Erection and NO override the vasoconstrictive effect of α-adrenergic stimulation in the rat penile vasculature

C. J. Wingard, Ronald W Lewis, T. M. Mills

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Studies in this laboratory are designed to determine the effects of vasoconstrictor agents on the erectile response in rats. We have previously demonstrated that the vasoconstrictor effect of endothelin-1 (ET-1) is sharply reduced by erection and by nitric oxide (NO) administration. The present study was performed to determine if vasoconstriction, resulting from aα-adrenergic stimulation, is altered by erection and NO. During continuous monitoring of corpus cavernosum pressure (CCP) and mean arterial pressure (MAP), erection was induced by electrical stimulation of the autonomic ganglion for the innervation of the penis. When the α-adrenergic agonist methoxamine (METH, 10 μg/kg) was injected before erection (ie, into the non-erect penis), the subsequent erectile response (CCP/MAP) was significantly reduced from 0.68 ± 0.03 before METH to 0.34 ± 0.08 after METH. Injection of METH into the erect penis (ie, during erection) reduced the vasoconstrictor action of METH; CCP/MAP was 0.74 ± 0.02 before METH and 0.55 ± 0.05 after METH (P < 0.05). The vasoconstrictor action of METH was slightly reduced when given in conjunction with NOR-1, a NO donor drug; CCP/MAP was 0.70 ± 0.05 before METH, 0.55 ± 0.09 after METH but this change was not significant. These results demonstrate that the response to α-adrenergic stimulation is attenuated during erection in response to ganglionic stimulation. Furthermore, it appears that NO, produced during erection, may serve to override agonist-induced vasoconstriction. These results support our hypothesis that NO acts to directly stimulate relaxation of cavernous smooth muscle and to inhibit the vasoconstrictor actions of agents like ET-1 and α-adrenergic agonists including norepinephrine.

Original languageEnglish (US)
Pages (from-to)212-220
Number of pages9
JournalInternational Journal of Impotence Research
Volume13
Issue number4
DOIs
StatePublished - Aug 25 2001

Fingerprint

Vasoconstrictor Agents
Adrenergic Agents
Nitric Oxide
Penis
Arterial Pressure
Pressure
Adrenergic Agonists
Endothelin-1
Vasoconstriction
Autonomic Ganglia
Methoxamine
Nitric Oxide Donors
Electric Stimulation
Smooth Muscle
Norepinephrine
Injections
Pharmaceutical Preparations

Keywords

  • Erectile dysfunction, smooth muscle
  • NO
  • α-adrenergic vasoconstriction

ASJC Scopus subject areas

  • Urology

Cite this

Erection and NO override the vasoconstrictive effect of α-adrenergic stimulation in the rat penile vasculature. / Wingard, C. J.; Lewis, Ronald W; Mills, T. M.

In: International Journal of Impotence Research, Vol. 13, No. 4, 25.08.2001, p. 212-220.

Research output: Contribution to journalArticle

@article{2b622582463c45788e3aef427e922cee,
title = "Erection and NO override the vasoconstrictive effect of α-adrenergic stimulation in the rat penile vasculature",
abstract = "Studies in this laboratory are designed to determine the effects of vasoconstrictor agents on the erectile response in rats. We have previously demonstrated that the vasoconstrictor effect of endothelin-1 (ET-1) is sharply reduced by erection and by nitric oxide (NO) administration. The present study was performed to determine if vasoconstriction, resulting from aα-adrenergic stimulation, is altered by erection and NO. During continuous monitoring of corpus cavernosum pressure (CCP) and mean arterial pressure (MAP), erection was induced by electrical stimulation of the autonomic ganglion for the innervation of the penis. When the α-adrenergic agonist methoxamine (METH, 10 μg/kg) was injected before erection (ie, into the non-erect penis), the subsequent erectile response (CCP/MAP) was significantly reduced from 0.68 ± 0.03 before METH to 0.34 ± 0.08 after METH. Injection of METH into the erect penis (ie, during erection) reduced the vasoconstrictor action of METH; CCP/MAP was 0.74 ± 0.02 before METH and 0.55 ± 0.05 after METH (P < 0.05). The vasoconstrictor action of METH was slightly reduced when given in conjunction with NOR-1, a NO donor drug; CCP/MAP was 0.70 ± 0.05 before METH, 0.55 ± 0.09 after METH but this change was not significant. These results demonstrate that the response to α-adrenergic stimulation is attenuated during erection in response to ganglionic stimulation. Furthermore, it appears that NO, produced during erection, may serve to override agonist-induced vasoconstriction. These results support our hypothesis that NO acts to directly stimulate relaxation of cavernous smooth muscle and to inhibit the vasoconstrictor actions of agents like ET-1 and α-adrenergic agonists including norepinephrine.",
keywords = "Erectile dysfunction, smooth muscle, NO, α-adrenergic vasoconstriction",
author = "Wingard, {C. J.} and Lewis, {Ronald W} and Mills, {T. M.}",
year = "2001",
month = "8",
day = "25",
doi = "10.1038/sj.ijir.3900688",
language = "English (US)",
volume = "13",
pages = "212--220",
journal = "International Journal of Impotence Research",
issn = "0955-9930",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - Erection and NO override the vasoconstrictive effect of α-adrenergic stimulation in the rat penile vasculature

AU - Wingard, C. J.

AU - Lewis, Ronald W

AU - Mills, T. M.

PY - 2001/8/25

Y1 - 2001/8/25

N2 - Studies in this laboratory are designed to determine the effects of vasoconstrictor agents on the erectile response in rats. We have previously demonstrated that the vasoconstrictor effect of endothelin-1 (ET-1) is sharply reduced by erection and by nitric oxide (NO) administration. The present study was performed to determine if vasoconstriction, resulting from aα-adrenergic stimulation, is altered by erection and NO. During continuous monitoring of corpus cavernosum pressure (CCP) and mean arterial pressure (MAP), erection was induced by electrical stimulation of the autonomic ganglion for the innervation of the penis. When the α-adrenergic agonist methoxamine (METH, 10 μg/kg) was injected before erection (ie, into the non-erect penis), the subsequent erectile response (CCP/MAP) was significantly reduced from 0.68 ± 0.03 before METH to 0.34 ± 0.08 after METH. Injection of METH into the erect penis (ie, during erection) reduced the vasoconstrictor action of METH; CCP/MAP was 0.74 ± 0.02 before METH and 0.55 ± 0.05 after METH (P < 0.05). The vasoconstrictor action of METH was slightly reduced when given in conjunction with NOR-1, a NO donor drug; CCP/MAP was 0.70 ± 0.05 before METH, 0.55 ± 0.09 after METH but this change was not significant. These results demonstrate that the response to α-adrenergic stimulation is attenuated during erection in response to ganglionic stimulation. Furthermore, it appears that NO, produced during erection, may serve to override agonist-induced vasoconstriction. These results support our hypothesis that NO acts to directly stimulate relaxation of cavernous smooth muscle and to inhibit the vasoconstrictor actions of agents like ET-1 and α-adrenergic agonists including norepinephrine.

AB - Studies in this laboratory are designed to determine the effects of vasoconstrictor agents on the erectile response in rats. We have previously demonstrated that the vasoconstrictor effect of endothelin-1 (ET-1) is sharply reduced by erection and by nitric oxide (NO) administration. The present study was performed to determine if vasoconstriction, resulting from aα-adrenergic stimulation, is altered by erection and NO. During continuous monitoring of corpus cavernosum pressure (CCP) and mean arterial pressure (MAP), erection was induced by electrical stimulation of the autonomic ganglion for the innervation of the penis. When the α-adrenergic agonist methoxamine (METH, 10 μg/kg) was injected before erection (ie, into the non-erect penis), the subsequent erectile response (CCP/MAP) was significantly reduced from 0.68 ± 0.03 before METH to 0.34 ± 0.08 after METH. Injection of METH into the erect penis (ie, during erection) reduced the vasoconstrictor action of METH; CCP/MAP was 0.74 ± 0.02 before METH and 0.55 ± 0.05 after METH (P < 0.05). The vasoconstrictor action of METH was slightly reduced when given in conjunction with NOR-1, a NO donor drug; CCP/MAP was 0.70 ± 0.05 before METH, 0.55 ± 0.09 after METH but this change was not significant. These results demonstrate that the response to α-adrenergic stimulation is attenuated during erection in response to ganglionic stimulation. Furthermore, it appears that NO, produced during erection, may serve to override agonist-induced vasoconstriction. These results support our hypothesis that NO acts to directly stimulate relaxation of cavernous smooth muscle and to inhibit the vasoconstrictor actions of agents like ET-1 and α-adrenergic agonists including norepinephrine.

KW - Erectile dysfunction, smooth muscle

KW - NO

KW - α-adrenergic vasoconstriction

UR - http://www.scopus.com/inward/record.url?scp=0034884487&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034884487&partnerID=8YFLogxK

U2 - 10.1038/sj.ijir.3900688

DO - 10.1038/sj.ijir.3900688

M3 - Article

C2 - 11494078

AN - SCOPUS:0034884487

VL - 13

SP - 212

EP - 220

JO - International Journal of Impotence Research

JF - International Journal of Impotence Research

SN - 0955-9930

IS - 4

ER -