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Background: Cerebrovascular disease may impair the autonomic control of peripheral organs including the male urogenital tract. This study investigates the effect of cortico-parietal focal ischaemia on the adrenergic and purinergic transmission in isolated epididymal and prostatic portion of rat vas deferens., Methods: Focal brain ischaemia was induced in male rats by photochemical activation following rose bengal intravenous injection. Twenty-four hours following brain ischaemia, cumulative and non-cumulative concentration-response curves were obtained for noradrenaline and alpha,beta-methylene ATP in the right and left epididymal and prostatic portions of the vas deferens. Both portions were also stimulated by single-pulse or pulse trains at 2-30 Hz to produce isometric contractions., Results: In both portions from ischaemic rats the response to exogenous noradrenaline was markedly depressed compared with controls. Acute cortico-parietal ischaemia almost completely abolished the adrenergic phase of the response to single-pulse stimulation in the epididymal portion of the vas deferens. In addition, brain ischaemia deeply depressed phasic and tonic contractions of the frequency-response curve in both portions of bisected vas deferens., Conclusions: Cortico-parietal ischaemia produces a selective noradrenergic impairment at the level of male sexual secondary organs that may contribute to sexual dysfunction after stroke.

1. Disturbances of the autonomic nervous system are common in right hemisphere stroke patients, including a marked decline in male sexual functions. There is a lack of information on the influence of stroke on male secondary sex organs such as the vas deferens. 2. This study investigates the effect of right brain focal ischaemia on the adrenergic and purinergic responses in isolated epididymal and prostatic portions of rat vas deferens. 3. In both epididymal and prostatic portions the concentration-response curves to noradrenaline are flattened resulting in a reduction (up to 67 - 76%) of the maximum contractile response in the tissue from ischaemic rats compared to the controls. In the prostatic portion from ischaemic rats the concentration-response curve to alpha,beta-methylene ATP was also depressed. 4. The first purinergic and the second delayed adrenergic phase to single pulse was not modified by brain ischaemia. In contrast both phasic and tonic components of the electrically induced contractions by trains of stimuli at high frequencies (2 - 30 Hz) were significantly depressed in the epididymal and prostatic portions from ischaemic rats. 5. These results demonstrate an autonomic imbalance at the level of male sexual secondary organs which may contribute to sexual impairment after stroke.

1. This study investigates the effect of acute in vivo and in vitro ethanol administration on the contractions evoked electrically and by exogenous noradrenaline and alpha,beta-methylene-ATP in the rat bisected vas deferens. 2. In vivo ethanol treatment (3 g kg(-1), i.p.) significantly potentiated the early purinergic (phase I) and the delayed adrenergic (phase II) phases evoked by single-pulse stimulation of the epididymal portion of the rat vas deferens, leaving unaffected both phases in the prostatic portion. In vitro 50 mM ethanol significantly depressed phase I leaving unaffected phase II in both portions from untreated rats. In vitro ethanol significantly depressed phase I in the epididymal portion from in vivo ethanol treated animals and potentiated phase II in both portions. 3. In vivo ethanol treatment (3.0 g kg(-1), i.p.) selectively impaired the response to noradrenaline only in the prostatic portion of rat vas deferens while it was devoid of any action on alpha,beta-methylene-ATP contractions. Ethanol 50 mM in vitro was devoid of any action on the response to exogenous noradrenaline and alpha,beta-methylene-ATP in both tissues. 4. In vivo ethanol treatment slightly but significantly increased the phasic response in the epididymal portion to trains of stimuli (2-30 Hz). In vitro 50 mM ethanol was ineffective against the phasic and tonic contractions elicited by the tetanus in both portions. 5. It is concluded that ethanol treatment affects purinergic and adrenergic pathways of transmission possibly leading to a disruption of physiological contractions necessary to seminal emission.

This study investigates the effect of acute in vivo or in vitro ethanol administration on the adrenergic and purinergic responses in the epididymal and prostatic portion of rat vas deferens. Acute in vivo ethanol treatment (3.0 g/kg, i.p.) selectively impaired the response to noradrenaline in the prostatic portion of rat vas deferens, leaving unaffected the epididymal portion. In addition, the response evoked by the maximal concentration of alpha, beta-methylene-ATP was significantly depressed by acute in vivo ethanol treatment in both the epididymal and prostatic segments. Ethanol 50 mM in vitro was devoid of any action on the response to exogenous noradrenaline in both tissues. Ethanol in vitro left unaltered the response to alpha,beta-methylene-ATP in the epididymal portion, while potentiated the contractile response in the prostatic one. These results provide, for the first time, evidence that ethanol in vitro and in vivo differentially affects the noradrenergic and purinergic responses in the bisected vas deferens, suggesting that this substance may alter the male reproductive tract function.

The present study was carried out compare the effects of nifedipine, verapamil, papaverine and chloroethylclonidine (CEC) on the electrically-induced contractions and on the contractions produced by exogenous noradrenaline and alpha, beta methylene-ATP in the epidydimal portion of rat vas deferens. Nifedipine inhibited in a concentration-dependent fashion the purinergic component (phase I) of the electrically evoked response. Verapamil (10(-7) M-10(-5) M) did not inhibit significantly or even potentiated phase I of the contractile response to single-pulse field stimulation but inhibited the response to alpha,beta methylene-ATP. Papaverine left unaffected phase I but depressed the response to alpha,beta methylene-ATP. CEC significantly potentiated the purinergic component of the electrically-evoked response and the response induced by alpha,beta methylene-ATP. Nifedipine was devoid of any inhibitory action on the noradrenergic component (phase II) of the response to single shock. Verapamil at the highest concentration used (10(-5) M) was able to partially inhibit phase II. Papaverine abolished in a concentration-dependent manner the noradrenergic component of the response to single shock. CEC abolished the phase II of single shock while was devoid of any inhibitory action on exogenous noradrenaline. The implications of these differences among the compounds studied in the present work are discussed in relation to roles of calcium channels.

1. The present study was carried out to look at the effect of different calcium antagonists on the response to noradrenaline in the whole and bisected rat vas deferens considering that the response consisted of three components (I) the phasic response (II) the tonic response and (III) the spikes (rhythmic contractions). 2. Nifedipine (3 x 10(-9)-1 x 10(-7) M) inhibited all the components at the same concentration range, verapamil (1 x 10(-7)-1 x 10(-5) M) inhibited the phasic and tonic response but not the rhythmic activity. This latter component, at a certain concentration range and especially in the prostatic portion was markedly potentiated. Diltiazem and flunarizine lay in an intermediate position. 3. Papaverine, a Ca2+ antagonist that acts mainly intracellularly, inhibited preferentially the tonic component; ryanodine was practically inactive. 4. Cromakalim inhibited only partially the phasic and tonic components but totally inhibited the rhythmic contractions. 5. These results can be explained by postulating two types of calcium channels opened by alpha-adrenoceptor stimulation. The first one is verapamil- and nifedipine-sensitive and allows the entry of Ca2+ directly available for the contraction and responsible for the phasic and partially responsible for the tonic component. The second channel is merely nifedipine-sensitive and allows the entry of Ca2+ trigger which can release Ca2+ from intracellular sites: the mobilized Ca2+ is able to sustain the tonic component and is the main one responsible for the rhythmic activity. There is the possibility that this second channel is associated with ATP-sensitive K+ channels.

1. The present study was carried out to look at the differences between the whole and bisected rat vas deferens in response to cumulative and non-cumulative administration of noradrenaline in terms of sensitivity and maximum response. An effort was made to quantify the parameters characterizing the various components of the mechanical response to single concentrations of the agonist. 2. The sensitivity, as measured by the -log EC50 value for noradrenaline, was significantly lower in the prostatic portion than in the whole vas deferens and epididymal portion. The maximum contractions reached by the epididymal and the prostatic half were 65.03 +/- 10.43% and 13.84 +/- 5.28% of the maximal contraction evoked by noradrenaline in the whole rat vas deferens. 3. Various concentrations of noradrenaline were tested as single concentrations in the three preparations. These components of the response to noradrenaline were individualized, i.e. an early rapid phasic component followed by a second slower tonic component with spikes superimposed. The time-course of these components, as well as their ratios, were different depending on the concentration of agonist tested and on which half of the vas deferens was considered. 4. The importance of oxidation of exogenous noradrenaline as well of the neuronal and extraneuronal uptake mechanisms was considered. EDTA was devoid of any action. Cocaine enhanced potency and the maximum contraction of noradrenaline and all the parameters related to the different phases of the contraction were increased. Hydrocortisone at the highest concentration employed (2 X 10-5 M) was able to reduce significantly the -log EC50 value of the cumulative concentration-response curve to noradrenaline and both the phasic and tonic components of the contradiction to noradrenaline (3 X 10-6 M). 5. In conclusion, our evaluation of the parameters of the mechanical response of the whole and bisected vas deferens to noradrenaline rationalize the, often contradictory, findings of the current literature. Chiefly, the attainment of a careful description of the features of the response to noradrenaline can offer a dependable approach to the study of the underlying mechanisms of the three components.

The present study was carried out to look at the influence of the K+ channel opener cromakalim, compared with suramin and prazosin, on the contractile response evoked by single-pulse field stimulation and exogenous agonists in epididymal and prostatic portions of rat vas deferens. In the epididymal portion suramin abolished the first phase of the response to single shock, prazosin deeply affected the second phase and a combination of both antagonists almost completely abolished both phases. Cromakalim was able to inhibit in a concentration-dependent manner the first purinergic phase (pD2 = 5.90 +/- 0.11), leaving practically unaffected the second, adrenergic phase. This inhibitory effect of cromakalim on the electrically evoked response was counteracted by glibenclamide. Cromakalim and prazosin, but not suramin, affected the response to exogenous noradrenaline. Suramin but not cromakalim was able to antagonize responses to alpha, beta-methylene-ATP. In the prostatic portion because of a less clear discrimination between adrenergic and purinergic phases of the electrically evoked response, the picture was less clear although the trend was identical. Cromakalim was not able to antagonize the response to ATP. It is concluded that in rat vas deferens cromakalim inhibits purinergic transmission by acting prejunctionally.

1 This study investigates the effect of acute in vivo and in vitro ethanol administration on the contractions evoked electrically and by exogenous noradrenaline and α,β-methylene-ATP in the rat bisected vas deferens. 2 In vivo ethanol treatment (3 g kg[sup –1] , i.p.) significantly potentiated the early purinergic (phase I) and the delayed adrenergic (phase II) phases evoked by single-pulse stimulation of the epididymal portion of the rat vas deferens, leaving unaffected both phases in the prostatic portion. In vitro 50 mM ethanol significantly depressed phase I leaving unaffected phase II in both portions from untreated rats. In vitro ethanol significantly depressed phase I in the epididymal portion from in vivo ethanol treated animals and potentiated phase II in both portions. 3 In vivo ethanol treatment (3.0 g kg[sup –1] , i.p.) selectively impaired the response to noradrenaline only in the prostatic portion of rat vas deferens while it was devoid of any action on α,β-methylene-ATP contractions. Ethanol 50 mMin vitro was devoid of any action on the response to exogenous noradrenaline and α,β-methylene-ATP in both tissues. 4 In vivo ethanol treatment slightly but significantly increased the phasic response in the epididymal portion to trains of stimuli (2–30 Hz). In vitro 50 mM ethanol was ineffective against the phasic and tonic contractions elicited by the tetanus in both portions. 5 It is concluded that ethanol treatment affects purinergic and adrenergic pathways of transmission possibly leading to a disruption of physiological contractions necessary to seminal emission. [ABSTRACT FROM AUTHOR]

1 Frequency–response curves (0.1–30 Hz) were obtained in the epididymal portion of rat vas deferens. At low frequencies (0.1–1 Hz), the parameters evaluated were the first twitch and the fourth twitch at each frequency. The responses to trains of stimuli at intermediate (2–5 Hz) and high (10–30 Hz) frequencies were biphasic consisting of phase I (the first rapid phase of tetanus) and of phase II (the secondary slowly developing one). 2 Prazosin inhibited the first and the fourth twitch but not when the frequency was <1 Hz. Suramin inhibited the first twitch while substantially depressing the fourth one. The combination of prazosin and suramin almost completely abolished all the twitches evoked by a train of stimuli at low frequencies. Nifedipine left almost unaltered the first twitch while markedly depressing the fourth one, especially at relatively high frequency (1 Hz). Verapamil was devoid of any inhibitory action. Papaverine depressed the first twitch while only at the highest concentration used (1×10-4 m) markedly inhibited the fourth one. Chloroethylclonidine (CEC) depressed the first twitch and increased the fourth. 3 When intermediate (2–5 Hz) and high (10–30 Hz) frequencies are considered, prazosin and suramin partially inhibited both phase I and phase II, while in combination they almost completely abolished both phases. Nifedipine and verapamil selectively suppressed phase II, leaving phase I unaffected. Papaverine completely abolished both phase I and phase II. CEC was able to completely abolish phase I but increased phase II. 4 These results suggest that the response to the first twitch of a train at low frequency is prevailingly noradrenergic, prazosin-sensitive, while when the twitches are close enough (i.e. at 1 Hz) a summation of stimuli takes place and a predominant purinergic component, both suramin- and nifedipine-sensitive, becomes evident. 5 At high frequencies, both phases are due to... [ABSTRACT FROM AUTHOR]

1 The present study was carried out compare the effects of nifedipine, verapamil, papaverine and chloroethylclonidine (CEC) on the electrically-induced contractions and on the contractions produced by exogenous noradrenaline and α,β methylene-ATP in the epidydimal portion of rat vas deferens. 2 Nifedipine inhibited in a concentration-dependent fashion the purinergic component (phase I) of the electrically evoked response. Verapamil (10--7 M-10--5 M) did not inhibit significantly or even potentiated phase I of the contractile response to single-pulse field stimulation but inhibited the response to α,β methylene-ATP. Papaverine left unaffected phase I but depressed the response to α,β methylene-ATP. CEC significantly potentiated the purinergic component of the electrically-evoked response and the response induced by α,β methylene-ATP. 3 Nifedipine was devoid of any inhibitory action on the noradrenergic component (phase II) of the response to single shock. Verapamil at the highest concentration used (10--5 M) was able to partially inhibit phase II. Papaverine abolished in a concentration-dependent manner the noradrenergic component of the response to single shock. CEC abolished the phase II of single shock while was devoid of any inhibitory action on exogenous noradrenaline. 4 The implications of these differences among the compounds studied in the present work are discussed in relation to roles of calcium channels. [ABSTRACT FROM AUTHOR]