Neurogenic contraction and relaxation of human penile deep dorsal vein

Abstract

1 The aim of the present study was to characterize neurogenic and pharmacological responses of human penile deep dorsal vein and to determine whether the responses are mediated by nitric oxide from neural or endothelial origin. 2 Ring segments of human penile deep dorsal vein were obtained from 22 multiorgan donors during procurement of organs for transplantation. The rings were suspended in organ bath chambers for isometric recording of tension. We then studied the contractile and relaxant responses to electrical ®eld stimulation and to vasoactive agents. 3 Electrical ®eld stimulation (0.5 ± 2 Hz) and noradrenaline (3610 710 ± 3610 75 M) caused frequencyand concentration-dependent contractions that were of greater magnitude in veins denuded of endothelium. The inhibitor of nitric oxide synthesis N G -nitro-L-arginine methyl ester hydrochloride (L-NAME, 10 74 M) increased the adrenergic responses only in rings with endothelium. 4 In preparations contracted with noradrenaline in the presence of guanethidine (10 76 M) and atropine (10 76 M), electrical stimulation induced frequency-dependent relaxations. This neurogenic relaxation was prevented by L-NAME, methylene blue (3610 75 M) and tetrodotoxin (10 76 M), but was una ected by removal of endothelium. 5 Acetylcholine (10 78 ± 3610 75 M) and substance P (3610 711 ± 3610 77 M) induced endotheliumdependent relaxations. In contrast, sodium nitroprusside (10 79 ± 3610 75 M) and papaverine (10 78 ± 3610 75 M) caused endothelium-independent relaxations. 6 The results provide functional evidence that the human penile deep dorsal vein is an active component of the penile vascular resistance through the release of nitric oxide from both neural and endothelial origin. Dysfunction in any of these sources of nitric oxide should be considered in some forms of impotence.

Modulation of Noradrenergic Neurotransmission in Isolated Rat Radial Artery

“…However, enhancement of adrenergic contraction seems to require the presence of an intact endothelial cell layer since L-NOARG did not affect the contraction of endotheliumdenuded radial arteries. In line with the present results, endothelial-derived NO attenuates adrenergic vasoconstriction in human gastroepiploic arteries and penile veins (10,11). Thus, neuronal NO is not likely to be involved in this potentiation.…”

Physiological regulation of penile arteries and veins

“…Numerous NOS nerve fibers and a marked NOmediated neurogenic vasodilatation similar to that of penile arteries has also been reported for the human deep dorsal vein, 14,58 which probably allows the vessel to accommodate the expansion of the CCs during erection. In contrast, no nitrergic relaxation was found in human circumflex veins, 62 which is consistent with the scarcity of NOS fibers 58 and suggests that a passive compression by engorgement of cavernous spaces rather than active neurogenic mechanisms is responsible for variations of venous outflow in the smaller penile veins.…”

“…In contrast, no nitrergic relaxation was found in human circumflex veins, 62 which is consistent with the scarcity of NOS fibers 58 and suggests that a passive compression by engorgement of cavernous spaces rather than active neurogenic mechanisms is responsible for variations of venous outflow in the smaller penile veins. 14,62 The contribution of the different isoforms of NOS to penile erection has been a subject of debate, specially because erectile function and mating behavior are preserved in mice lacking the genes for eNOS and nNOS. 63,64 This was initially ascribed to a compensatory upregulation of eNOS to compensate for insufficient nNOS expression in mice lacking nNOS.…”

“…9,10 In addition to this mechanical restriction of the venous outflow, there is an active regulation of venous resistance, and several vasoconstrictor and vasodilator stimuli can regulate penile venous tone to the same extent as arterial and cavernous smooth muscle. [11][12][13][14][15][16][17] The active control of penile veins probably accommodates blood flow from the penis to the hemodynamic changes that take place in the CC during erection and detumescence.…”

Immunohistochemical and functional evidence for a noradrenergic regulation in the horse penile deep dorsal vein

“…Penile veins seem to be regulated by both vasoconstrictor and vasodilator agents to the same degree as arterial smooth muscle. 16,17 The neurogenic and pharmacological responses of the deep dorsal and circumflex veins, which are the main venous drainage from the corpus cavernosum, may represent an active component of the penile vascular bed during the processes of detumescence and erection. The fact that in horse deep penile dorsal vein, electrical field stimulation-evoked contractions were abolished by the blockers of the noradrenergic transmission and neuronal sodium channels, guanethidine and tetrodotoxin, respectively, and reduced by the a 1 -and a 2 -receptor antagonist, prazosin and rauwolscine, respectively, indicates that neurogenic contractions are associated with the release of noradrenaline from noradrenergic nerves acting on a 1 -and a 2 -adrenoceptors.…”