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Vascular norepinephrine regulation in hypertension
Frontiers ira Catecholamine Research
vii
in cholinergic neuronal activity, ACh turnover and in the appearance of parkinsonian symptoms . If such a link between DA and ACh' neurons existed in the limbic system which has been proposed to be involved in the antipsychotic action of neuroleptic drugs - it could be speculated that this action is connected with the activation of cholinergic neurons by blockade of DA receptors. However, the neuroleptics do not modify the ACh liberation from the perfused nucleus accumbens septi of the cat - the area of the limbic system with the most dense DA network - although they markedly enhance the DA turnover in that region . This suggests that (1) a .cholinergio-dopaminergic connection similar to that in the striatum is not present in the limbic system ; (2) the antipsychotic effect of neuroleptics may not be mediated by cholinergic neurons. The latter is supported by the observation that anticholinergic compounds ameliorate the parkinsoniaa symptoms induced by neuroleptics without diminishing the antipsychotic action of these drugs. VASCULAR NOREPIIVEPHRINE REDULATION IIV HYPERTENSION Barry Berkowitz, Trajko Trajkov, James Tarver and Sydney Spector floche Institute of Molecular Biology, Pharmacology Section, Nutley, New Jereey 07110, U .S .A .
The role of the sympathetic nervous system as a causative factor in hyper tension remains controversial. However, it well accepted that many antihypertetisive drugs lower blood pressure by influencing the disposition or synthesis of the norepinephrine of sympathetic neurons in the vasculature. We have examined the influence of hypertension on the en zymes of catecholamine metabolism in the blood vessels as well as the heart in order to determine whether during the course of this disease there are endogenous homeostatic controls capable of influencing cardiovascular, vascular catecholamine disposition. In the spontaneously hypertensioe rats there is a decrease in the activities of tyrosine hydroxylase, as well as dopamine-~i-hydroxylase in the mesenteric artery whereas the activity of the degradative enzyme catechol-O-methyl trans ferase was elevated . We have also examine another hypertensioe model, the uniniphrectomized deoxycorticosterone-salt treated rat. In this specie, tyrosine hydroxylase activity is also diminished and the activity of catechol-O-methyl transferase is increased. Thus in these hypertensioe animals the enzymes of catecholamine metabolism appear to change in a direction to diminish synthesis of norepinephriae and accelerate catabolism at the vascular level.
vii
in cholinergic neuronal activity, ACh turnover and in the appearance of parkinsonian symptoms . If such a link between DA and ACh' neurons existed in the limbic system which has been proposed to be involved in the antipsychotic action of neuroleptic drugs - it could be speculated that this action is connected with the activation of cholinergic neurons by blockade of DA receptors. However, the neuroleptics do not modify the ACh liberation from the perfused nucleus accumbens septi of the cat - the area of the limbic system with the most dense DA network - although they markedly enhance the DA turnover in that region . This suggests that (1) a .cholinergio-dopaminergic connection similar to that in the striatum is not present in the limbic system ; (2) the antipsychotic effect of neuroleptics may not be mediated by cholinergic neurons. The latter is supported by the observation that anticholinergic compounds ameliorate the parkinsoniaa symptoms induced by neuroleptics without diminishing the antipsychotic action of these drugs. VASCULAR NOREPIIVEPHRINE REDULATION IIV HYPERTENSION Barry Berkowitz, Trajko Trajkov, James Tarver and Sydney Spector floche Institute of Molecular Biology, Pharmacology Section, Nutley, New Jereey 07110, U .S .A .
The role of the sympathetic nervous system as a causative factor in hyper tension remains controversial. However, it well accepted that many antihypertetisive drugs lower blood pressure by influencing the disposition or synthesis of the norepinephrine of sympathetic neurons in the vasculature. We have examined the influence of hypertension on the en zymes of catecholamine metabolism in the blood vessels as well as the heart in order to determine whether during the course of this disease there are endogenous homeostatic controls capable of influencing cardiovascular, vascular catecholamine disposition. In the spontaneously hypertensioe rats there is a decrease in the activities of tyrosine hydroxylase, as well as dopamine-~i-hydroxylase in the mesenteric artery whereas the activity of the degradative enzyme catechol-O-methyl trans ferase was elevated . We have also examine another hypertensioe model, the uniniphrectomized deoxycorticosterone-salt treated rat. In this specie, tyrosine hydroxylase activity is also diminished and the activity of catechol-O-methyl transferase is increased. Thus in these hypertensioe animals the enzymes of catecholamine metabolism appear to change in a direction to diminish synthesis of norepinephriae and accelerate catabolism at the vascular level.