scholarly journals Are the Vascular Effects of Naloxone Attributable to the Preservatives Methyl- and Propylparaben?

1983 ◽  
Vol 3 (3) ◽  
pp. 395-398 ◽  
Author(s):  
Lennart Brandt ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt ◽  
Bengt Ljunggren ◽  
John D. Pickard
Keyword(s):  
Cerebrospinal Fluid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Rapid Onset ◽  
Vascular Effects ◽  
Prostaglandin F

In vitro, the Nalonee® preparation of naloxone caused a concentration-dependent relaxation of human pial cortical arteries contracted by potassium, noradrenaline, serotonin, prostaglandin F2α (PGF2α), and haemorrhagic cerebrospinal fluid, or inhibited contractions elicited by these agents. However, the preservatives in the Nalonee preparation, methyl- and propylparaben, had similar effects. Pure naloxone alone had no effect on potassium or PGF2α-induced contractions. It is suggested that the relaxant effects on vascular smooth muscle of Nalonee can be attributed to the alkylparabens rather than to naloxone. The pronounced relaxations induced by the alkylparabens had a rapid onset, and they were stable and could easily be cleared after rinsing.

Effects of the β-Receptor Antagonists Propranolol, Oxprenolol and Labetalol on Human Vascular Smooth-Muscle Contraction

1978 ◽  
Vol 55 (3) ◽  
pp. 235-240
Author(s):  
R. F. W. Moulds ◽  
R. A. Jauernig ◽  
J. D. Hobson ◽  
J. Shaw
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Barium Chloride ◽  
Smooth Muscle Contraction ◽  
Hypotensive Activity ◽  
Inhibitory Effects ◽  
Vascular Effects ◽  
High Concentrations ◽  
Β Receptor

1. Spiral strips of human digital arteries have been studied in vitro to investigate whether dl-propranolol, d-propranolol, oxprenolol and labetalol have peripheral vascular effects in man. 2. Labetalol was a potent inhibitor of contractile responses to noradrenaline, but had less effect on responses to 5-hydroxytryptamine and barium chloride. 3. dl-and d-propranolol were equally effective inhibitors of responses to barium chloride. They were only weak antagonists of noradrenaline responses, but stronger, non-competitive antagonists of 5-hydroxytryptamine responses. 4. Oxprenolol was only a weak inhibitor of the responses to both noradrenaline and 5-hydroxytryptamine and had little effect on responses to barium chloride. 5. It is concluded that labetalol has specific α-adrenoreceptor-blocking properties, which are probably relevant to its therapeutic action in man. Propranolol has non-specific inhibitory effects on vascular smooth muscle, which might contribute to its hypotensive activity at high concentrations, but oxprenolol has only slight peripheral effects that are probably therapeutically insignificant.

Vascular effects of some opioid receptor agonists

1991 ◽  
Vol 69 (6) ◽  
pp. 846-851 ◽  
Author(s):  
T. Y. El-Sharkawy ◽  
M. F. Al-Shireida ◽  
C. W. T. Pilcher
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Endogenous Opioids ◽  
Vascular Effects ◽  
High Potassium ◽  
Opioid Agonists ◽  
Low Concentrations ◽  
Prostaglandin F ◽  
High Concentrations ◽  
High Doses

Opioid peptides have been implicated in shock-associated hypotension. Our aim was to find out whether opioid agonists have direct vasodilator actions on vascular smooth muscle. The study was conducted on rat abdominal aortic rings. In rings precontracted with either norepinephrine, prostaglandin F2α, or high potassium Krebs (HPK), the effects of the opioid agonists tested (morphine, U50488H, ethylketocyclazocine (EKC), and bremazocine) depended on the precontracting agent used. HPK-precontracted rings were relaxed by all agonists tested. In norepinephrine-precontracted rings, all caused contraction at low concentrations and relaxation at high concentrations except bremazocine, which caused only relaxation. In prostaglandin F2α-precontracted rings, U50488H produced contraction at low concentrations and relaxation at high concentrations while EKC caused only relaxation and morphine or bremazocine caused only contraction. All relaxant responses were endothelium-independent and were antagonized by verapamil but not by a number of antagonists including naloxone, MR2266, propranolol, diphenhydramine, cimetidine, and indomethacin. They may reflect calcium channel blockade. Morphine-induced vasoconstriction was antagonized by high concentrations of naloxone or mepyramine and may be due to release of histamine by a naloxone-sensitive mechanism. We conclude that (a) the opioid agonists tested exert direct actions on vascular smooth muscle; (b) the nature of the response depended not only on the agonist used and its concentration but also on the agent used to precontract the tissue; and (c) it is unlikely that direct actions of endogenous opioids contribute to the shock-associated hypotension because high doses were needed to elicit them.Key words: vascular smooth muscle, opioids, neurohormonal peptides, circulatory shock.

scholarly journals Effects of Hyperglycemia on Vascular Smooth Muscle Ca2+Signaling

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Nahed El-Najjar ◽  
Rashmi P. Kulkarni ◽  
Nancy Nader ◽  
Rawad Hodeify ◽  
Khaled Machaca
Keyword(s):  
Insulin Resistance ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Vascular Smooth Muscle ◽  
Complex Disease ◽  
Prolonged Exposure ◽  
In Vitro System ◽  
A7r5 Cells

Diabetes is a complex disease that is characterized with hyperglycemia, dyslipidemia, and insulin resistance. These pathologies are associated with significant cardiovascular implications that affect both the macro- and microvasculature. It is therefore important to understand the effects of various pathologies associated with diabetes on the vasculature. Here we directly test the effects of hyperglycemia on vascular smooth muscle (VSM) Ca2+signaling in an isolated in vitro system using the A7r5 rat aortic cell line as a model. We find that prolonged exposure of A7r5 cells to hyperglycemia (weeks) is associated with changes to Ca2+signaling, including most prominently an inhibition of the passive ER Ca2+leak and the sarcoplasmic reticulum Ca2+-ATPase (SERCA). To translate these findings to the in vivo condition, we used primary VSM cells from normal and diabetic subjects and find that only the inhibition of the ER Ca2+leaks replicates in cells from diabetic donors. These results show that prolonged hyperglycemia in isolation alters the Ca2+signaling machinery in VSM cells. However, these alterations are not readily translatable to the whole organism situation where alterations to the Ca2+signaling machinery are different.

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