Abstract
Penile erection (PE) is a hemodynamic event that results from a neuroendocrine process, and it is influenced by the cardiovascular status of the patient. However, it may also modulate an individual’s cardiovascular events. The present study provides the mechanisms involved in the association of PE and cardiovascular function. Erection upsurges the cardiac rate, blood pressure, and oxygen uptake. Sex-enhancing strategies, such as phosphodiesterase inhibitors, alprostadil, and testosterone also promote vasodilatation and cardiac performance, thus preventing myocardial infarction. More so, drugs that are used in the treatment of hypertensive heart diseases (such as angiotensin system inhibitors and β-blockers) facilitate vasodilatation and PE. These associations have been linked with nitric oxide- and testosterone-dependent enhancing effects on the vascular endothelium. In addition, impaired cardiovascular function may negatively impact PE; therefore, impaired PE may be a pointer to cardiovascular pathology. Hence, evaluation of the cardiovascular status of an individual with erectile dysfunction (ED) is essential. Also, employing strategies that are used in maintaining optimal cardiac function may be useful in the management of ED.
Authors’ contributions
Conceptualization and design: ARE. Funding acquisition: ABA, HAS, and ARE. Investigation: ABA, HAS, and ARE. Methodology: ARE. Project administration: ABA, HAS, and ARE. Supervision: ARE. Validation: ARE. Writing-original draft: ABA, HAS, and ARE. Writing-review and editing and final approval: ABA, HAS, and ARE.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The data used to support the findings of the present study are available from the corresponding author upon request.