0 ng/min/10(7) cells, P < 0.01), SPF (33.0 +/- 3.3 ng/min/10(7) cells, P < 0.05), and SPF+ (49.4 +/- 5.1 ng/min/10(7) cells, P < 0.01) groups. Analysis of dose-response curves showed that the maximal secretory response was produced by the same concentration of GHRH (10 nM) in the four groups and was lower (P < 0.01) in UREM than SAL and SPF+ rats (34.9 +/- 5.0 versus 115.7 +/- 28.4 and 98.9 +/- 9.8 ng/min/10(7) cells). The concentration of GHRH that caused the half of maximal effect was identical, close to 1 nM, in the four groups of animals. This study provides direct evidence that the ability of pituitary cells to secrete GH in response to GHRH is depressed in severe CRF. The lower secretory capacity of pituitary gland is only partly dependent on caloric malnutrition associated with CRF. Data of dose-response curves suggest that decreased GH secretion may be related to a lesser number of pituitary receptors for GHRH.

Role of cyclic nucleotides in contraction induced by oxytocin in the testicular capsule of the rat in vitro.

The effects of phosphodiesterase inhibitors, an activator and an inhibitor of guanylyl cyclase, and cAMP and cGMP analogs on oxytocin-induced contractions have been studied in the testicular capsule of rats. The nonspecific phosphodiesterase inhibitors, theophylline and caffeine, attenuated the oxytocin-induced contractions via mechanisms that seem to be related to an increase in cAMP levels, since a similar effect was produced by dibutyryl cAMP. Sodium nitroprusside facilitated oxytocin-induced contractions. This effect was mimicked by dibutyryl cGMP. Methylene blue, an inhibitor of soluble guanylyl cyclase, decreased oxytocin-induced contractions, which suggests an involvement of guanylyl cyclase in the oxytocin effect. These results suggest that cAMP modulates the contraction and that cGMP, contrary to what happens in most smooth muscles, could participate in oxytocin-induced contractions in the testicular capsule of rats.

Chronic renal failure and human growth hormone treatment do not modify endothelium-dependent reactions in the rat aorta in vitro.

1. Growth hormone (GH) increases glomerular filtration rate and renal plasma flow and decreases renal vascular resistance. Sustained GH-induced hyperfiltration might be undesirable in children with chronic renal failure (CRF) who are receiving recombinant human GH (rhGH) therapy. 2. In order to determine the effect of CRF on vascular reactivity and the modifications induced by rhGH administration, two endothelium-dependent effects, acetylcholine relaxation and decrease of contractile response to noradrenaline, were studied in aorta segments of various groups of male Sprague-Dawley rats: CRF rats (CRF, n = 8) with serum urea nitrogen (SUN) 68 +/- 16 mg dl-1 (mean +/- SEM), CRF rats treated with intraperitoneal rhGH at 10 IU kg-1 day-1 for 13 days (CRFGH, n = 6, SUN = 88 +/- 15 mg dl-1), sham operated rats (SHAM, n = 8, SUN: 21 +/- 1 mg dl-1) and control rats (CONTROL, n = 8, SUN 20 +/- 1 mg dl-1), housed in identical conditions but without undergoing surgical intervention or manipulation. CRF was induced by 5/6 two stage nephrectomy. 3. Rats were sacrificed and a segment of thoracic aorta was immediately removed, cut into spirals, and suspended in organ baths according to standard procedures. First, dose-response curves to noradrenaline and acetylcholine relaxation, in strips previously exposed to noradrenaline, were determined. Then, the endothelium was removed and both dose-response curves were repeated. Acetylcholine induced a greater relaxation, P < 0.05, in the aorta of CONTROL rats (82.6 +/- 6.1%) as compared with SHAM (60.3 +/- 4.7%), CRF (60.0 +/- 6.8%) and CRFGH (54.8 +/- 8.2%) rats. 4. Endothelium removal only caused a greater contractile response to noradrenaline (10(-9) and 3 x 10(-9)M) in the CONTROL group, P < 0.05. 5. No differences to acetylcholine and noradrenaline responses were found among the SHAM, CRF and CRFGH groups. 6. These results suggest that the endothelium-dependent vascular reactivity was modified by the experimental protocol to induce chronic renal failure but no further changes resulted from uraemia and rhGH treatment.

Mechanisms involved in the spasmolytic effect of extracts from Sabal serrulata fruit on smooth muscle.

1. The effects of two extracts from Sabal serrulata fruits [total lipidic (L) and saponifiable (S)] on smooth muscle contractions have been assayed. 2. Both extracts (0.1-1 mg/ml) relaxed the tonic contraction induced by norepinefrine (30 nM) on rat aorta [EC50, 0.53 +/- 0.05 mg/ml (L) and 0.5 +/- 0.04 mg/ml (S)] and by KCl (60 mM) on rat uterus. The Sabal extracts (0.3-1 mg/ml) also antagonized the dose-response curve of contractions induced by acetylcholine (0.1-100 microM) on urinary bladder. 3. dL-Propranolol (1 microM) but not the inactive (R)-(+)-propranolol(1 microM) potentiated the Sabal extracts relaxant effect by lowering the EC50 (0.35 +/- 0.2 vs 0.20 +/- 0.01 mg/ml for L and 0.43 +/- 0.02 vs 0.19 +/- 0.02 mg/ml, P < 0.01, for S extract). 4. Cycloheximide (10 micrograms/ml) antagonized the effect of extracts from Sabal. However, actinomycin D (5 micrograms/ml) significantly (P < or = 0.01) antagonized the effect of the total lipidic extract without modifying that of the saponifiable extract. 5. The relaxant effect of both extracts was not modified by the tyrosine kinase inhibitor genistein (10 microM) or the ornithine decarboxylase inhibitor alpha-difluoromethyl-ornithine (10 mM).

Mechanisms involved in the relaxant effect of estrogens on rat aorta strips.

The effects of estrogens 17beta-estradiol (17beta-E2), 17alpha-estradiol (17alpha-E2) and diethylstilbestrol (DES) on CaCl2 (3mM)-induced contractions on rat aorta strips have been assayed. Both 17alpha-E2 and DES, but not the 17beta-E2 relaxed and inhibited the contraction induced by CaCl2. The antiestrogen tamoxifen (0.1, 1 and 3 microM) antagonizes, in a concentration-dependent way, the relaxant effect of 17alpha-E2 but the relaxation induced by DES is only significantly antagonized with 3 microM of tamoxifen. Cycloheximide (0.1 and 0.3 mM) does not modify the 17alpha-E2 or DES effects. However, the inhibitors of cAMP-dependent protein kinase TPCK (1 microM) and Rp-cAMPS (10 microM) inhibit the relaxation induced by 17alpha-E2 and DES. The elimination of endothelium by rubbing, significantly inhibits the effect of DES but does not modify the effect of 17alpha-E2. Our results suggest that estrogen-induced relaxation is a non-genomic effect possibly or presumably produced by activation of estrogenic receptors and mediated by cAMP. The DES-effect is partially endothelium-dependent but the effect of 17alpha-E2 is independent of endothelium.

Pharmacological dissociation of UTP- and ATP-elicited contractions and relaxations in isolated rat aorta.

Effects of UTP have been described in many tissues, but it is not clear whether these are due to purinoceptors. Specific receptors for UTP, 'pyrimidinoceptors', and 'nucleotide receptors' have also been proposed. We pharmacologically characterized the receptors involved in the ATP- and UTP-induced contraction under basal tone and the relaxation of raised tone elicited by noradrenaline in isolated rat aorta. The rank order of potency for the agonists for the contraction was alpha,beta-methylene ATP > > ATP, and the desensitization by alpha,beta-methylene ATP suggests that ATP contractions were mediated via P2X purinoceptors which were located on the vascular smooth muscle. The rank order of potency of the agonists for relaxation was 2-methyl-thio ATP > > ATP, which is suggestive of a P2Y purinoceptor. However, the relaxation seems to be unrelated to the classical P2Y subtype and a heterogeneous population of purinoceptors might therefore exist. The evidence comes from the distinct location and the different pharmacological effect of reactive blue 2 on 2-methyl-thio ATP and ATP receptors. 2-Methyl-thio ATP produced an endothelium-dependent relaxation while ATP-induced relaxation was produced via endothelium-dependent and endothelium-independent mechanisms, unrelated to adenosine receptors. It is unlikely that UTP-induced contractions and the endothelium-dependent relaxation were produced via purinoceptors since the pharmacology is not consistent with that of the classical P2 purinoceptors studied. Furthermore, UTP-sensitive receptors showed a pharmacological property that was also distinct from that of the 'nucleotide' or P2U receptor reported. The results suggest the presence of a heterogeneous population of purinoceptors and pyrimidinoceptors pharmacologically different from the receptors for ATP.

Influence of hormonal status in relaxant effect of diethylstilbestrol and nifedipine on isolated rat uterus contraction.

1. The effects of diethylstilbestrol (DES, 10(-7)-10(-5) M) and nifedipine (10(-10)-10(-7) M) on KCl (60 mM)-induced tonic contraction in the uterus of ovariectomized and 17 beta-estradiol (0.1 mg/kg/day, s.c.)-, 17 alpha-estradiol (0.1 mg/kg/day, s.c.)-, or progesterone (2 mg/kg/day, s.c.)-treated rats have been assayed. 2. The dose-dependent relaxation produced by nifedipine in ovariectomized rats (EC50 = 5.59 +/- 1.25 x 10(-9) M) is potentiated in uterus of rats treated with 17 beta-estradiol and progesterone (EC50 = 0.59 +/- 0.1 and 0.49 +/- 0.1 x 10(-9) M, respectively) but not in the 17 alpha-estradiol-treated rats (3.01 +/- 0.6 x 10(-9) M). 3. The relaxation produced by DES on ovariectomized rats (EC50 = 0.84 +/- 0.14 x 10(-6) M) is reduced when the rats are treated with 17 beta-estradiol (EC50 = 2.22 +/- 0.2 x 10(-6)M) or progesterone (EC50 = 1.24 +/- 0.08 x 10(-6) M), but unmodified by 17 alpha-estradiol (EC50 = 0.58 +/- 0.01 x 10(-6) M). 4. The nifedipine-induced relaxation is reversed with Bay K 8644 (10(-10)-10(-6) M) in all experimental conditions. However, Bay K 8644 counteracted the relaxation of DES at 45.7% on ovariectomized rats but this was lower than 30% in the other groups. 5. Our results suggest that in ovariectomized rats the effects of both nifedipine and DES are similar, but 17 beta-estradiol and progesterone produce a contrary effect on the relaxation induced by nifedipine and DES (by increasing the nifedipine and decreasing the DES effects).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of preanesthetic and anesthetic drugs on endothelium-dependent responses in the rat aorta.

1. Acetylcholine often fails to induce endothelium-dependent relaxation in human vessels in vitro. Due to the fact that most of these vessels come from surgery, we examined the influence of drugs used in anesthesia on endothelium-dependent responses in rat aorta. 2. Groups of male Wistar rats of the following treatments were utilized: P group, diazepam+promethazine+atropine; I group, pentothal+succinylcholine; IG group, halothane+nitrous oxide; M group, morphine+pancuronium; C group, untreated rats. Dose-response curves to noradrenaline and acetylcholine were determined in rat aorta in vitro, in the presence and absence of endothelium. 3. Acetylcholine induced more relaxation (P < 0.05) in the rat aorta of IG group compared with that of the C group. 4. In the rat aorta from P and IG groups, the contractions produced by several concentrations of noradrenaline were significantly smaller (P < 0.05) when the endothelium was removed. Similar effects occurred in aorta strips of animals previously treated with either atropine, promethazine, cimetidine or halothane. 5. Our results suggest that drugs currently used in anesthesia interfere with some endothelium-dependent effects on isolated rat aorta but according to these results they do not seem to be responsible for the lack of acetylcholine relaxation sometimes described in human vessels in vitro.

Influences of age and sex on endothelium-dependent vascular responses and arterial blood pressure in the rat.

1. Vascular reactivity related to age and sex on two endothelium-dependent effects in isolated rat aorta (acetylcholine-induced relaxation and modulation of noradrenaline response) and blood pressure decreases by acetylcholine administration were studied. Group of male Wistar rats aged 2, 4, 8, 16 and 24 months plus female rats of 4 months were used. 2. Blood pressure was measured by using a standard tail-cuff technique. Acetylcholine in vivo administration (0.002 mg/kg i.v.) significantly reduced diastolic pressures in the 2 month old males and 4 month old females, but not in other age groups. 3. Isolated helical strips of rat aorta were used to determine the endothelium-dependent reactivity. The maximal relaxation from different groups of male rats induced by acetylcholine was: 100% in those of 2 months; 53.2 +/- 6.0% in those of 4 months; 61.8 +/- 6.1% in those of 8 months; 57.6 +/- 5.0% in those of 16 months and 31.0 +/- 4.9% in those of 24 months. Concentration-response curves to noradrenaline were significantly greater only when endothelial cells were removed from aorta strips of 2 month old rats. In aorta strips with endothelium the maximal contraction to noradrenaline was significantly greater in 2 month old rats when compared with the other groups and smaller in aorta strips from 24 month old rats. 4. These results suggest that the endothelium-dependent effects studied and the noradrenaline-induced contraction decreased according to the age of the rats.

Influence of mechanical endothelium removal techniques and conservation conditions on rat aorta responses.

Endothelial denudation of aortas induces a lack of relaxation to acetylcholine and enhancement of response to noradrenaline. These modified responses have been studied in rat aorta by using different techniques for mechanical removal of the endothelial layer and maintenance conditions. Rubbing the artery with cotton inside the organ bath preserves the enhancement of response to noradrenaline, and this effect is not present by rubbing the aortas with filter paper outside the organ bath. Both techniques abolished the relaxant response to acetylcholine. The endothelium dependent effects are not observed by conservation of the artery at room temperature during 1 h. The relaxant response to acetylcholine after this period is approximately 29% of the control. These effects were preserved when the conservation temperature was maintained at 4 degrees C and/or the solution was being bubbled with oxygen.

[Calcium dependence of the contractile response of the aorta in the rat, rabbit and guinea pig and in the human uterine artery]. / Dependencia del calcio de la respuesta contráctil de aorta de rata, conejo y cobaya y arteria uterina humana.

The influence of extracellular Ca2+ on the contraction produced by noradrenaline (NA) (3 x 10(-6) M), KCl (60 mM) and BaCl2 (30 mM) on human uterine arteries (AUH) and aortic strips from rats, rabbits and guinea-pigs have been studied. The vessels were cut spirally and incubated in Krebs solution containing 2.5 mM Ca2+ (KN), 0 mM Ca2+ (K-0Ca) or 0 mM Ca2+ + 3 mM EDTA (K-EDTA). Both phases (fast and slow) of the response of aortic strips to NA and of the AUH to NA, KCl and BaCl2 were significantly smaller in solutions without Ca2+. Only in rabbit aortic strips the slow phase was significantly more reduced than the fast phase. Overall, the contractions of the rat aortic strips were most resistant to the absence of extracellular Ca2+. These results confirm the variability of the responses of blood vessels from different vascular beds and species to the removal of extracellular Ca2+.

Effects of tyramine on the human uterine artery in vitro.

1. We have studied the effects of tyramine on the human uterine artery (HUA) in order to assess its site of action. 2. Tyramine (5 x 10(-5) to 10(-3) M) contracts the isolated human uterine artery. Tachyphylaxis appeared when concentration-response curves were repeated and the contraction was diminished by prazosin (10(-8), 10(-7) and 10(-6) M). The maximal contraction induced by tyramine (10(-3) M) was 25% of the maximal response to noradrenaline (10(-5) M). 3. After 2 hr of tyramine perfusion a decrease of the contractile response to KCl, 30 and 60 mM (15.0 and 12.9%) and noradrenaline 10(-6) M (83.2%) is shown. 4. However, when tyramine was previously added for 3 min to the bath, the response to KCl increased while the response to noradrenaline was lower. 5. A possible postsynaptic antagonistic effect for tyramine in the HUA is suggested in addition to its usual presynaptic effect.

Effects of verapamil and nifedipine on human uterine artery "in vitro".

We have studied, in isolated human uterine arteries, the effects of verapamil and nifedipine on the contractions induced by noradrenaline (NA) and KCl in standard Krebs and those produced by CaCl2 and NA added to a free-calcium medium (128.5 mM K+). Both calcium antagonists reduce in a dose-dependent way the contractions induced by NA, KCl and CaCl2. Smaller doses of nifedipine were needed to produce the same inhibitory effects. The maximal doses of calcium antagonists utilized had no effect on the contractions induced by NA when the calcium was removed from the medium. NA, in equal doses, had similar contractile effect whether after incubation with the maximal doses of verapamil and nifedipine or in a calcium-free medium. The inhibitory effects produced by verapamil and nifedipine are only adequately explained by a blockage of the entry of calcium. Other intracellular changes do not seem to play a role in this case.

[Characterization of beta-2 adrenergic receptors in the human uterine artery]. / Caracterización de receptores adrenérgicos beta-2 en arteria uterina humana.

The actions of the hexoprenaline, salbutamol and terbutaline on adrenalin-induced effects in the human artery were studied in vitro. The human uterine artery has a two-part response to adrenalin: The first, rapid (phasic component), and the second, slow and sustained (tonic component). Both beta-2 stimulators relax the tonic component and reduced the amplitude of the phasic component. The depressor effect of the responses to adrenalin is reduced in the presence of butoxamine and intensified in the presence of caffeine. These results suggest the existence on the human uterine artery of beta-2 adrenergic receptors acting as mediators of smooth muscle relaxation, and suggest also that the mechanism of this relaxation is most likely cAMP dependent.

[Different behavior of the rat vas deferens of castrated animals and those treated with cyproterone acetate]. / Diferente comportamiento del conducto deferente de rata de animales castrados y tratados con acetato de ciproterona.

The effects of castration and treatment with the antiandrogen cyproterone acetate (CPA) on the responses of the vas deferens of the rat induced by phenylephrine, KCl and BaCl2 has been studied. Both castration and CPA induced a spontaneous motility in the rat vas deferens. Castration produces a decrease of the response amplitude induced by phenylephrine and KCl and an increase of those induced by BaCl2 in animals killed 30 days after castration. CPA increases the response amplitude induced by phenylephrine and KCl without modifying those induced by BaCl2. These results suggest that the antiandrogen CPA produces modifications qualitatively different from castration.