An investigation of an autonomic innervation of the vertebral artery using monoamine histofluorescence.

Blood flow to the hindbrain, via the paired vertebral arteries, must be uncompromised for adequate neurological functioning of its vital centres. Therefore, it would seem unlikely that the intracranial vertebral artery would need to vasoconstrict, thus reducing its blood flow. In order to investigate the existence and location of a noradrenaline-mediated constrictor mechanism in the wall of the intracranial vertebral artery, transverse sections of ten baboon and ten monkey vessels were stained with sucrose-potassium phosphate-glyoxylic acid (counterstained with malachite-green). This method allows the visualisation of catecholaminergic nerves when the sections are exposed to ultraviolet light. In this study of primate vascular tissue, however, none of the monkey or baboon vertebral artery sections showed the presence of noradrenergic nerves in the tunica media - tunica adventitia junction or penetrating the tunica media of the arteries. These findings indicate that the intracranial vertebral artery does not have a neurogenic vasomotor function in primates.

Weakness of sympathetic neural control of human pial compared with superficial temporal arteries reflects low innervation density and poor sympathetic responsiveness.

BACKGROUND AND PURPOSE: The primary goal of these studies was to understand and investigate the capacity of perivascular nerves to influence the tone of human pial arteries and to compare them with other human cephalic arteries, the superficial temporal and middle meningeal. METHODS: Responses to electrical activation of intramural nerves and related features of fresh segments of human cephalic arteries-the pial (PA; 478+/-34 microm ID), middle meningeal (MMA; 540+/-41 microm ID), and superficial temporal (STA; 639+/-49 microm ID)-obtained from patients aged 15 to 82 years during surgical procedures were studied on a resistance artery myograph. RESULTS: The PA segment responses to electrical nerve activation and to norepinephrine (NE; 10[-5] mol/L) were 1% and 21% of tissue maximum, respectively, compared with 6% and 34% for the MMA and 14% and 90% for the STA. Tissue maximum was defined as the force increase to 127 mmol/L KCl plus arginine vasopressin (1 microm). All arteries dilated well to acetylcholine. Possible explanations for the PA marginal neurogenic responses were assessed. NE ED50 was 5.4+/-2.2 X 10(-7) mol/L and did not vary with age or diameter. NE responsiveness did not increase in vessels with spontaneous or raised potassium-induced tone. Relaxation to isoproterenol was variable and propranolol did not increase the neurogenic response. Neither N(G)-monomethyl-L-arginine, N(G)-nitro-L-arginine methyl ester, endothelium removal, nor indomethacin consistently influenced the contractions to NE or neurogenic reactivity. The weak PA neurogenic response is in keeping with its poor innervation. As determined by catecholamine histofluorescence, innervation in the PA is sparse, with density increasing in the order PA, MMA, and STA. The incidence of nerve structures in the PA adventitio-medial junction was only 3% of those in the STA, and these were situated more than 3 microm from the closest smooth muscle cell. CONCLUSIONS: We conclude that the weak neurogenic response of adult human pial artery reflects its poor innervation and responsiveness to NE, implying that these features are not important in the regulation of its diameter.

Vascular innervation in atherogenesis.

Although collar-induced atherosclerosis continues to be used as an investigative tool, the underlying mechanism has not been established. Two primary mechanisms suggested are adventitial ischemia due to reduction in vasa vasorum, and perivascular denervation. We have examined the effect of injuring the common carotid artery in the pattern produced by the ends of a silastic collar, and have correlated the effect on innervation with change in intima/media ratios in normal and cholesterol-fed rabbits. The serum cholesterol of cholesterol-fed rabbits was significantly elevated by 10 days following initiation of cholesterol feeding, and further elevated at 21 days. No structural difference was detected between the uninjured carotid arteries of control and cholesterol-fed rabbits. At the site of injury in freeze injured carotid arteries there was a thickening of the intima which was increased in cholesterol-fed rabbits. The intima at the site of injury was composed of lipid-laden cells embedded in a matrix of collagen and elastin fibres. In carotid artery segments, between two sites of freeze injury, denervation was established by immunohistochemistry and electron microscopy. The denervated segments were not morphologically different from uninjured carotid arteries in either control or cholesterol-fed rabbits. While injury induced intimal thickening and foam cell development, denervation did not. It is concluded that perivascular denervation is a consequence of silastic collar application and is not involved in the induction of atherosclerosis.