Recovery of erectile function after brief aggressive antihypertensive therapy

Taben Hale, H. Okabe, T. L. Bushfield, J. P W Heaton, M. A. Adams

Research output: Contribution to journalArticle

71 Citations (Scopus)

Abstract

Purpose: We have previously demonstrated that antihypertensive therapy could structurally modulate blood vessels in the penis, although the impact on erectile function was not established. Given the importance of inadequate penile arterial inflow as a cause of erectile dysfunction we determined in spontaneously hypertensive rats the impact of brief aggressive antihypertensive therapy on structurally based penile vascular resistance, erectile function and mean arterial pressure during and after treatment. Materials and Methods: Young (15-week-old) and aged (40-week-old) spontaneously hypertensive rats were treated for 2 weeks (enalapril 30 mg./kg. daily plus a low salt diet). Mean arterial pressure was continuously monitored via radio telemetry. Erectile responses were assessed by administering apomorphine (80 μg./kg. subcutaneously) before, during and after treatment. Structurally based vascular resistance was determined in the isolated, perfused penile vasculature 2 weeks after stopping treatment in aged spontaneously hypertensive rats. Certain responses were determined, including resistance at maximum dilatation (lumen size) and at maximum constriction (medial bulk), and EC50 of the α-adrenoceptor agonist methoxamine. Results: In the period after the cessation of drug treatment there was a persistent reduction in the level of arterial pressure (16%) and a doubling of erectile responses compared with pretreatment. Cardiac and vascular structure regressed, as determined by the mean decrease plus or minus standard deviation in vascular resistance at maximum dilatation (21% ± 4.5%) and mean reduction in left ventricle mass (10.4% ± 3.7%). Furthermore, treatment induced a significant right shift in α1-adrenoceptor concentration response curve in treated versus control rats (mean EC50 1.09 ± 0.111 versus 0.76 ± 0.111). Conclusions: The improvement in erectile function after brief aggressive treatment may be related to improvement in structurally based vascular resistance within the penis and the decrease in responsiveness of α1-adrenoceptor mediated erectolytic signaling. These findings are suggestive of a new therapeutic strategy for hypertension and erectile dysfunction.

Original languageEnglish (US)
Pages (from-to)348-354
Number of pages7
JournalJournal of Urology
Volume168
Issue number1
StatePublished - 2002
Externally publishedYes

Fingerprint

Recovery of Function
Antihypertensive Agents
Vascular Resistance
Inbred SHR Rats
Adrenergic Receptors
Arterial Pressure
Penis
Erectile Dysfunction
Therapeutics
Blood Vessels
Dilatation
Methoxamine
Sodium-Restricted Diet
Telemetry
Withholding Treatment
Enalapril
Apomorphine
Radio
Constriction
Heart Ventricles

Keywords

  • Antihypertensive agents
  • Hypertension
  • Impotence
  • Penis
  • Rats, inbred SHR

ASJC Scopus subject areas

  • Urology

Cite this

Hale, T., Okabe, H., Bushfield, T. L., Heaton, J. P. W., & Adams, M. A. (2002). Recovery of erectile function after brief aggressive antihypertensive therapy. Journal of Urology, 168(1), 348-354.

Recovery of erectile function after brief aggressive antihypertensive therapy. / Hale, Taben; Okabe, H.; Bushfield, T. L.; Heaton, J. P W; Adams, M. A.

In: Journal of Urology, Vol. 168, No. 1, 2002, p. 348-354.

Research output: Contribution to journalArticle

Hale, T, Okabe, H, Bushfield, TL, Heaton, JPW & Adams, MA 2002, 'Recovery of erectile function after brief aggressive antihypertensive therapy', Journal of Urology, vol. 168, no. 1, pp. 348-354.
Hale T, Okabe H, Bushfield TL, Heaton JPW, Adams MA. Recovery of erectile function after brief aggressive antihypertensive therapy. Journal of Urology. 2002;168(1):348-354.
Hale, Taben ; Okabe, H. ; Bushfield, T. L. ; Heaton, J. P W ; Adams, M. A. / Recovery of erectile function after brief aggressive antihypertensive therapy. In: Journal of Urology. 2002 ; Vol. 168, No. 1. pp. 348-354.
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AB - Purpose: We have previously demonstrated that antihypertensive therapy could structurally modulate blood vessels in the penis, although the impact on erectile function was not established. Given the importance of inadequate penile arterial inflow as a cause of erectile dysfunction we determined in spontaneously hypertensive rats the impact of brief aggressive antihypertensive therapy on structurally based penile vascular resistance, erectile function and mean arterial pressure during and after treatment. Materials and Methods: Young (15-week-old) and aged (40-week-old) spontaneously hypertensive rats were treated for 2 weeks (enalapril 30 mg./kg. daily plus a low salt diet). Mean arterial pressure was continuously monitored via radio telemetry. Erectile responses were assessed by administering apomorphine (80 μg./kg. subcutaneously) before, during and after treatment. Structurally based vascular resistance was determined in the isolated, perfused penile vasculature 2 weeks after stopping treatment in aged spontaneously hypertensive rats. Certain responses were determined, including resistance at maximum dilatation (lumen size) and at maximum constriction (medial bulk), and EC50 of the α-adrenoceptor agonist methoxamine. Results: In the period after the cessation of drug treatment there was a persistent reduction in the level of arterial pressure (16%) and a doubling of erectile responses compared with pretreatment. Cardiac and vascular structure regressed, as determined by the mean decrease plus or minus standard deviation in vascular resistance at maximum dilatation (21% ± 4.5%) and mean reduction in left ventricle mass (10.4% ± 3.7%). Furthermore, treatment induced a significant right shift in α1-adrenoceptor concentration response curve in treated versus control rats (mean EC50 1.09 ± 0.111 versus 0.76 ± 0.111). Conclusions: The improvement in erectile function after brief aggressive treatment may be related to improvement in structurally based vascular resistance within the penis and the decrease in responsiveness of α1-adrenoceptor mediated erectolytic signaling. These findings are suggestive of a new therapeutic strategy for hypertension and erectile dysfunction.

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