The effects of chronic alterations in plasma
adrenaline levels, on the development of a raised blood pressure in young spontaneously hypertensive (SHR) rats, have been investigated. Bilateral adrenal demedullation (at 4 weeks) significantly reduced plasma
adrenaline levels and attenuated the development of
hypertension. Pressor responses to
phenylephrine (0.3-10 micrograms, i.v.), measured in the pithed animals 11 weeks after demedullation, were unaffected although neurogenic pressor responses were significantly reduced. Subcutaneous implants of
procaterol and
salbutamol (0.005 and 0.165 mumol/kg, respectively) restored
hypertension development in demedullated rats and significantly enhanced neurogenic pressor responses, while responses to i.v.
phenylephrine remained unaltered, in the pithed rats. Implants of
adrenaline (0.165 and 0.5 mumol/kg, s.c.) also restored
hypertension development. However, pressor responses to
phenylephrine were reduced and neurogenic responses only slightly enhanced when compared to those obtained in untreated pithed demedullated rats. The pro-hypertensive effect of
adrenaline (0.5 mumol/kg, s.c.) was abolished by treatment with the beta 2-adrenoreceptor selective antagonist
ICI 118551 (25 mg/kg/day, p.o.). In the subsequently pithed rats, neurogenic pressor responses were slightly reduced when compared to those in animals treated with
adrenaline alone. In control demedullated rats,
ICI 118551 had no effect on blood pressure nor on the neurogenic and
phenylephrine-induced pressor responses. However, in
sham-operated animals,
ICI 118551 attenuated the development of
hypertension and significantly reduced neurogenic pressor responses in the subsequently pithed rats. Responses to
phenylephrine remained unaltered. The results support the suggestion that a beta 2-adrenoreceptor-mediated facilitation of sympathetic neurotransmission may be involved in mediating the pro-hypertensive effects of circulating
adrenaline in the SHR rat.