Pharmacology and Physiology of Perivascular Nerves Regulating Vascular Function

Abstract

ABSTRACT-Maintenance of blood pressure is mostly dependent on sympathetic "tone", and the sympathetic nerve innervates the entire vascular bed, excepting the capillaries. Although norepinephrine (NE) is the principal neurotransmitter released upon sympathetic nerve stimulation, neuropeptide Y and ATP are cotransmitters in various vascular tissues. In addition, dopamine and epinephrine, as well as acetylcholine, have been shown to be sympathetic neurotransmitters in specific vasculatures. Transmitter NE release is modified by a number of endogenous substances including the transmitter itself. Chronic denervation of the preganglionic fiber induces an increase in NE release per pulse, indicating postganglionic neuronal supersensitivity. So far, three main adrenoceptor types have been shown, =1, =2 and > , each of which is further divided into at least three subtypes, as well as the = 1L-adrenoceptor, a phenotype of the cloned = 1a-adrenoceptor, in the blood vessel. Thus, the response of vessels with different receptor types to a transmitter varies quantitatively and even qualitatively from one vessel to another. The remarkable diversity in the sympathetic innervation mechanism in the vascular system may play an important role in regional variations in the regulation of blood flow. The sympathetic nerve also exerts long-term trophic action on the blood vessel. In conclusion, the sympathetic nervous system plays an important role not only in the regulation of cardiovascular dynamics but in the maintenance of the vessel structure, as well.

Genetic Ablation of Ca V 3.2 Channels Enhances the Arterial Myogenic Response by Modulating the RyR-BK Ca Axis

“…Perhaps, the loss of smooth muscle feedback in Ca V 3.2 −/− arteries is compensated by enhanced dilatory feedback from the endothelium. Other functional compensation may have occurred in this global knockout independent of vascular smooth muscle 29 ; in this context, establishing a smooth muscle–specific Ca V 3.2 knockout model would be valuable. It should also be recognized that for the proposed Ca V 3.2/RyR/BK Ca feedback mechanism to effectively drive a blood pressure response, it should be ideally present in a full range of vascular beds.…”

Molecular Targets of Antihypertensive Peptides: Understanding the Mechanisms of Action Based on the Pathophysiology of Hypertension

“…Sympathetic nervous system stimulates the release of catecholamines (norepinephrine and epinephrine) from postganglionic neurons [ 78 ]. The release of catecholamines activates the hypertrophic growth of cardiomyocytes [ 79 ].…”

“…The release of renin subsequently activates RAS and results in increased blood pressure through the production of Ang II ( Figure 3 ). Ang IAng II also amplifies the response of the sympathetic nervous system by a peripheral mechanism, that is, pre-synaptic facilitatory modulation of norepinephrine release [ 77 , 78 ]. Additionally, ROS and ET-1 may also stimulate the sympathetic activity and its effects on the vasculature [ 78 , 80 ].…”

ECM-Based Materials in Cardiovascular Applications: Inherent Healing Potential and Augmentation of Native Regenerative Processes

“…The release of neurotransmitter and chemical signalling occurs in small enlargements along the nerve fibres. Nerve stimulation can elicit different responses, in terms of type and amplitude, at different areas of the vascular system [234,235]. Neurogenic vasocontrol can thus follow different patterns depending on which molecules are released and what local reactions they trigger.…”