Regulation of tone in penile cavernous smooth muscle. Established concepts and new findings.
Since Benson, in 1983, reported on a potent nonadrenergic, noncholinergic (NANC) transmitter postulated to relax penile vessels and the corpus cavernosum, much new information on the mechanisms of contraction and relaxation of corporeal smooth muscle and penile vasculature has been obtained. The information currently available suggests that NANC transmitters may be involved in both contractile and relaxant responses of penile erectile tissues. There is good experimental evidence to allow the assumption that neurogenic nitric oxide (NO) is a mediator of penile erection, but even if NO probably is the most important factor for relaxation of penile vessels and the corpus cavernosum, this does not exclude the possibility that other agents released from nerves may have a modulatory function in this process. However, the roles of, for example, vasoactive intestinal polypeptide and related peptides as neurotransmitters and/or neuromodulators in the nervous control of penile erection have yet to be established. The restricted availability of human penile erectile tissues has led to the use of cavernous tissue and penile vessels from animals, both for screening and for detailed analysis of mechanisms previously demonstrated to exist also in human tissues. When interpreting the results obtained, it is important to stress that there may be important differences between human and animal tissues, that each of the tissues only gives a piece of information on the complex process of penile erection, and that the physiological and clinical importance of results from such experiments may be limited. The differing responses in different parts of the vasculature within the penis and the multiplicity of putative transmitters present in the corpus cavernosum and in perivascular nerves make further investigations necessary, as do the interactions between transmitters and neuromodulators at the neuromuscular junction, and between the neural and endothelial control of vascular tone.
Andersson
K E
KE
Department of Clinical Pharmacology, Lund University Hospital, Sweden.
Holmquist
F
F
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology / Q000502:physiology; D015740:Calcitonin Gene-Related Peptide / Q000494:pharmacology / Q000502:physiology; D016232:Endothelins / Q000494:pharmacology / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D006632:Histamine / Q000494:pharmacology / Q000502:physiology; D006801:Humans; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000098:blood supply / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology; D009478:Neuropeptide Y / Q000494:pharmacology / Q000502:physiology; D009569:Nitric Oxide / Q000494:pharmacology / Q000502:physiology; D010410:Penile Erection / Q000187:drug effects / Q000502:physiology; D010413:Penis / Q000098:blood supply / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D011453:Prostaglandins / Q000494:pharmacology / Q000502:physiology; D013373:Substance P / Q000494:pharmacology / Q000502:physiology; D009435:Synaptic Transmission; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology / Q000502:physiology
D016232:Endothelins; D009478:Neuropeptide Y; D011453:Prostaglandins; D001127:Arginine Vasopressin; D009569:Nitric Oxide; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D006632:Histamine; D000255:Adenosine Triphosphate; D015740:Calcitonin Gene-Related Peptide