Article date: February 1980
By: K.P. KLUGMAN, F. LEMBECK, S. MARKOWITZ, G. MITCHELL, C. ROSENDORFF in Volume 71, Issue 2, pages 623-629
Hypothalamic blood flow (HBF) was measured in conscious rabbits by the 133xenon washout technique.
Substance P in a dose of 50 or 500 ng increases HBF while 5 ng is without effect.
Cholinoceptor blockade, with either atropine or mecamylamine abolishes the vasodilator effect of substance P.
Chemical sympathectomy of the hypothalamus with 6‐hydroxydopamine, or adrenoceptor blockade with either propranolol or phenoxybenzamine abolishes the effect of substance P on HBF.
Destruction of the intracerebral noradrenergic pathway (INP), or blockade of its vasodilator action, with barbiturate or bicarbonate, likewise prevent the vasodilator action of substance P.
These results suggest that substance P may cause an increase in HBF via the release of endogenous acetylcholine, which in turn stimulates the INP.
Hypothalamic blood flow (HBF) was measured in conscious rabbits by the 133xenon washout technique.
Substance P in a dose of 50 or 500 ng increases HBF while 5 ng is without effect.
Cholinoceptor blockade, with either atropine or mecamylamine abolishes the vasodilator effect of substance P.
Chemical sympathectomy of the hypothalamus with 6‐hydroxydopamine, or adrenoceptor blockade with either propranolol or phenoxybenzamine abolishes the effect of substance P on HBF.
Destruction of the intracerebral noradrenergic pathway (INP), or blockade of its vasodilator action, with barbiturate or bicarbonate, likewise prevent the vasodilator action of substance P.
These results suggest that substance P may cause an increase in HBF via the release of endogenous acetylcholine, which in turn stimulates the INP.
DOI: 10.1111/j.1476-5381.1980.tb10982.x
View this article