For Research Use Only. VIP is intended exclusively for in vitro and preclinical research. It is not approved for human use, is not a drug, and should never be administered to humans or to animals outside of an authorized research protocol.
VIP and the Respiratory System
The respiratory system is a major site of VIP biology, with high expression of VIP-containing nerve fibers throughout the airways and high expression of VPAC1 receptors on multiple cell types in the lungs. VIP-containing nerves innervate airway smooth muscle, submucosal glands, blood vessels, and other structures in the respiratory tract, providing the basis for VIP signaling at multiple sites within the lungs.
The recognition of VIP as a respiratory neuropeptide came shortly after its original isolation in the 1970s. Subsequent research characterized the role of VIP in the regulation of airway tone, in the modulation of inflammatory responses in the lungs, and in various other respiratory functions in research models. The lung research base on VIP is one of the more developed areas of the broader VIP literature.
For more on the receptor pharmacology that underlies these pulmonary effects, see our companion article on VIP receptor research and VPAC1/VPAC2 signaling in research models.
VIP and Airway Smooth Muscle
Airway smooth muscle tone is one of the major regulators of airflow through the lungs, and the modulation of airway smooth muscle is a central topic in pulmonary research. VIP has been characterized as a potent bronchodilator in research models, producing relaxation of airway smooth muscle through VPAC1 receptor activation on these cells.
The mechanism of VIP-induced bronchodilation involves VPAC1 activation, downstream cyclic AMP signaling, and protein kinase A-mediated relaxation of airway smooth muscle. This mechanism is analogous to the bronchodilator effects of beta-adrenergic agonists, which also work through cyclic AMP elevation, but VIP acts through a different receptor system. The complementary nature of these mechanisms has been one of the topics of interest in pulmonary research.
Research on VIP and airway smooth muscle has used isolated tracheal preparations, lung slice methods, and whole-animal pulmonary function measurements to characterize the bronchodilator effects of VIP in research models. The published findings consistently support potent and reproducible bronchodilation, making VIP one of the more well characterized non-adrenergic bronchodilators in research literature.
VIP and Pulmonary Inflammation
Beyond its effects on airway smooth muscle, VIP has been studied for its effects on inflammation in the respiratory tract. The lungs contain multiple immune cell populations including alveolar macrophages, lymphocytes, and other inflammatory cells, all of which can express VPAC receptors and respond to VIP signaling. The published findings generally support anti-inflammatory effects of VIP in pulmonary research models, consistent with the broader anti-inflammatory profile of VIP discussed in our companion article on VIP neuroinflammation research and animal model studies.
Studies have used various rodent models of pulmonary inflammation to characterize VIP effects, including LPS-induced lung inflammation, asthma research models with allergen challenge, and other inflammation protocols. The findings include reductions in inflammatory cell infiltration, reductions in pro-inflammatory cytokine production in lung tissue, and improvements in functional pulmonary endpoints in some models.
The combined effects of VIP on airway smooth muscle (bronchodilation) and on pulmonary inflammation (anti-inflammatory) provide a coordinated profile in respiratory research models that has made VIP one of the more conceptually interesting peptides in pulmonary research.
VIP in Asthma Research Models
Asthma research models are one of the more common contexts for studying VIP effects in the respiratory system. These models typically involve sensitization with an allergen followed by challenge protocols that produce airway hyperresponsiveness, inflammatory cell infiltration, and other features characteristic of asthma. VIP has been studied in these models for its effects on multiple endpoints, including airway hyperresponsiveness measurements, inflammatory cell counts in bronchoalveolar lavage fluid, and lung tissue histology.
The published findings generally support beneficial effects of VIP in asthma research models, with reductions in airway hyperresponsiveness, inflammatory cell infiltration, and tissue inflammation. The mechanism involves the combined bronchodilator and anti-inflammatory effects of VIP, both mediated by VPAC1 signaling on the relevant cell types.
These asthma model findings have made VIP a useful research tool for studying neuropeptide modulation of airway disease in animal models. The convergence of bronchodilator and anti-inflammatory effects in a single peptide is one of the features that distinguishes VIP from purely bronchodilator or purely anti-inflammatory tools.
VIP and Pulmonary Vascular Effects
The pulmonary vasculature is another site where VIP has been studied in respiratory research. VIP-containing nerves innervate pulmonary blood vessels, and VPAC receptors are expressed on pulmonary vascular smooth muscle. VIP has been characterized as a potent pulmonary vasodilator in research models, producing relaxation of pulmonary vascular smooth muscle through receptor activation and downstream cyclic AMP signaling.
The pulmonary vasodilator effects of VIP have been studied in research models of pulmonary hypertension and in normal pulmonary vasculature. The mechanism is similar to the airway smooth muscle effects, involving VPAC receptor activation and cyclic AMP-mediated smooth muscle relaxation. The combination of airway and vascular effects in the lung makes VIP a particularly interesting research tool for studies of pulmonary biology.