The
arteriolar vasodilation induced by minoxidil activates the peripheral sympathetic nervous system (SNS) via carotid and aortic baroreceptor reflexes. In tandem with activation of the SNS, both the pulse rate and cardiac output increase (11,12). Minoxidil administration evokes an increase in plasma renin activity, largely due to activation of the SNS (13-15). The activation of the renin-angiotensin axis elicits an increase in plasma and urinary aldosterone levels (13-15). As well as, minoxidil possesses alpha-adrenoceptor agonist activity in addition to potassium-channel opening activity (16). As a part of erection biology, the peripheral nervous system helps transmit the central impulses to the end organ.
Sympathetic pathways generally provide inhibitory impulses,
whereas parasympathetic and somatic innervation is
pro-erectogenic,
the most important component responsible for penile erection is the corpus cavernosum;
smooth muscle relaxation within this tissue is the endpoint of all stimuli resulting in an erection, Alpha-adrenergic agents induce smooth muscle contraction and result in DE tumescence (17). Antagonism of alpha-adrenergic signaling
enables other independent relaxatory pathways to predominate within the penile trabecular smooth muscle (18). Allergic dermatitis which manifested by the patient as itchy and burning scalp, which is seen on examination as an erythematous and scratched scalp, leads to increase in absorption of topical minoxidil systematically. This increase
in absorption leads to low blood pressure values manifested as dizziness.
Because of arteriolar vasodilatation caused by absorbed minoxidil and the direct adrenergic effect of minoxidil; sympathetic system activated. Sympathetic system activation flagged by chest tightness and racing heart also
led to corpus cavernosum smooth muscle
contraction and result in DE tumescence. In the patient reported here, the absence of organic and psychological cause of erectile dysfunction, and the indirect effect on minoxidil.