PubMed · 34915
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E Milroy. 1979. Pharmacological management of common urodynamic problems.. https://pubmed.ncbi.nlm.nih.gov/34915/
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The Authors examine the antihypertensive effectiveness of the beta-adrenergic receptor blocking agents, according to their personal experience and a review of the bibliography. It is not cleared yet how these drugs reach their hypotensive effect. It is reasonable to assume however that several factors are involved: cardiac output, intravascular volume changes, plasma renin activity and peripheral resistance. Thirty patients suffering from essential hypertension not complicated by cardiac or renale failure were treated. Patients were allocated at random into one of three subsets of ten. In group A oxprenolol was given for 8 weeks and the dose was gradually increased up to 300 mgs daily. Oxprenolol was administered in combination with clortalidone in group B and with phentolamine in group C. A clinically satisfactory reduction in blood pressure was attained in no subset, despite the significant decrease of mean blood pressure. The blockade of beta-adrenergic receptors alone has proved to be less effective than the combined administration of oxprenolol and clortalidone or of oxprenolol and phentolamine. No differences were observed between the two combinations.
The depolarization (15 mM K+)-induced release of 3H-NA from superfused rat brain synaptosomes and the effects of alpha-noradrenergic drugs thereon were studied. Noradrenaline (NA; in the presence of the uptake inhibitor desipramine) reduced synaptosomal 3H-NA release. Reduction of the concentration of calcium ions in the medium during K+ stimulation greatly enhanced the sensitivity of 3H-NA release to alpha-receptor-mediated inhibition. Under these conditions NA dose-dependently inhibited 3H-NA release from synaptosomes obtained from cortex or hypothalamus, but did not affect 3H-NA release from striatal (i.e dopaminergic) synaptosomes. Adrenaline, clonidine and oxymetazoline potently inhibited 3H-NA release from cortex synaptosomes at concentrations in the nanomolar range. Phentolamine by itself did not affect synaptosomal 3H-NA release, but antagonized the inhibitory effects of both noradrenaline and adrenaline. The data obtained further substantiate the hypothesis that the alpha-receptors mediating a local negative feedback control of NA release are localized on the varicosities of central noradrenergic neurons, Furthermore, noradrenergic nerve terminals in the hypothalamus appear to be less senstive to alpha-receptor-mediated presynaptic inhibition than those in the cortex.
A variety of alpha-adrenergic agonists encompassing a broad range of concentrations were used to investigate the existence and nature of a putative alpha-adrenergic mechanism inhibitory to renin release, which may operate at the level of the juxtaglomerular apparatus. For this purpose rat renal cortical tissue incubated in vitro was used. Concentrations of noradrenaline, adrenaline and methoxamine of 10(-6), 10(-5), 10(-4) and 10(-3) M caused significant dose-related inhibition of renin release. The inhibition of release by these doses was reversed completely by 10(-4) M phentolamine. In contrast, phenylephrine, oxymetazoline and clonidine did not inhibit renin release. The results support the concept of an alpha-adrenergic mechanism inhibitory to renin release and show that high concentrations of alpha-adrenergic agonist are required for its operation in vitro. The manner in which this inhibitory mechanism affects renin release under physiological circumstances remains to be demonstrated.