The Role of Alpha-adrenergic Receptor Mechanism in ... - JST

Tohoku J. exp. Med., 1972, 108, 337-352

The Role of Alpha-adrenergic Receptor Mechanism

in Ejaculation

YUKIO KIMURA, KOYO MIYATA, KUNIAKI ADACHI and SATOSHI MATSUMURADepartment of Urology,* Tohoku University School of Medicine, Sendai

KIMURA, Y., MIYATA, K., Anaoni, K. and MATSUMURA, S. The Role of

Alpha-adrenergic Receptor Mechanism in Ejaculation. Tohoku J. exp. Med.,

1972, 108 (4), 337-352 - The effects of autonomic drugs on seminal emission

and ejaculation were investigated in mongrel dogs. Changes in the posterior

urethral pressure (posterior urethrogram) and the volume of seminal emission during

continuous hypogastric nerve stimulation were measured in test animals. The

seminal emission induced by hypogastric nerve stimulation caused continuous rise

in the posterior urethral pressure. When the pressure reached the maximum level,

rhythmic alterations of the pressure which was considered to be a phenomenon

associated with ejaculation occurred. The drugs were administered into the

abdominal aorta just above its bifurcation. Tetrodotoxin (1-5ƒÊg) abolished

both seminal emission and rhythmic alterations of the posterior urethral pressure.

Phenylephrine (10-100ƒÊg) and methoxamine (10-30ƒÊg) increased markedly the

seminal emission and induced the rhythmic alterations. Phentolamine (1-10

mg) and phenoxybenzamine (1-10mg) abolished both seminal emission and the

rhythmic alterations. Administration of isoproterenol (10-30ƒÊg) or propranolol

(1-10mg) affected neither seminal emission nor rhythmic alterations. Acetyl

-choline (1-10ƒÊg) or atropine (1-10ƒÊg) did not show any definite effect on both

seminal emission and the rhythmic alterations. No significant effect of DMPP

(10-30ƒÊg) on seminal emission and rhythmic alterations were observed. No signi

ficant change in seminal emission was caused by hexamethonium (100-500ƒÊg).

The rhythmic alterations were not affected by this agent in many dogs. From

these results it is concluded that both seminal emission and ejaculation are pre-

dominantly under the influence of adrenergic nervous system, particularly through

an a-adrenergic receptor mechanism seminal emission; ejaculation; a-

adrenergic receptor

It is generally accepted that the mechanism of "ejaculation" depends on the

autonomic nervous functions and that it can be separated from seminal emission,

i.e., rhythmic elections of the semen from the external urethral orifice.

Numerous reports have been published on the presence or absence of the a-

and ƒÀ-receptor mechanisms and of cholinergic receptor one in the internal male

sexual organs of the various mammals, such as the prostatic gland (Smith 1967,

Smith and Lebeaux 1970, Smith 1968, Farrell and Lyman 1937, Ochiai 1953), vas

deferens (Mantegazza 1967, Sexana 1970, Naimzadda 1966, Large 1965, Bhargava

Received for publication, April 18, 1972.

* Director: Prof. S. Shishito.

337

338 Y. Kimura et al,

et al. 1965) and seminal vesicle (Sexana 1970, Naimzadda 1966, Takeda and

Nakanishi 1965, Endo 1965). However, little information is available on the role

of these receptors in the integral functions of these organs, that is, seminal

emission and ejaculation, and it involves a risk to regard a response of an individual

organ as a response of the whole organs.

In the present report how these receptor mechanisms are working in seminal

emission and ejaculation was studied using a series of autonomic drugs.

For this purpose the authors used the posterior urethrogram, measurement

of pressure changes in the posterior urethra during hypogastric nerve stimulation

(Kimura 1971).

MATERIALS AND METHODS

For the present study 110 male adolescent mongrel dogs weighing 10-15kg were

used. The effect of each drug on the posterior urethrogram was investigated in more than

5 dogs and the effect on the seminal volume in other 3 dogs or more. The present study

was carried out from April to October, since the seminal emission caused by hypogastric

nerve stimulation was noted to decrease in the colder seasons.

1) Isolation and stimulation of the hypogastric nerve

The experimental animals were anesthetized by intravenous injection of pentobarbital.

The anesthesia was maintained by repeated administration of small doses of the drug in

such depth as that pupillary reflex was sustained throughout the experiment.

Through a lower abdominal midline incision, the hypogastric nerves were exposed and

cut on both sides of the sigmoid colon. The pelvic and pudendal nerves were left intact.

Bipolar stimulating electrodes consisting of silver wire 200ƒÊ in diameter were attached to

the peripheral end of both cut hypogastric nerves. The nerves were stimulated with

square pulses of 2V and 2 msec at a frequency of 10 Hz for various periods by use of an

electronic stimulator, MSE-3R (Nihon Koden Co.). By this stimulation seminal emission

was made.

2) Measurement of the posterior urethral pressure (posterior urethrogram)

A No. 6 polyethylene tube was inserted into the urethra through the external

urethral orifice, so that the tip of the tube was positioned in the prostatic region of the

urethra. A Satensky's clamp was applied at the neck of the urinary bladder to prevent

the seminal fluid from regurgitating into the bladder, and the external urethral orifice was

ligated to increase resistance in the anterior urethra (Fig. 1).

The changes of the pressure in the posterior urethra due to seminal emission and/or

administration of drugs were recorded by connecting the tube to an electric manometer.

The recording was made with a Multipurpose Recorder, twin, with a Carrier Ampliphier

RP-2 (Nihon Koden Co.).

3) Measurement of seminal emission

A No. 6 polyethylene tube was also inserted into the posterior urethra through the

external urethral orifice and the same procedure was done on the urethra as in the posterior

urethrogram. The amount of the semen excreted through the tube was measured for 3

minutes before and after administration of drugs. Upon administration of drugs the

measurement was begun immediately after termination of the administration.

4) Drugs and administration

A catheter (2mm in diameter) was inserted into the femoral artery, following Seldinger's

Alpha-adrenergic Receptor Mechanism in Ejaculation 339

Fig. 1. Assembly to measure posterior urethrogram . A No. 6 polyethylene tube was inserted into the urethra , so that the tip of the tube

was positioned in pars prostate of the urethra .

1) Control:

2) Effect of tetrodotoxin on rhythmic alterations in posterior urethral pressure:

3) Effect on the rise in the posterior urethral pressure:

Fig. 2. Effect of tetrodotoxin on posterior urethrogram (P.U.G.). N.H.S.: hypogastric nerve stimulation.

i) The control response obtained before administration of tetrodotoxin (TTX). ii) the response after 5µg of TTX were given during the occurrence of rhythmic alterations

in the posterior urethral pressure. The alterations disappeared immediately after the injection. iii) The posterior urethrogram after 5µg of TTX were given. No rise in

the posterior urethral pressure was observed after administration of the drug in spite of hypogastric nerve stimulation. Chart speed: 0.5mm/sec (timer 1 cps).

method (Seldinger 1953), and the tip of the catheter reached the abdominal aorta just above its bifurcation.

The drugs dissolved in 1ml of physiologic saline were instilled into the catheter. This was immediately followed by instantaneous instillation of 1ml of physiologic saline to flush the drug solutions into the abdominal aorta, since the inside volume of the catheter was made to be 1ml.

The following drugs were used: tetrodotoxin (Sankyo), phenylephrine hydrochloride

(Kowa Chemicals), methoxamine hydrochloride (Nihon Shinyaku), l-isoproterenol hydrochloride (Nikken), phentolamine mesylate (Chiba), phenoxybenzamine hydrochloride

340 Y. Kimura et al.

TABLE 1. Effect of tetrodotoxin on the volume of semen secreted by

hypogastric nerve stimulation (tetrodotoxin 5ƒÊg)

Abbreviation TTX: tetrodotoxin.

1) Effect of phenylephrine on the rise of the posterior urethral pressure induced by hypogastric nerve stimulation.

i) Control

ii) Administration of 100µg of phenylephrine:

Fig. 3. Effects of a-stimulants and a-blockers on posterior urethrogram.

H.N.S.: hypogastric nerve stimulation.

i) Posterior urethral pressure curve obtained before administration of phenylephrine.

ii) Posterior urethral pressure curve obtained after 100ƒÊg of phenylephrine was

given. Scarcely any rise in the posterior urethral pressure was observed after

administration of phenylephrine alone. When the hypogastric nerve stimulation was

applied, a continuous rise in the pressure was observed, and when the pressure reached

the maximum level, rhythmic alterations of the pressure occurred. Chart speed:

0.83mm/sec (timer 1 cycle/min).

(Smithin and French), propranolol hydrochloride (Sumitomo Chemicals), acetylcholine chlo

ride (Daiiehi Seiyaku), atropine sulfate (Takeda Yakuhin), 1,1-dimethy-1-4-phenylpipera

zinium iodide (Aldrich), and hexamethonium bromide (Yamanouchi Seiyaku). These

drugs were given in terns of salts except for TTX.

RESULTS

1) Effect of tetrodotoxin

i) The posterior urethral pressure.

When the bilateral hypogastric nerves were stimulated continuously, the


2) Effects of phenylephrine and phentolamine on rhythmic alterations in the posterior urethral pressure

i) Control:

ii) Administration of phenylephrine and phentolamine:

iii) Administration of phentolamine:

iv) After phentolamine way ulin nistercd:


H.V.S.: hypogastric nerve stimulation.

Figures i), ii) and iv) were obtained from the same dog.

i) Posterior urethral pressure curve obtained before administration. ii) Hypogastric

nerve stimulation was discontinued when the posterior urethral pressure reached to

nearly maximum level, and phenylephrine was given. As seen in the figure phenyl

ephrine caused rhythmic alterations in the posterior urethral pressure. These rhythmic

alterations were abolished with 5 mg of phentolamine. iii) Phentolamine in a dose

of 10 mg caused disappearance of the rhythmic alterations in the posterior urethral

pressure which had been induced by hypogastric nerve stimulation and without a-

stimulant. iv) After 10mg of phentolamine was given, no rise in the pressure was

caused with hypogastric nerve stimulation. Additional administration of 100ƒÊg of

phenylephrine did not affect the curve. Chart speed: 0.83mm/sec (timer 1 cycle/

min).


3) Effects of methoxamine and phentolamine.



Thirty ƒÊg of methoxamine induced the rhythmic alterations in the posterior urethral

pressure when the pressure was raised nearly to maximum level with hypogastric nerve

stimulation. These alterations were abolished by phentolamine. Chart speed: 0.83

mm/sec (timer 1 cycle/min).

4) Effect of phenoxybenzamine (P.B.):



Upper tracing shows that the rhythmic alterations in the posterior urethral pressure

with hypogastric nerve stimulation were abolished by 5mg of phenoxybenzamine.

Lower tracing shows that no rise in the posterior urethral pressure occurred after

administration of 5mg of phenoxybenzamine. Chart speed: 0.83mm/sec (timer I

cycle/min).

posterior urethral pressure gradually increased with seminal emission and reached

a steady level. Then, the rhythmic alterations in the pressure occurred (Fig. 2,

upper panel). These alterations were maintained long enough to evaluate the

effects of drugs, as far as hypogastric nerve stimulation was continued and the

intra-urethral pressure was not artificially reduced.

When 1 to 5ƒÊg of tetrodotoxin were given during the rhythmic alterations,

these alterations disappeared immediately (Fig. 2, middle panel). A prior admini-


TABLE 2. Effect of a-stimulants on the volume of semen secreted by

hypogastric nerve stimulation

1) Phenylephrine in a dose of 10ƒÊg:

2) Methoxamine in a dose of 30ƒÊg:

TABLE 3. Effect of a-blockers on the volume of semen secreted by hypogastric nerve stimulation

1) Phentolamine in a dose of 1mg:

2) Phenoxybenzamine in a dose of 3mg:

stration of these doses of tetrodotoxin prevented completely the increase in the

posterior urethral pressure in response to hypogastric nerve stimulation (Fig. 2,

lower panel).

ii) Changes in the volume of seminal emission.

The mean volume of semen secreted by continuous hypogastric nerve

stimulation was markedly reduced after the administration of 5ƒÊg of tetrodotoxin

(Table 1).


i) Control:

ii) Administration of isoproterenol in a close of 10ƒÊg:

Fig. 7. Effects of ƒÀ-stimulant and ƒÀ-blocker on posterior urethrogram.


i) The control response obtained before administration of isoproterenol. ii) Posteri-

or urethrogram after an administration of 10ƒÊg. Isoproterenol caused no rise in the

posterior urethral pressure. The pressure was raised by hypogastric nerve stimulation as seen before the administration. The rhythmic alterations occurred in the same

way as in the control. Chart speed: 0.83mm/sec (timer 1 cycle/min).

2) Effects of a-stimulants and a-blockers


A single injection of 10-100ƒÊg of phenylephrine or 10-30ƒÊg of methoxamine

without hypogastric nerve stimulation caused scarcely any rise in the posterior

urethral pressure. There was a very little difference in the rise of the posterior

urethral pressure induced by continuous hypogastric nerve stimulation before and

after the administration of either phenylephrine or methoxamine (Fig. 3).

Administration of phenylephrine or methoxamine in the above-mentioned

doses induced the rhythmic alterations in the posterior urethral pressure when

the pressure was raised to near the maximum level by hypogastric nerve stimula

tion (Figs. 4 and 5).

Phentolamine in a dose of 1-10mg or phenoxybenzamine, 1-10mg abolished

the rhythmic alterations in the posterior urethral pressure caused either by

hypogastric nerve stimulation or by the administration of phenylephrine (Figs.

4, 5 and 6). After the administration of phentolamine or phenoxybenzamine, the

hypogastric nerve stimulation caused no rise in the pressure (Figs. 4 and 6).


Phenylephrine and methoxamine increased markedly the amount of seminal

emission induced by continuous hypogastric nerve stimulation (Table 2). Phento

lamine and phenoxybenzamine decreased the amount markedly (Table 3).

3) Effects of ƒÀ-stimulant and ƒÀ-blocker


The administration of 10-30ƒÊg of isoproterenol without hypogastric nerve


2) Effects of isoproterenol and propranolol .

Fig. 8. Effects of ƒÀ-stimulant and ƒÀ-blocker on posterior urethrogram.

H.N.S.: hypogastric nerve stimulation .

Upper tracing shows that the rhythmic alterations in the posterior urethral pressure

were not affected by propranolol. Lower tracing shows that the posterior urethral

pressure curve after an administration of 4mg of propranolol is similar to the curve

obtained before the administration. Chart speed: 0.83mm/sec (timer 1 cycle/min) .

TABLE 4. Effects of #-stimulant and ƒÀ-blocker on the volume of semen

secreted by hypogastric nerve stimulation

1) Isoproterenol in a dose of 10ƒÊg:

2) Propranolol in a dose of 5mg:

stimulation did not affect the pressure in the posterior urethra (Fig. 7).Isoproterenol did not induce the rhythmic alterations in the posterior urethral

pressure even when the pressure was raised to near the maximum level by continuous hypogastric nerve stimulation.

Propranolol in a dose of 1-10mg showed no effect on the rhythmic alterations in the posterior urethral pressure (Fig. 8).

The rise in the posterior urethral pressure caused by continuous hypogastric nerve stimulation was not affected by propranolol (Fig. 8).


Effect of acetylcholine.

Fig. 9. Effects of acetylcholine and atropine on posterior urethrogram.


In the upper tracing it is seen that acetylcholine without hypogastric nerve stimulation

caused a transient rise in the posterior urethral pressure. In the lower tracing it is seen

that acetyleholin, which was administered when the posterior urethral pressure was

raised by continuous hypogastric nerve stimulation, caused a transient rise in the

pressure but did not induce the rhythmic alterations. However, the rhythmic altera

tions occurred when the pressure was raised to the maximum level by hypogastric

nerve stimulation. Chart speed: 0.83mm/sec (timer 1 cycle/min).


No significant change in the volume of semen secreted by continuous

hypogastric nerve stimulation was seen before and after the administration of

isoproterenol or propranolol (Table 4).

4) Effects of parasympathomimetics and parasynapatholytics


The administration of 1-10ƒÊg of acetylcholine either before or during

continuous hypogastric nerve stimulation showed a transient rise in the posterior

urethral pressure (Fig. 9).

Acetylcholine in the same dose did not induce the rhythmic alterations in

most dogs even when the pressure was raised to near the maximum level (Fig. 9).

In 3 out of 8 dogs rhythmic alterations caused by hypogastric nerve stimula

tion were abolished by atropine in dose as small as 10ƒÊg. However, in the other

5 dogs the rhythmic alterations were resistant to blockade by atropine in a dose

as large as 110ƒÊg (Fig. 10).

After the administration of atropine, the rise in the posterior urethral

pressure occurred very slowly and the pressure was not raised to more than 30

cm H2O (Fig. 10).


The amount of seminal emission induced by continuous hypogastric nerve

stimulation was slightly increased after the administration of acetylcholine.

Atropine, however, decreased seminal emission considerably (Table 5).


Effect of atropine.

i) Control:

ii) Effect of atropine on the rythmic alterations in the posterior urethral pressure (I):

iii) Effect of atropine on the rhythmic alterations in the posterior urethral pressure (2):

iv) Effect of atropine on the rhythmic alterations in the posterior urethral pressure (3) :

v) Effect of atropine on the rise in the posterior urethral pressure:

Fig. 10. Effects of acetylcholine and atropine on posterior urethrogram.


Figures i), iii) and v) were obtained from the same dog.

The rhythmic alterations in the posterior urethral pressure were abolished by 10ƒÊg

of atropine in ii), 21ƒÊg in iii), and were not affected by more than 100ƒÊg in iv).

Atropine inhibited a rise in the posterior urethral pressure as shown in v). Chart

speed: 1mm/sec in i), iii), iv) and v) (timer 1 cps); 0.83mm/sec in ii) (timer 1

cycle/min).

5) Effects of ganglion stimulant and ganglion blocker


There was a slight transient rise in the posterior urethral pressure when 10-30ƒÊ

g of DMPP was given either with continuous hypogastric nerve stimulation or


TABLE 5. Effect of acetylcholine and atropine on the volume of semen

secreted by hypo gastric nerve stimulation

1) Ach in a dose of 10ƒÊg:

2) Atropine in a dose of 10ƒÊg:

TABLE 6. Effect of ganglion stimulant and blocker on the volume of semen

secreted by hypogastric nerve stimulation

1) DMPP in a dose of 10ƒÊg:

2) Hexamethonium in a dose of 500ƒÊg:

without the stimulation (Figs. 11 and 12). There was a very little difference in the rise of the posterior urethral pressure induced by continuous hypogastric nerve stimulation before and after the administration of DMPP . DMPP of the above-mentioned dosage did not induce the rhythmic alterations in the posterior urethral

pressure even when the pressure was raised to near the maximum level by hypogastric nerve stimulation (Fig. 12).


1) Effect on rise of the posterior urethral pressure .i) Control:

ii) Administration of DMPP:

Fig. 11. Effects of ganglion stimulant and ganglion blocker on posterior urethrogram.


i) Control response to test effects of the drug. ii) When 10ƒÊg of DMPP was given,

a slight transient rise in the posterior urethral pressure occurred, but the rise of the

pressure was not significantly changed by DMPP. The rhythmic alterations appeared, when the pressure reached the maximum level by hypogastric nerve

stimulation. Chart speed: 0.83mm/sec.

By the administration of hexamethonium (100-500ƒÊg) the rhythmic altera

tions in the posterior urethral pressure disappeared in 3 of 5 dogs examined (Fig.

12), but they remained unchanged in the remaining 2 dogs. In the latter case

the rhythmic alterations disappeared when the dose of hexamethonium was

increased by more than 1mg (Fig. 13).


A slight increase in the amount of seminal emission secreted by continuous

hypogastric nerve stimulation was obtained after the administration of DMPP, and

a slight decrease in the amount of seminal emission was noted after the administ

ration of hexamethonium.

DISCUSSION

It has been well known that "ejaculation" consists of two factors, secretion

of semen into the posterior urethra (seminal emission) and rhythmic ejections of

semen from the posterior urethra to outside of the body (ejaculation). In the

previous papers (Kimura 1971, Kimura 1972) it was reported that the rise of the


2) Effect of DMPP and hexamethonium on rise and rhythmic alterations of the

posterior urethral pressure.

Fig. 12. Effects of ganglion stimulant and ganglion blocker on posterior urethrogram.


DMPP caused a slight transient rise in the posterior urethral pressure irrespective of

application of hypogastric nerve stimulation. The agent did not induce rhythmic

alterations in the pressure when the pressure was raised to near the maximum level.

In this dog the rhythmic alterations were abolished by 100ƒÊg of hexamethonium.

Chart speed: 0.83mm/sec.

Fig. 13. Effects of ganglion stimulant and ganglion blocker.H.N.S.: hypogastric nerve stimulation.In some dogs it required hexamethonium in the doses of 1 mg and upward to abolish

the rhythmic alterations of the posterior urethral pressure. Chart speed: 0.83mm/sec (timer 1 cycle/min).

pressure in the posterior urethra by continuous hypogastric nerve stimulation indicated seminal emission, and that the rhythmic alterations, which occurred when the pressure reached the maximum level, were identical with the pressure changes in the posterior urethra during ejaculation in actual coitus.

In the present experiments seminal emission was induced by bilateral electric stimulation of the hypogastric nerve and the measurement of the posterior urethral pressure was performed with the method reported previously (Kimura 1971). The intra-aortic administration of the drugs used in the present experiments reduced the systemic effects of the drugs to minimum.

It has been shown that both the cholinergic and adrenergic innervations are


present in the internal male sexual organs of the dog, such as the prostatic

gland, vas deferens and epididymis (S)ostrand 1965, Sasaki 1971). Farrell and

Lyman (1937) and Ochiai (1953) showed that sympathomimetic drugs had

secretogogue effect on the prostatic gland in dogs, and that sympatholytic drugs

had depressing effect on prostatic secretion . Recently, Smith and his co-worker

(Smith 1967, Smith 1968, Smith and Lebeaux 1970) insisted that in dogs the

prostatic secretion was mediated through a cholinergic mechanism. The reports

which concern the receptor mechanisms in the vas deferens and epididymis of the

dog are very scanty. Based on the reports in the other mammals it can be

presumed that the ƒ¿- and ƒÀ-adrenergic and. cholinergic receptors are present inn

these organs of the dog.

In this study administration of both phenylephrine and methoxamine, a-

stimulants, considerably increased the amount of seminal emission caused by

hypogastric nerve stimulation and induced the rhythmic alterations of the

posterior urethral pressure. In accord with this, phentolamine and phenoxybenza

mine, ƒ¿-blockers, were found to depress seminal emission caused by hypogastric

nerve stimulation and to abolish the rhythmic alterations. These results clearly

indicate that an ƒ¿-adrenergic mechanism is involved in both seminal emission and

ejaculation.

In contrast, seminal emission and rhythmic alterations in the posterior

urethral pressure caused by hypogastric nerve stimulation were not affected by

isoproterenol, a pure ƒÀ-stimulant, or by propranolol, a ƒÀ-blocker. Consequently,

it seems unlikely that the ƒÀ-receptor plays an important role in both seminal

emission and ejaculation.

The results obtained by use of acetylcholine and atropine lead us to the

conclusion that seminal emission and ejaculation are not predominantly under

the influence of the cholinergic receptor mechanism. The reasons are as follows :

(1) The changes in seminal emission after the administration of acetylcholine was

so small as compared with those obtained with ƒ¿-stimulants and ƒ¿-blockers. (2)

Only an uncertain result on the rhythmic alterations was obtained by administra

tion of acetylcholine or atropine.

Smith and Lebeaux (1970) and Smith and Ilievski (1969) reported the

presence of the synapse in the hypogastric nerve and near or within the internal

sexual organs of the dog. However, in the present study the effect of DMPP and

hexamethonium on seminal emission and ejaculation were not so clear as those of

a-stimulants and ƒ¿-blockers. Therefore, it appears that in dogs the majority of

the nerve fibers which concern seminal emission and ejaculation may not change

neurons near or within the target organs.

Acknowledgment

We wish to express our gratitude to Prof. Sentaro Shishito, our director, and Profs.

Koroku Hashimoto and Norio Taira of Department of Pharmacology and Department

of Experimental Therapeutics, Tohoku University School of Medicine for their suggestions

throughout the experiments and in the preparation of the manuscript.


References

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adrenergic mechanisms in the guinea-pig. isolated nerve vas deferens preparation.

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2) Endo, M. (1965) Analysis of the adrenergic receptive mechanism of mouse seminal

vesicle. Bull. Osaka med. Sch., 11, 73-78.

3) Farrell, J.I. & Lyman, Y. (1937) A study of the secretory nerves of, and the action

of certain drugs on, the prostate gland. Amer. J. Physiol., 118, 64-70.

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The Role of Alpha-adrenergic Receptor Mechanism in ... - JST