Search

OBJETIVO: Realizar un diagnóstico sobre cómo se desarrolla la comunicación asertiva, para mejorar el clima laboral y eficientar los procesos dentro de las organizaciones públicas MATERIAL Y MÉTODO: Esta investigación es descriptiva, con un enfoque: cualitativo, tomando en consideración las variables del clima laboral. Los datos obtenidos, se llevaron a cabo por medio de la aplicación de encuestas, las cuales se analizaron de acuerdo a las respuestas proporcionadas por la población. RESULTADOS: Se obtuvo como resultado que una parte de los encuestados dijo que sí se da la comunicación y otra parte mencionó que no se siente satisfecho, ni motivado, reconocido y que el clima laboral no es tan agradable. CONCLUSIONES: El clima laboral en las organizaciones es base fundamental para el desempeño de las personas, que se sientan confiadas, valoradas, motivadas, reconocidas, todo esto se verá reflejado en la producción de su organización, en el caso de las instituciones públicas o gubernamentales lo sentirán los usuarios o beneficiarios de los derechos fundamentales.

Purpose. This study investigates whether functionality and/or expression changes of transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential ankyrin 1 (TRPA1) channels, oxidative stress, and hydrogen sulfide (H2S) are involved in the bladder dysfunction from an insulin-resistant obese Zucker rat (OZR). Materials and Methods. Detrusor smooth muscle (DSM) samples from the OZR and their respective controls, a lean Zucker rat (LZR), were processed for immunohistochemistry for studying the expression of TRPA1 and TRPV1 and the H2S synthase cystathionine beta-synthase (CBS) and cysthathionine-γ-lyase (CSE). Isometric force recordings to assess the effects of TRPA1 agonists and antagonists on DSM contractility and measurement of oxidative stress and H2S production were also performed. Results. Neuronal TRPA1 expression was increased in the OZR bladder. Electrical field stimulation- (EFS-) elicited contraction was reduced in the OZR bladder. In both LZR and OZR, TRPA1 activation failed to modify DSM basal tension but enhanced EFS contraction; this response is inhibited by the TRPA1 blockade. In the OZR bladder, reactive oxygen species, malondialdehyde, and protein carbonyl contents were increased and antioxidant enzyme activities (superoxide dismutase, catalase, GR, and GPx) were diminished. CSE expression and CSE-generated H2S production were also reduced in the OZR. Both TRPV1 and CBS expressions were not changed in the OZR. Conclusions. These results suggest that an increased expression and functionality of TRPA1, an augmented oxidative stress, and a downregulation of the CSE/H2S pathway are involved in the impairment of nerve-evoked DSM contraction from the OZR.

Como muchas ciudades latinoamericanas, Buenos Aires, durante la década de 1990, fue escenario de una serie de cambios vertiginosos que se asociaron, con mayor o menor énfasis, al imperativo de entrar en un escenario global. Zonas que décadas atrás eran orgullo de la metrópolis y donde el auge constructor del siglo XIX había afincado el poderío de un Estado-Nación en crecimiento comenzaron a ser abandonadas en favor de barrios nuevos o reciclados que insinuaban una impronta estética y cultural. El neoliberalismo imprimió de esta manera sus signos en la ciudad: se produjo la formación, mpulsada por el Estado, de nuevos barrios (como Puerto Madero), el reciclaje de otros con una activa vida previa y en manos de emprendimientos privados (el barrio porteño de Palermo), el surgimiento de shoppings basados en la reconversión de antiguas estructuras industriales abandonadas, entre otros ejemplos. Después de la gran crisis argentina del año 2001, estos procesos fueron inscriptos en una oposición que sugería una ruptura entre la década neoliberal de los noventa y la década siguiente. Este artículo sostiene, por el contrario, que existe una continuidad cultural entre ambas décadas y que esa continuidad se expresa en la perpetuación y potenciación de espacios denominados "globales" y en las prácticas de consumo cultural que los caracterizan. As many cities in Latin America, during the 1990s Buenos Aires City was the scene of various dizzyng changes associated, with greater or lesser emphasis, to the imperative of entering on a global stage. Some areas that decades ago were the reason of the metropolis' pride, and where the nineteenth century, through the urban boom, had installed a symbol of the power of the emerging nation-state, began to be abandoned in favor of new or recycled neighborhoods that revealed an aesthetic or cultural mark. In this way, the neoliberalism succeeded in printing its signs in the city: the setting-up of new neighborhoods (Puerto Madero, for example); the recycling of other existing neighborhoods by private actions (Palermo), the emergence of shopping malls situated in converted old and abandoned structures, and so on. After the great argentinian crise in 2001, these processes were integred into an emphasized opposition that suggested a breakdown between the "neoliberal decade" (the 1990s) and the following decade. This article proposes, on the contrary, that it is a cultural continuity between the 1990s and the 2000s city, and suggests that this continuity is expressed in the perpetuation and empowerment of spaces called "global spaces", as well as it is expressed in some urban practices associated to the cultural consummerism.

Aims Neuronal and non-neuronal bradykinin (BK) receptors regulate the contractility of the bladder urine outflow region. The current study investigates the role of BK receptors in the regulation of the smooth muscle contractility of the pig intravesical ureter. Methods Western blot and immunohistochemistry were used to show the expression of BK B1 and B2 receptors and myographs for isometric force recordings. Results B2 receptor expression was consistently detected in the intravesical ureter urothelium and smooth muscle layer, B1 expression was not detected where a strong B2 immunoreactivity was observed within nerve fibers among smooth muscle bundles. On ureteral strips basal tone, BK induced concentration-dependent contractions, were potently reduced by extracellular Ca2+ removal and by B2 receptor and voltage-gated Ca2+ (VOC) channel blockade. BK contraction did not change as a consequence of urothelium mechanical removal or cyclooxygenase and Rho-associated protein kinase inhibition. On 9,11-dideoxy-9a,11a-methanoepoxy prostaglandin F2α (U46619)-precontracted samples, under non-adrenergic non-cholinergic (NANC) and nitric oxide (NO)-independent NANC conditions, electrical field stimulation-elicited frequency-dependent relaxations which were reduced by B2 receptor blockade. Kallidin, a B1 receptor agonist, failed to increase preparation basal tension or to induce relaxation on U46619-induced tone. Conclusions The present results suggest that BK produces contraction of pig intravesical ureter via smooth muscle B2 receptors coupled to extracellular Ca2+ entry mainly via VOC (L-type) channels. Facilitatory neuronal B2 receptors modulating NO-dependent or independent NANC inhibitory neurotransmission are also demonstrated.

Metabolic syndrome (MS) is a known risk factor for lower urinary tract symptoms. This study investigates whether functional and expression changes of cannabinoid CB1 and CB2 receptors are involved in the bladder dysfunction in an obese rat model with insulin resistance. Bladder samples from obese Zucker rat (OZR) and their respective controls lean Zucker rat (LZR) were processed for immunohistochemistry and western blot for studying the cannabinoid receptors expression. Detrusor smooth muscle (DSM) strips from LZR and OZR were also mounted in myographs for isometric force recordings. Neuronal and smooth muscle CB1 and CB2 receptor expression and the nerve fiber density was diminished in the OZR bladder. Electrical field stimulation (EFS) and acetylcholine (ACh) induced frequency- and concentration-dependent contractions of LZR and OZR DSM. ACh contractile responses were similar in LZR and OZR. EFS-elicited contractions, however, were reduced in OZR bladder. Cannabinoid receptor agonists and antagonists failed to modify the DSM basal tension in LZR and OZR In LZR bladder, EFS responses were inhibited by ACEA and SER-601, CB1 and CB2 receptor agonists, respectively, these effects being reversed by ACEA plus the CB1 antagonist, AM-251 or SER-601 plus the CB2 antagonist, AM-630. In OZR bladder, the inhibitory action of ACEA on nerve-evoked contractions was diminished, whereas that SER-601 did not change EFS responses. These results suggest that a diminished function and expression of neuronal cannabinoid CB1 and CB2 receptors, as well as a lower nerve fiber density is involved in the impaired excitatory neurotransmission of the urinary bladder from the OZR.

Background and purpose: The aim of the current study was to investigate the role of arachidonic acid (AA) metabolism via cyclooxygenase (COX) in the endothelial dysfunction of penile arteries from pre-diabetic, obese Zucker rats (OZR). Experimental approach: Penile arteries from OZR and from lean Zucker rats (LZR) were mounted in microvascular myographs to assess vascular function and COX expression was determined by immunohistochemistry. Key results: Acetylcholine (ACh) and AA elicited relaxations that were impaired in arteries from OZR. Inhibition of both COX-1 and COX-2 reduced the relaxant effects of ACh and AA in LZR but not in OZR. Inhibitors of COX-1 and of the TXA2/PGH2 (TP) receptor enhanced the relaxations induced by AA in both LZR and OZR, whereas COX-2 inhibition enhanced these responses only in OZR. TP receptor blockade did not restore ACh relaxant responses in arteries from OZR. Inhibition of COX-1 increased basal tension in OZR and this contraction was blunted by TP receptor blockade. The vasoconstrictor responses to noradrenaline were augmented by indomethacin and by COX-2 inhibition in LZR but not in OZR. Immunohistochemical staining showed that both COX-1 and COX-2 are expressed in the endothelium of penile arteries from both LZR and OZR. Conclusions and implications: Vasoactive prostanoids were formed via constitutively active COX-1 and COX-2 pathways in normal rat penile arteries. Under conditions of insulin resistance, the release and/or effects of vasodilator prostanoids were impaired, contributing to the blunted endothelium-dependent vasodilatation and to the enhanced vasoconstriction.

BACKGROUND AND PURPOSE 5-Hydroxytryptamine (5-HT) is one of the inhibitory mediators in the urinary bladder outlet region. Here we investigated mechanisms involved in 5-HT-induced relaxations of the pig bladder neck. EXPERIMENTAL APPROACH Urothelium-denuded strips of pig bladder were mounted in organ baths for isometric force recordings of responses to 5-HT and electrical field stimulation (EFS). KEY RESULTS After phenylephrine-induced contraction, 5-HT and 5-HT receptor agonists concentration-dependently relaxed the preparations, with the potency order: 5-carboxamidotryptamine (5-CT) > 5-HT = RS67333 > (+/-)-8-hydroxy-2-dipropylaminotetralinhydrobromide > m-chlorophenylbiguanide > alpha-methyl-5-HT > ergotamine. 5-HT and 5-CT relaxations were reduced by the 5-HT(7) receptor antagonist (2R)-1-[(3-hydroxyphenyl)sulphonyl]-2-[2-(4-methyl-1-piperidinyl)ethyl]pyrrolidine hydrochloride and potentiated by (S)-N-tert-butyl-3-(4-(2-methoxyphenyl)-piperazin-1-yl)-2-phenylpropanamide dihydrochloride (WAY 100135) and cyanopindolol, 5-HT(1A) and 5-HT(1A/1B) receptor antagonists respectively. Inhibitors of 5-HT(1B/1D), 5-HT(2), 5-HT(2B/2C), 5-HT(3), 5-HT(4), 5-HT(5A) and 5-HT(6) receptors failed to modify 5-HT responses. Blockade of monoamine oxidase A/B, noradrenergic neurotransmission, alpha-adrenoceptors, muscarinic and purinergic receptors, nitric oxide synthase, guanylate cyclase and prostanoid synthesis did not alter relaxations to 5-HT. Inhibitors of Ca(2+)-activated K(+) and ATP-dependent K(+) channels failed to modify 5-HT responses but blockade of neuronal voltage-gated Na(+)-, Ca(2+)- and voltage-gated K(+) (K(v))-channels potentiated these relaxations. Adenylyl cyclase activation and cAMP-dependent protein kinase (PKA) inhibition potentiated and reduced, respectively, 5-HT-induced responses. Under non-adrenergic, non-cholinergic, non-nitrergic conditions, EFS induced neurogenic, frequency-dependent, relaxations which were resistant to WAY 100135 and cyanopindolol. CONCLUSIONS AND IMPLICATIONS 5-HT relaxed the pig urinary bladder neck through muscle 5-HT(7) receptors linked to the cAMP-PKA pathway. Prejunctional 5-HT(1A) receptors and K(v) channels modulated 5-HT-induced relaxations whereas postjunctional K(+) channels were not involved in such responses. 5-HT(7) receptor antagonists could be useful in the therapy of urinary incontinence produced by intrinsic sphincter deficiency.

The present study was designed to characterize the neurogenic contraction of rat radial artery. Electrical field stimulation (EFS) evoked frequency-dependent contraction that was abolished by tetrodotoxin (neuronal Na+ channel blocker), guanethidine (sympathetic neuron blocker), or phentolamine (α-adrenoceptor blocker). The α1-adrenoceptor antagonist prazosin inhibited endothelium-independent contractions to EFS, noradrenaline (NA), and the α1-adrenoceptor agonist phenylephrine. Rauwolscine, an α2-adrenoceptor antagonist, augmented nerve-mediated contractions and reduced sensitivity to NA and the α2-adrenoceptor agonist BHT-920. The β-adrenoceptor antagonist propranolol diminished EFS-elicited contractions, while sensitivity to NA was enhanced by propranolol. Relaxations evoked by isoproterenol, a β-adrenoceptor agonist, were abolished by propranolol. NG-Nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, increased both nerve-mediated and NA-induced responses in endothelium-intact, but not in endothelium-denuded arteries. Moreover, endothelium-dependent responses to BHT-920 and isoproterenol were modified by L-NOARG. Tetraethylammonium (TEA) or 4-amynopyridine, the Ca2+-activated (KCa) or voltage-dependent K+ (KV) channel blockers, respectively, enhanced the neurogenic contractions observed. TEA but not 4-amynopyridine increased NA-induced contractions. The ATP-sensitive K+ (KATP)–channel blocker glibenclamide failed to modify adrenergic contractions. Blockade of capsaicin-sensitive primary afferents increased EFS-induced contractions. In conclusion, adrenergic contractions are predominantly mediated by muscular α1-adrenoceptors, while endothelial α2- and β-adrenoceptors play a minor role. Presynaptic α2- and β-adrenoceptors cannot be precluded. Noradrenergic neurotransmission in rat radial artery seems to be modulated by both stimulation of endothelial NO, KCa, and KV channels and sensory C-fiber activation. Keywords:: rat radial artery, electrical field stimulation, adrenergic receptor, nitric oxide, K+ channel

Recent studies have suggested that endogenous vasopressin (AVP) acts as a spasmogen during coronary artery bypass grafting (CABG). Given that AVP could induce vasospasm in the grafted vessel, we assessed the release of this peptide during and after CABG, and explored ways of counteracting its contractile effect on the internal mammary artery (IMA).Plasma levels of AVP were determined by radioimmunoassay in 16 patients before, during and after CABG. Using isometric force recording techniques, we also investigated the mechanisms involved in the contractile effect of AVP in ring preparations of IMA specimens taken from 95 patients.Plasma AVP levels peaked after the start of cardiopulmonary bypass (CPB) and correlated well with serum osmolality (Pearson's r=0.9490; P0.0001; n=16). An inverse correlation was observed between plasma AVP levels recorded at this stage and the maximal contraction induced in vitro by AVP in vascular rings from the same patients (Pearson's r=-0.6968; P0.01; n=16). No change in the AVP response was produced by endothelium removal, exposure to the NO precursor (3 x 10(-4)M L-arginine), inhibition of nitric oxide (NO) synthase (3 x 10(-5) M L-NAME) or soluble guanylate cyclase (3 x 10(-6) M 1H-[1,2,4]oxadiazol [4,3,-alpha]quinoxalin-1-one (ODQ)), removal of the superoxide anion (100 U/ml superoxide dismutase (SOD) plus 1200 U/ml catalase) or hydroxyl radical (10(-4) M deferoxamine), or specific alpha1 - (10(-6) M prazosin) or endothelin (10(-5) M bosentan) receptor antagonism. In contrast, adenylate cyclase activation (3 x 10(-8) M forskolin) reduced the contractile response to AVP, while prostanoid synthesis (3 x 10(-6) M indomethacin) inhibition and blockade of Ca2+ -activated potassium channels (KCa) (10(-3) M tetraethylammonium (TEA)) enhanced AVP contraction. Age, gender and smoking also modified the AVP response.Our findings suggest a role for AVP as a modulator of vascular tone in human IMA. The effect of AVP is dependent on prostanoids and Ca2+ -activated K+ channels, so its dysfunction in pathophysiological cardiovascular processes could mean that AVP, among other factors, produces vasospasm in IMA grafts.

Background and purpose: As pituitary adenylate cyclase-activating polypeptide 38 (PACAP 38)- and vasoactive intestinal peptide (VIP) are widely distributed in the urinary tract, the current study investigated the receptors and mechanisms involved in relaxations induced by these peptides in the pig bladder neck. Experimental approach: Urothelium-denuded strips were suspended in organ baths for isometric force recordings and the relaxations to VIP and PACAP analogues were investigated. Key results: VIP, PACAP 38, PACAP 27 and [Ala11,22,28]-VIP produced similar relaxations. Inhibition of neuronal voltage-gated Ca2+ channels reduced relaxations to PACAP 38 and increased those induced by VIP. Blockade of capsaicin-sensitive primary afferents (CSPA), nitric oxide (NO)-synthase or guanylate cyclase reduced the PACAP 38 relaxations but failed to modify the VIP responses. Inhibition of VIP/PACAP receptors and of voltage-gated K+ channels reduced PACAP 38 and VIP relaxations, which were not modified by the K+ channel blockers iberiotoxin, charybdotoxin, apamin or glibenclamide. The phosphodiesterase 4 inhibitor rolipram and the adenylate cyclase activator forskolin produced potent relaxations. Blockade of protein kinase A (PKA) reduced PACAP 38- and VIP-induced relaxations. Conclusions and implications: PACAP 38 and VIP relax the pig urinary bladder neck through muscle VPAC2 receptors linked to the cAMP-PKA pathway and involve activation of voltage-gated K+ channels. Facilitatory PAC1 receptors located at CSPA and coupled to NO release, and inhibitory VPAC receptors at motor endings are also involved in the relaxations to PACAP 38 and VIP, respectively. VIP/PACAP receptor antagonists could be useful in the therapy of urinary incontinence produced by intrinsic sphincter deficiency. British Journal of Pharmacology (2006) 149, 100–109. doi:10.1038/sj.bjp.0706832

The mechanisms and receptors involved in the vasoactive intestinal peptide (VIP)- and pituitary adenylate cyclase-activating polypeptide (PACAP)-induced relaxations of the pig intravesical ureter were investigated. VIP, PACAP 38 and PACAP 27 concentration-dependently relaxed U46619-contracted ureteral strips with a similar potency. [Ala11,22,28]-VIP, a VPAC1 agonist, showed inconsistent relaxations. The neuronal voltage-gated Ca2+ channel inhibitor, ω-conotoxin GVIA (ω-CgTX, 1 μM), reduced the VIP relaxations. Urothelium removal or blockade of capsaicin-sensitive primary afferents, nitric oxide (NO) synthase and guanylate cyclase with capsaicin (10 μM), NG-nitro-L-arginine (L-NOARG, 100 μM) and 1H-[1,2,4]-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 5 μM), respectively, did not change the VIP relaxations. However, the PACAP 38 relaxations were reduced by ω-CgTX, capsaicin, L-NOARG and ODQ. The VIP and VIP/PACAP receptor antagonists, [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (1 μM) and PACAP (6–38) (0.4 μM), inhibited VIP and VIP and PACAP 38, respectively, relaxations. The nonselective and large-conductance Ca2-activated K+ channel blockers, tetraethylammonium (3 mM) and charybdotoxin (0.1 μM), respectively, and neuropeptide Y (0.1 μM) did not modify the VIP relaxations. The small-conductance Ca2-activated K+ channel blocker apamin (1 μM) did not change the PACAP 27 relaxations. The cAMP-dependent protein kinase A (PKA) blocker, 8-(4-chlorophenylthio)adenosine-3′,5′-cyclic monophosphorothioate (Rp-8-CPT-cAMPS, 100 μM), reduced VIP relaxations. The phosphodiesterase 4 inhibitor rolipram and the adenylate cyclase activator forskolin relaxed ureteral preparations. The rolipram relaxations were reduced by Rp-8-CPT-cAMPS. Forskolin (30 nM) evoked a potentiation of VIP relaxations. These results suggest that VIP and PACAP relax the pig ureter through smooth muscle receptors, probably of the VPAC2 subtype, linked to a cAMP-PKA pathway. Neuronal VPAC receptors localized at motor nerves and PAC1 receptors placed at sensory nerves and coupled to NO release, seem also to be involved in the VIP and PACAP 38 relaxations. British Journal of Pharmacology (2004) 141, 123–131. doi:10.1038/sj.bjp.0705582

1 This study was designed to investigate the effect of 5-hydroxytryptamine (5-HT) and to characterize the 5-HT receptors involved in 5-HT responses in the pig intravesical ureter. 2 5-HT (0.01-10 microM) concentration-dependently increased the tone of intravesical ureteral strips, whereas the increases in phasic contractions were concentration-independent. The 5-HT(2) receptor agonist alpha-methyl 5-HT, mimicked the effect on tone whereas weak or no response was obtained with 5-CT, 8-OH-DPAT, m-chlorophenylbiguanide and RS 67333, 5-HT(1), 5-HT(1A), 5-HT(3) and 5-HT(4) receptor agonists, respectively. 5-HT did not induce relaxation of U46619-contracted ureteral preparations. Pargyline (100 microM), a monoaminooxidase A/B activity inhibitor, produced leftward displacements of the concentration-response curves for 5-HT. 3 5-HT-induced tone was reduced by the 5-HT(2) and 5-HT(2A) receptor antagonists ritanserine (0.1 microM) and spiperone (0.2 microM), respectively. However, 5-HT contraction was not antagonized by cyanopindolol (2 microM), SDZ-SER 082 (1 microM), Y-25130 (1 microM) and GR 113808 (0.1 microM), which are respectively, 5-HT(1A/1B), 5-HT(2B/2C), 5-HT(3), and 5-HT(4) selective receptor antagonists. 4 Removal of the urothelium did not modify 5-HT-induced contractions. Blockade of neuronal voltage-activated sodium channels, alpha-adrenergic receptors and adrenergic neurotransmission with tetrodotoxin (1 microM), phentolamine (0.3 microM) and guanethidine (10 microM), respectively, reduced the contractions to 5-HT. However, physostigmine (1 microM), atropine (0.1 microM) and suramin (30 microM), inhibitors of cholinesterase activity, muscarinic- and purinergic P(2)-receptors, respectively, failed to modify the contractions to 5-HT. 5 These results suggest that 5-HT increases the tone of the pig intravesical ureter through 5-HT(2A) receptors located at the smooth muscle. Part of the 5-HT contraction is indirectly mediated via noradrenaline release from sympathetic nerves.

Objective: Peripheral arterial disease is one of the macrovascular complications of type 2 diabetes mellitus. This study addresses femoral artery regulation in a prediabetic model of obese Zucker rats (OZR) by examining cross-talk between endothelial and neural factors. Methods and Results: Arterial preparations from lean (LZR) and OZR were subjected to electrical field stimulation (EFS) on basal tone. Nitric oxide synthase (NOS) and cyclooxygenase (COX) isoform expression patterns were determined by immunohistochemical labelling and Western blotting. Results indicate significantly reduced noradrenergic contractions in preparations from OZR compared with those of LZR. Functional inhibition of endothelial NOS (eNOS) indicated a predominant role of this isoform in LZR and its modified activity in OZR. Neural (nNOS) and inducible NOS (iNOS) were activated and their expression was higher in femoral arteries from OZR. Neurotransmission modulated by largeconductance Ca 2+ -activated (BK Ca ) or voltage-dependent (K V ) K + channels did not seem compromised in the obese animals. Endothelial COX-1 and COX-2 were expressed in LZR and an additional adventitial location of COX-2 was also observed in OZR, explaining the higher COX-2 protein levels detected in this group. Prostanoids derived from both isoforms helped maintain vasoconstriction in LZR while in OZR only COX-2 was active. Superoxide anion inhibition reduced contractions in endothelium-intact arteries from OZR. Conclusions: Endothelial dysfunction led to reduced neurogenic vasoconstriction in femoral arteries from OZR. In a setting of obesity, NO-dependent nNOS and iNOS dilation activity could be an alternative mechanism to offset COX-2- And reactive oxygen species-mediated vasoconstriction, along with impaired endothelial NO relaxation.

Our aim was to study the presence of noradrenergic nerves and to characterize the alpha-adrenergic receptors involved in the contractions to electrical field stimulation and to alpha-adrenergic agonists of the horse penile deep dorsal vein. Noradrenergic fibres were visualized by immunohistochemistry using an antibody against dopamine-beta-hydroxylase (DBH). For functional studies, the responses of the venous rings to electrical field stimulation and to alpha-adrenergic agonists (noradrenaline, phenylephrine and BHT 920) were studied in the absence and the presence of noradrenergic transmission- and neuronal sodium channel-blockers (guanethidine and tetrodotoxin, respectively) and of alpha1- and alpha2-adrenergic antagonists (prazosin and rauwolscine, respectively). DBH-immunoreactive fibres were present in the adventitia and in the media layer of the venous rings. Electrical field stimulation (0.5-32 Hz) caused frequency-dependent contractions that were abolished by guanethidine (10(-6) M) and tetrodotoxin (10(-6) M) and reduced by prazosin (10(-9)-10(-7) M) and rauwolscine (3 x 10(-8)-3 x 10(-7) M). Noradrenaline, phenylephrine and BHT 920 induced equipotent contractions of the rings. Prazosin and rauwolscine competitively antagonized the contractions to phenylephrine and BHT 920, respectively. In conclusion, DBH-immunoreactive nerve fibres are present in the horse penile dorsal vein. Both transmural nerve stimulation and alpha-adrenergic agonists induce contraction of the venous rings through a heterogeneous population of alpha1- and alpha2-adrenoceptors.

The present investigation was designed to evaluate the effect of histamine on isolated rings of horse deep dorsal penile vein. Under precontracted or basal conditions, histamine evoked an endothelium-independent contraction. Preincubation of the vein rings with the selective H1 receptor antagonist, mepyramine, shifted the concentration-response curve for histamine and to the H1 receptor agonist 2-pyridylethylamine to the right in a competitive manner. Pretreatment with cimetidine, a specific H2 receptor antagonist, did not modify the pEC50 and maximal contraction of the histamine response. Cimetidine and propranolol failed to induce a change in the relaxation caused by dimaprit, the H2 receptor agonist. Histamine contraction was unaffected by thioperamide, the specific H3 receptor antagonist. (R)-alpha-methylhistamine, the H3 receptor agonist, also induced contractions which persisted in the presence of either thioperamide or tetrodotoxin. These data indicate that horse deep dorsal penile vein shows an endothelium-independent contraction response to histamine, mainly mediated by H1 receptors.

The effects of specific histamine agonists and antagonists on isolated rabbit penile dorsal artery segments were explored using in vitro isometric techniques. Histamine caused the constriction of both precontracted and resting segments. In precontracted arterial rings treated with the H, receptor antagonist mepyramine, histamine evoked a vasodilatation, followed by contraction at higher concentrations, The vasoconstrictor effect of histamine and the H 1 receptor agonist, 2-pyridylethylamine (PEA) on preparations under conditions of basal tone, was competitively antagonized by mepyramine (10 -9 -10 -8 M), The relaxant effect of histamine, unmasked by mepyramine, was abolished by cimetidine. Dimaprit, the H 2 receptor agonist, provoked a relaxation of precontracted segments that was also competitively inhibited by cimetidine (10 -6 -10 -5 M). Selective H 3 receptor activation with the agonist (R)α-methylhistamine (10 -10 -10 -4 M) produced no effect in penile dorsal artery. The biphasic response to histamine was unaffected by endothelium removal or the nitric oxide inhibitor N G -nitro-L-arginine methyl ester (L-NAME) (3 x 10 -4 M) and its precursor, L-arginine (3 x 10 -4 M). Similarly, the cyclooxygenase inhibitor, indomethacin (3 x 10 -6 M) and a combination of Ca 2+ -activated K + channel blockers apamin (5 x 10 -7 M) and charybdotoxin (10 -7 M) showed no effect on the histamine-induced relaxation or contraction. In conclusion, contraction, the predominant effect of histamine, is mediated by the activation of H, receptors that mask the relaxant effect brought about by H 2 receptors. Both these effects appear to be mediated by direct action on the smooth muscle, with no participation of nitric oxide or cyclooxygenase products or Ca 2+ -activated K + channels.