Penile erection is a part of the human male sexual response, involving desire, excitation (erection), orgasm (ejaculation), and resolution, and autonomic nerves are involved in all phases. Autonomic innervation of smooth-muscle cells of the erectile tissue is provided by the cavernous nerve. Motor and sensory innervation is derived from the pudendal nerves and their terminal branches, that is, the dorsal nerves of the penis, which carry impulses from receptors harbored in the penile skin, prepuce, and glans. Erection begins with an increased flow in the pudendal arteries and dilatation of the cavernous arteries and helicine arterioles in association with relaxation of the smooth muscles of the trabecular network, causing engorgement of blood in the corpora. This leads to compression of subtunical venules by the resistant tunica albuginea and erection. During detumescence these events are reversed.
Mohammed H. Abdulla and Edward J. Johns
A potential role for the renal innervation was first described in 1859 by Claude Bernard, who observed an increase in urine flow following section of the greater splanchnic nerve, which included the renal nerves. Subsequent studies provided little further clarity, leading Homer Smith in 1951 to declare that the renal innervation had little or no significance in controlling kidney hemodynamic or excretory function. However, since the 1960s, there has been increased attention to how the renal nerves may contribute to the deranged control of blood pressure and heart function cardiovascular diseases. The efferent (sympathetic) nerves have neuroeffector junctions which provide close contact with all vascular and tubular elements of the kidney. Activation of the sympathetic nerves at the resistance vessels, that is, the interlobular arteries afferent and even arterioles, modulates both renal blood flow and glomerular filtration rate; at the juxtaglomerular granular cells, they cause renin release and subsequent angiotensin II generation, and at the tubules there is a neurally stimulated increase in epithelial cell sodium transport. Less is known of the role of the afferent nerves, which primarily innervate the renal pelvis, and to a lesser degree the cortex and medulla. Their role is uncertain but sensory information passing to the brain can influence renal efferent nerve activity, forming the basis of both inhibitory and excitatory reno-renal reflexes. Increasingly, it is perceived that in a range of cardiovascular diseases such as cardiac failure, chronic renal disease, and hypertension, there is an inappropriate sympatho-excitation related to alterations in afferent renal nerve activity, which exacerbates the disease progression. The importance of the renal innervation in these disease processes has been emphasized in clinical studies where renal denervation in humans has been found to reduce blood pressure in resistant hypertensive patients and to ameliorate the progression of cardiac and kidney diseases, diabetes, and obesity and hypertension. The importance of both systemic and renal inflammatory responses in activating the neurohumoral control of the kidney is a continuing source of investigation.