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Pneumadins (PNM) is a decapeptide originally isolated from the lungs of mammals and exerts an effective antidiuretic effect by stimulating the release of arginine vasopressin (AVP). PNM is present in the bronchial mucosa and is discharged into the lumen. The presence of PNM was found in the cerebral cortex, thyroid gland, adrenal gland, and pyloric sinus of the stomach. In addition to the release of AVP, PNM is also able to increase the plasma concentrations of atrial natriuretic peptide and aldosterone. Acute administration of very low concentrations (<4 nmol) of PNM stimulates the large pituitary-adrenal axis, which acts on the secretory activity of the intramedullary CRH/ACTH and AVP systems, resulting in the release of corticosterone and aldosterone. In addition, PNM may participate in the regulation of respiratory physiology during life after birth and may regulate the growth of thymocytes.
Mechanism of action
Pneumadins can cause rapid and significant antidiuretic effects and reduce Na+ and Cl- excretion in the body without altering mean arterial pressure, right atrial pressure, heart rate or hematocrit. In addition, PNM can activate PLC and IP3 through specific receptors to increase [Ca2+]i in vivo. PNM causes a rapid increase in [Ca2+]i in a concentration-dependent manner similar to other Gq receptor agonists. The increase in IP3 level is consistent with the trend of [Ca2+]i increase, which varies with the change of PNM. When PNM is higher than 5nM, both IP3 and [Ca2+]i elevation decrease in a concentration-dependent manner. Thus, PN can participate in the vasoconstriction response, which contributes to an increase in VSM tone and/or vascular hypertrophy.
Application of Pneumadins
PNM can act as a normal regulatory substance in the human body. Because of its promotion of [Ca2+]i, PNM can have a significant direct vascular effect in the presence of elevated glucocorticoid levels and can be applied to Cushing's syndrome or for glucocorticoid therapy. Since PNM can alter circulating AVP levels, injection of PNM can cause antidiuretic effects.
1. Batra, V. K., Mathur, M., Mir, S. A., Kapoor, R., & Kumar, M. A. (1990). Pneumadin: a new lung peptide which triggers antidiuresis. Regulatory peptides, 30(2), 77-87.
2. Batra, V. K., Hopfner, R. L., Gopalakrishnan, V., & McNeill, J. R. (1999). Pneumadin-evoked intracellular free Ca2+ responses in rat aortic smooth muscle cells: effect of dexamethasone. Biochemical pharmacology, 58(1), 177-182.