Viprostol [(dl)-15-deoxy-16-hydroxy-16(alpha/beta)-vinyl-
prostaglandin E2 methyl ester; CL 115 347] is a new orally and transdermally active
antihypertensive agent that exerts its major
antihypertensive action by vasodilation. The present studies were conducted to examine its effects on the
adrenergic nervous system. In cats,
viprostol did not inhibit renal sympathetic nerve discharge (RSND) monitored at the postganglionic region, indicating that nerve transmission or conduction was not blocked at the
ganglion or the pre- or postganglionic fibres. In cat nictitating membrane preparations in situ,
viprostol partially blocked the membrane contractile response to exogenous
epinephrine and
norepinephrine, as well as to electrical stimulation of pre- and postganglionic fibres. In spontaneously hypertensive rats (SHR),
viprostol partially blocked the vasopressor response of exogenous
norepinephrine and
epinephrine specifically without influencing that of
angiotensin II. All these suggest that
viprostol produced weak alpha-
adrenoceptor blockade.
Viprostol did not antagonize the
tachycardia induced by stimulation of the discrete segments at C7-T1 (cardio-accelerator) of the spinal cord in pithed SHR, suggesting that
viprostol did not activate the presynaptic alpha-
adrenoceptors.
Viprostol significantly inhibited the increase in blood pressure induced by electrical stimulation of the spinal cord at T7-T9 in pithed SHR, probably due to postsynaptic alpha-
adrenoceptor blockade. In conclusion,
viprostol produced weak, but statistically significant alpha-
adrenoceptor blockade which may contribute partially to its
antihypertensive action.