Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
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Query: UMLS:C1832526 (
PCC
)
5,967
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Specific receptor antagonists were used to examine the role of
endothelin-1
(
ET-1
) in the erectile response of the rat. In these studies, intact rats were cannulated to permit the continuous recording of mean arterial pressure (MAP) and intracavernosal pressure (
CCP
). Erection was induced by electrical stimulation of the autonomic ganglion, which regulates blood flow to the penis. The animals were subjected to intracavernosal injection with vehicle only (Cont) or with an antagonist to the endothelin-A receptor (ET(A)) or to the endothelin-B receptor (ET(B)). Blockade of the ET(A) or the ET(B) had no effect on the erectile response (
CCP
/MAP) during maximal ganglionic stimulation. When
ET-1
was injected into Cont rats, there was a marked vasoconstriction with a sharp rise in MAP and a decline in
CCP
as the cavernosal arterioles constricted and limited inflow. The injection of the ET(A) antagonist prevented the vasoconstriction after
ET-1
injection into Cont rats, whereas blockade of the ET(B) had no effect on the vasoconstrictive effect to
ET-1
. Similar results were obtained during submaximal ganglionic stimulation. With minimal levels of ganglionic stimulation,
ET-1
injection led to a moderated degree of vasodilation in the presence of the ET(A) antagonist. The ET(B) antagonist failed to alter the
CCP
response during minimal stimulation, but it did have a marked effect on the MAP response to
ET-1
injection. The results of these studies confirm that cavernosal tissue of the rat penis is highly responsive to
ET-1
. However, the failure of the
ET-1
antagonists to affect penile erection in response to ganglionic stimulation reflects a minimal role of
ET-1
in the erectile response in the rat.
...
PMID:Receptor-specific influence of endothelin-1 in the erectile response of the rat. 1089 60
Recent evidence indicates that
endothelin-1
(
ET-1
) might be a principal vasoconstrictor in the penis. We report that
ET-1
injection into the cavernous sinuses before erection sharply reduced the magnitude of subsequent erections. Corpus cavernosum pressure-to-mean arterial pressure ratios (
CCP
/MAP), with maximal ganglionic stimulation, were 0.62 +/- 0.05 before
ET-1
injection and 0.31 +/- 0.05 after, indicating that
ET-1
acted as a vasoconstrictor. When
ET-1
was injected during a maximal neurally induced erection, the ability of
ET-1
to attenuate subsequent erections was diminished (
CCP
/MAP 0.75 +/- 0.02 before
ET-1
, 0.61 +/- 0.03 after). At submaximal stimulation voltages, injection of
ET-1
during erection also attenuated its vasoconstrictive effect. Similarly, when
ET-1
was injected during erection induced by intracavernosal injection of the nitric oxide (NO) donor NOR-1, subsequent erections were not significantly suppressed (
CCP
/MAP 0.53 +/- 0.04 before
ET-1
, 0.45 +/- 0.04 after). These findings that
ET-1
-induced vasoconstriction is attenuated during erection are consistent with the hypothesis that NO mediates erection both by initiating pathways that cause smooth muscle relaxation and by inhibiting the vasoconstrictive actions of
ET-1
.
...
PMID:Endothelin-1-induced vasoconstriction is inhibited during erection in rats. 1144 50
