The effect of hypertonic saline administration or stalk transection on histamine and histamine N-methyltransferase in the rat posterior pituitary

• Published in: Agents and Actions 1986-08, Vol.18 (5-6), p.494-498
• Main Authors: Verburg, K M, Bowsher, R R, Zerbe, R L, Henry, D P
• Format: Article
• Language: English
• Subjects: Animals; Arginine Vasopressin - metabolism; Histamine N-Methyltransferase - metabolism; Histamine Release - drug effects; Kinetics; Male; Methyltransferases - metabolism; Pituitary Gland - drug effects; Pituitary Gland - enzymology; Pituitary Gland - physiology; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic - pharmacology; Sodium Chloride - pharmacology
• ISSN: 0065-4299; 1420-908X
• DOI: 10.1007/BF01964952

There is evidence to suggest that histamine is a neurotransmitter in the CNS and functions in the regulation of arg-vasopressin (AVP) secretion. The posterior pituitary contains high levels of histamine and histamine N-methyltransferase (HNMT). Therefore, posterior pituitary histamine could also modulate the release of AVP. Paralleling the effect on AVP levels, the concentration of histamine in the rat posterior pituitary decreased from 18.8 +/- 2.7 ng/mg protein (x +/- SEM) to 12.9 +/- 1.9 ng/mg protein following 2 days of 2% (w/v) hypertonic saline administration and to 11.5 +/- 0.9 ng/mg protein with 7 days of treatment. Conversely, posterior pituitary HNMT activity was significantly elevated after hypertonic saline administration. Pituitary stalk transection did not reduce the concentration of histamine in the rat posterior pituitary although HNMT activity was reduced from 18.8 +/- 0.82 munits/gland to 9.22 +/- 1.56 munits/gland (x +/- SEM). These results indicate that histamine released from posterior pituitary mast cells could facilitate AVP release as part of the overall mechanism for osmotic stimulation of AVP secretion and support the concept that most posterior pituitary histamine is not neuronally derived from the brain. HNMT, on the other hand, may be contained in neurons disrupted by stalk section.